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EFFECTS OF LOW-INTENSITY EXERCISE CONDITIONING ON BLOOD PRESSURE, HEART RATE, RATE-PRESSURE-PRODUCT AND CARDIAC AUTONOMIC FUNCTION IN HYPERTENSIVE WOMEN by CATHERINE LINDSAY BAINES A thesis submitted to the School of Nursing in conformity with the requirements for the degree of Master of Science Queen‘s University Kingston, Ontario, Canada September 2008 Copyright © Catherine Lindsay Baines, 2008 ii ABSTRACT The effects of a twelve-week low-intensity exercise conditioning program on blood pressure (BP), heart rate (HR), rate-pressure-product (RPP) and cardiac autonomic function were examined in menopausal and post menopausal women with hypertension. Eligible participants (n=50) were counterbalanced to either the exercise group or the control group. Using a pretest-posttest design, participants were tested at the beginning and the end of the 12-week study period, in which BP, HR, RPP, heart rate variability and spontaneous baroreflex sensitivity were measured at rest and during standing and low intensity steady-state exercise. The exercise group participated in a 12-week, lowintensity walking program, 5 days/week, while the comparison group continued with usual activity. The exercise group adhered to 4 walking sessions per week while the control group averaged 0.6 walking sessions per week. Repeated measures analysis of variance (ANOVA) demonstrated a reduction in systolic and diastolic BP and RPP in hypertensive women. Additionally, the low intensity exercise conditioning program attenuated the physiological response to stress (standing, exercise). This was evidenced by decreased systolic and diastolic BP and RPP in the exercise group and increased diastolic BP in the control group. Postmenopausal women demonstrated decreased log transformed high frequency power and total power in comparison to menopausal women. However, postmenopausal women also showed decreased low frequency power in comparison to menopausal women. It was concluded that a 12-week, low-intensity exercise conditioning program reduced systolic and diastolic BP and RPP in hypertensive women while attenuating their physiological responses to stress. iii ACKNOWLEDGEMENT I would like to express my sincere gratitude to Dr Ann Brown for her guidance and support throughout this project. Ann, I truly appreciate the time you spent helping me develop my skills as a researcher; your supervision and attention to detail has allowed me to gain a solid foundation for my career in research to be built upon. This project could not have been accomplished without the patience and dedication of Dr Sylvia Hains. Sylvia, thank you for your teaching in statistics; you‘re help was invaluable. The success of this study is also credited to my committee; Dr Barbara Kisilevsky and Dr Richard Birtwhistle. Thank you for donating your time, knowledge and experience to this endeavor. I am most grateful to the women who participated in this study. Their dedication and unwavering will to walk through all of natures elements enabled our pursuit of knowledge. Many women came from far and wide and sacrificed their time and energy in the spirit of true volunteerism. On a more personal note, I would like to thank my family for believing in me throughout my academic career. I would not be enjoying all of my successes without their perseverance. I am greatly appreciative to my classmates and close friends whose friendship and support carried me through the last two years. And last but certainly not least, my boyfriend Craig, thank you for your savvy computer skills in addition to your continuous love and support. iv TABLE OF CONTENTS Abstract……………………….…………………………………………………………...ii Acknowledgement……………………………………………………………………..…iii Table of Contents…………………………………………………………………………iv List of Tables…………………………………………………………………………....viii List of Figures………………………………………………………………………….....ix List of Abbreviations…………………………………………………………………….xii CHAPTER ONE Introduction………………………………………………………………………..1 CHAPTER TWO Literature Review……………………………………………………………………….…3 Cardiovascular Disease……………………………………………………………3 Hypertension……………………………………………………………………....3 Regulation of Heart Rate and Blood Pressure…………………………………….5 Autonomic Regulation of Heart Rate……………………………………………..7 Heart Rate Variability……………………………………………………………..8 Measurement of Heart Rate Variability…………………………………………...9 Arterial Baroreflex……………………………………………………………….12 Measurement of Arterial Baroreflex……………………………………………..13 Physiological Factors Which Effect Cardiac Autonomic Function.......................16 v Hypertension……………………………………………………………..16 Aging……………………………………………………………………..18 Gender……………………………………………………………………19 Menopause……………………………………………………………….20 Body Posture……………………………………………………………..21 Respiratory Rate…………………………………………….……………22 Antihypertensive Medications…………………………………………...25 Acute Exercise…………………………………………………………...26 Effects of Exercise Conditioning on the Cardiac Autonomic Nervous System....27 Relevant Work by Other Investigators at Queen‘s University………………..…30 Exercise Adherence……………………………………………………………...32 Rationale and Hypothesis……………………………………………………..…34 Rationale………………………………………………………………....34 Hypothesis………………………………………………………………..35 CHAPTER THREE Method…………………………………………………………………………...36 Participants……………………………………………………………….36 Equipment and Instruments……………………………………………...38 Procedure………………………………………………………………...42 Data Analysis…………………………………………………………….47 Analysis of Heart Rate Variability……………………………….47 Analysis of Baroreflex Sensitivity……………………………….48 Statistical Analysis……………………………………………………….49 vi CHAPTER FOUR Results……………………………………………………………………………51 Demographic, Physiological and Lifestyle Measures……………………51 Antihypertensive Medications…………………………………………...53 BpTRU Blood Pressure and Heart Rate Measures over Time…………...54 BpTRU Systolic Blood Pressure…………………………………54 BpTRU Diastolic Blood Pressure………………………………..56 BpTRU Heart Rate……………………………………………….58 BpTRU RPP……………………………………………………...59 Comparison of Body Mass Index and Waist Circumference over Time...62 Heart Rate Variability Measures…………………………………………63 Low Frequency Power…………………………………………...65 High Frequency Power………………………………………..…67 Total Power………………………………………………………69 PNS Indicator…………………………………………………….70 SNS Indicator…………………………………………………….72 Baroreflex Measures…………………………………………………..…76 Baroreflex Slope…………………………………………………78 Systolic Finapres Arterial Blood Pressure……………………….79 R-R Interval……………………………………………………...81 Exercise Compliance…………………………………………………….84 CHAPTER FIVE Discussion………………………………………………………………………..85 Conclusions………………………………………………………………94 vii REFERENCES…………………………………………………………………………..96 APPENDIX A Research Information Consent Form…………………………...131 APPENDIX B Physical Activity Readiness Questionnaire………...…………..135 APPENDIX C Measuring Your Pulse and Your Target Heart Rate……………137 APPENDIX D Borg‘s Rating of Perceived Exertion Scale…………………….138 APPENDIX E Walking Protocol……………………………………………….139 APPENDIX F Exercise Log……………………………………………………140 APPENDIX G Activity Log…………………………………………………….141 APPENDIX H Study Advertisement……………………………………………142 APPENDIX I Demographic and Data Form…………………………………...143 APPENDIX J Editing Heart Rate Variability Data…………………………….144 APPENDIX K Editing Spontaneous Baroreflex Sensitivity Data………………146 APPENDIX L Means (±SD) for BpTRU Systolic and Diastolic Blood Pressure, Heart Rate and Rate-Pressure-Product in Both Control and Exercise Group at Week 1 and Week 12 .……………………...147 APPENDIX M Means (±SD) for Log Transformed Heart Rate Variability Measures for Both Control and Exercise Group at Week 1 and Week 12 ………………………………………………………..148 APPENDIX N Means (±SD) for Spontaneous Baroreflex Measures for Both Control and Exercise Group at Week 1 and Week 12………….150 APPENDIX O Summary of Study Sample and Reasons for Attrition………….151 APPENDIX P Other Demographic Data at Baseline Testing………………….152 APPENDIX Q Chi-squared/ANOVA Summary Tables……………..…………153 viii LIST OF TABLES Table 1 Means (±SD) for demographic, physiological and lifestyle measures at week 1……………………………………………………………………52 Table 2 Antihypertensive medication classification……………………………...53 Table 3 Means (±SD) for log transformed heart rate variability measures at week 1………………………………………………………………………….64 Table 4 Means (±SD) for spontaneous baroreflex sensitivity measures at week 1 ……………………………………………………………………………77 ix LIST OF FIGURES Figure 1 Study Design……………………………………………………………..42 Figure 2 Mean systolic blood pressure as a function of time for the control and exercise group……………………………………………………………55 Figure 3 Mean systolic blood pressure in three conditions for the control and exercise group……………………………………………………………55 Figure 4 Mean diastolic blood pressure as a function of time for the control and exercise group……………………………………………………………57 Figure 5 Mean diastolic blood pressure in three conditions for the control and exercise group……………………………………………………………57 Figure 6 Mean heart rate in three conditions for week 1 and week 12…………..58 Figure 7 Mean Rate-Pressure-Product as a function of time for the control and exercise group……………………………………………………………60 Figure 8 Mean Rate-Pressure-Product in three conditions for the control and exercise group……………………………………………………………60 Figure 9 Mean body mass index as a function of time for the control and exercise group…………………………………………………………………… .62 x Figure 10 Mean of the log transformed low frequency power in three conditions as a function of time…………….…………………………………………….66 Figure 11 Mean of the log transformed low frequency power as a function of menopausal state…………………………………………………………66 Figure 12 Mean of the log transformed high frequency power in three conditions for the control and exercise group…………………………………………...68 Figure 13 Mean of the log transformed high frequency power as a function of menopausal state for the control and exercise group…………………….68 Figure 14 Mean of the log transformed total power as a function of menopausal state………………………………………………………………………69 Figure 15 Mean of the log transformed PNS Indicator in three conditions for the control and exercise group……………………………………………….71 Figure 16 Mean of the log transformed PNS Indicator in three conditions for menopausal and postmenopausal women…………………………….71 Figure 17 Mean of the log transformed SNS Indicator in three conditions for the control and exercise group…………………………………………….…72 Figure 18 Mean of the log transformed SNS Indicator in 3 conditions as a function of menopausal state for a) control group and b) exercise group………....74 xi Figure 19 Mean baroreflex slope in three conditions for the control and exercise group……………………………………………………………………..78 Figure 20 Mean systolic Finapres arterial blood pressure in three conditions as a function of time………………………………………………………….80 Figure 21 Mean systolic Finapres arterial blood pressure in three conditions for the control and exercise group……………………………………………….80 Figure 22 Mean R-R interval in three conditions for the control and exercise group …………………………………………………………………………....81 Figure 23 Mean R-R interval in 3 conditions as a function time for a) menopausal women and b) postmenopausal women……………………………........ 83 xii Abbreviations HR Heart Rate BP Blood Pressure PNS Parasympathetic Nervous System SNS Sympathetic Nervous System HRV Heart Rate Variability SBR Spontaneous Baroreflex PSD Power Spectral Density VLF Very Low Frequency LF Low Frequency HF High Frequency FFT Fast Fourier transform TP Total Power 1 CHAPTER ONE Introduction It is estimated that a Canadian dies from heart disease or stroke every seven minutes (Heart and Stroke Foundation of Canada [HSFC], 2008). Although the rate of heart disease and stroke are declining, they remain the leading causes of death and disability in Canada (HSFC, 2007). The incidence of cardiovascular disease increases with age and is exaggerated during menopause (Rosano & Panina, 1999). Hypertension increases the risk of developing cardiovascular disease by three fold (HSFC, 2008). After 45 years of age, one out of every three Canadians has high blood pressure; with a higher proportion of women affected than men. Hypertension can cause damage to the heart, blood vessels and autonomic nervous system. Hypertensive individuals experience increased sympathetic and decreased parasympathetic cardiac modulation, reduced baroreflex sensitivity and enhanced vasomotor sympathetic modulation (Julius & Majahalme, 2000; Pagani & Lucini, 2001; Souza, Ballejo, Salgado, Da Silva & Salgado, 2001). These factors are detrimental because they decrease an individual‘s ability to maintain blood pressure within a normal range, react to stressful stimuli and avoid cardiovascular injury (stroke, heart disease and death). Autonomic balance is further compromised as women transition though menopause. Menopause causes the protective effect of estrogen to become attenuated and there is increased sympathetic and decreased parasympathetic modulation of the heart and decreased R-R interval (Farag, Bardwell, Nelesen, Dimsdale & Mills, 2003; Rosano & Panina, 1999). 2 Exercise conditioning is known to lower blood pressure and improve autonomic function in hypertensive women (Davy, Willis & Seals, 1997; Whelton, Chin, Xin & He, 2002). Exercise is commonly recommended at high- or moderate-intensity to reduce blood pressure (Cleroux, Feldman & Petrella, 1999; Parati & Lantelme, 2005). However, high-intensity exercise can be harmful as it increases sympathetic activity and BP which could result in cardiovascular injury such as stroke or sudden death. If low-intensity exercise offers comparable cardiovascular benefits without increasing plasma catecholamines it would be advantageous. Low-intensity exercise does not put an individual at risk for injury as there are no drastic fluctuations in sympathetic activity or BP (Brown, Wolfe, Hains, Pym and Parker, 1994). Walking has been found to be a suitable low intensity exercise that is recommended for hypertensive individuals (Lesniak & Dubbert, 2001). The purpose of this study was to test the effects of a low-intensity exercise conditioning intervention on heart rate, blood pressure, heart rate variability and baroreflex sensitivity in hypertensive women. This study will aim to address the following research questions: 1. What are the effects of a 12 week low intensity exercise conditioning program on blood pressure, heart rate, rate-pressure-product and cardiac autonomic function in women with hypertension? 2. How does menopausal state influence blood pressure, heart rate, rate-pressureproduct and cardiac autonomic function in women with hypertension? 3 CHAPTER TWO Literature Review Cardiovascular Disease Cardiovascular disease is a major cause of illness, disability and death in Canada. The cardiovascular system consists of the heart, the blood and the blood vessels (arteries, veins, capillaries) throughout the body and within the brain. The function of this system is to move oxygen and metabolites to and from cells for the purpose of maintaining internal homeostasis. The Heart and Stroke Foundation of Canada (HSFC) (2007) defines cardiovascular disease as any injury of the heart, the blood vessels of the heart or the peripheral blood vessels. Many Canadians have a high prevalence rate of the major risk factors for cardiovascular disease: smoking, physical inactivity, high blood pressure (hypertension), dyslipidemias, obesity, and diabetes. There is a disparity in risk factors that exist among men and women, various age groups and between different geographical regions of the country. The Heart and Stroke Foundation of Canada (1999) recommends that available resources be targeted at individuals and communities in order to help reduce risk factors for heart disease and stroke. Hypertension Hypertension is defined as blood pressure (BP) that is chronically high (more than or equal to 140/90 mm Hg). BP is a measure of the force that blood exerts against the walls of arteries. The numerator represents the highest pressure as the heart contracts and pushes blood out (systolic) and the denominator is the lowest pressure when the heart 4 relaxes between beats (diastolic) (HSFC, 2007). The Canadian Hypertension Education Program (2007) defines hypertension as mild (140-159 / 90-99 mmHg), moderate (160179 / 100-109) and severe (>180 / >110). The risk of being diagnosed with hypertension increases with age (Wolf-Maiser, Cooper, Banegas, 2003). It is anticipated that 90% of individuals will suffer from the disease at some point in their life due to lifestyle patterns. Hypertension can cause serious cardiovascular consequences including stroke, ischemic heart disease, myocardial infarction, congestive heart failure, peripheral vascular disease, renal failure, impotence, left ventricular hypertrophy and left ventricular diastolic dysfunction (Esler & Kaye, 2000; HSFC, 2007; Piccirillo, Germano, Vitarelli, Ragazzo, di Carlo, De Laurentis et al., 2006). Untreated hypertension ultimately results in death. Hypertension signifies a huge public health burden and efforts should be directed at primary prevention (Vasan, Beiser, Seshadri, Larson, Kannel, D'Agostino et al., 2002). There are three common types of hypertension. Essential hypertension constitutes 90-95% of cases and is considered idiopathic. Secondary hypertension is responsible for 5-10% of cases are instigated by underlying renal (acute glomerulonephritis, chronic renal disease, polycystic disease, renal artery stenosis, renal vasculitis, renin-producing tumors), endocrine (adrenocortical hyperfunction, exogenous hormones, pheochromocytoma, acromegaly, hyperthyroidism, hypothyroidism, pregnancy induced), cardiovascular (coarctation of the aorta, polyarteritis nodosa, increased intravascular volume/output, rigidity of the aorta) and neurologic (psychogenic, increased intracranial pressure, sleep apnea, acute stress) causes. Malignant hypertension is less common and is accountable for 5% affected individuals. It is characterized by rapidly rising BP which leads to death within two years if untreated (Cotran, Kumar, Collins, 1999). 5 Regulation of Heart Rate and Blood Pressure BP is directly determined by two elementary hemodynamic principles: cardiac output and total peripheral resistance. Cardiac output is the product of heart rate (HR) multiplied by stroke volume and represents the total amount of blood ejected from the heart per minute. It is influenced by cardiac contractility and venous return. Total peripheral resistance is the cumulative resistance of all peripheral vasculature and dependent on arteriole lumen size. Lumen size is determined by neural and hormonal influences which cause vasoconstriction and vasodilatation (Cotran, Kumar, Collins, 1999). Hypertension is exemplified by high peripheral vascular resistance and reduced cardiac output (Sowers & Lester, 2000). BP control can be understood at a more multifaceted level by investigating the effect the nervous system has on regulation. There are two components of the nervous system, the first is the central nervous system which consists of the brain and spinal cord which integrate incoming afferent information and determine if an efferent response is necessary. The second is the peripheral nervous system which is comprised of exposed nerves which branch out from the spinal cord and innervate different regions of the body. The peripheral nervous system is divided into the somatic nervous system and the autonomic nervous system. The somatic nervous system controls conscious body movements through perception of external stimuli and efferent control of skeletal muscle. The autonomic nervous system is predominantly made up of efferent nerves which transmit impulses from the central nervous system to peripheral organ systems for the purpose of maintaining homeostasis without conscious control. The autonomic nervous 6 system is responsible for control of HR, force of cardiac contraction, constriction /dilatation of blood vessels, contraction and relaxation of smooth muscle in various organs, visual accommodation, pupillary size and secretions from exocrine and endocrine glands (Cotran, Kumar, Collins, 1999). The autonomic nervous system is subdivided into the parasympathetic nervous system (PNS) and the sympathetic nervous system (SNS). The vagus nerve is the origin of all parasympathetic nerve fibers and the only cranial nerve that starts in the brainstem and extends into the abdomen. The vagus nerve is made up of motor neurons that begin in the medulla oblongata (in cells that lie in the nucleus ambiguous) and travel alongside the carotid arteries into the thorax where they synapse with the sinoatrial (SA) /atrioventricular (AV) nodes and atrial muscle. The right vagi innervates SA node firing while the left innervates AV node conduction (Malik & Camm, 1995). Sympathetic motor neurons originate in the intermediolateral columns of the spinal cord (C1-C2, T1T5), synapse with paravertebral chains of ganglia and join with PNS fibers to form a plexus of cardiac nerves which stimulate the heart. Sympathetic postganglionic fibers innervate the SA/AV node and the atrial and ventricular myocardium (Batulevicius, Skripka, Pauziene & Pauza, 2008; Malik & Camm, 1995). The SNS is well known for the sympatho-adrenal response it exhibits to accelerate HR. The PNS acts to slow HR. The SNS and PNS are antagonists of each other and have reciprocal actions. HR is determined by the rate of depolarization of the sinoatrial (SA) node. It represents the net effect of sympathetic and parasympathetic innervation. In a resting state, the SNS and PNS are both active but the PNS is dominant. 7 If there were no PNS influence, the SNS would prevail and intrinsic HR would exceed 100 beats per minute. The average resting adult HR is 70 beats per minute when it is mediated by the PNS (Berne & Levy, 2001). Both divisions of the autonomic nervous system use neurotransmitters for synaptic communication in order to produce a chronotropic effect. The PNS is mediated by acetylcholine, which travels from the vagus nerve to muscarinic receptors in the SA node in order to inhibit cardiac pacemaker activity and slow HR. HR is effected immediately (<400ms) by vagal stimulation/withdraw (Batulevicius et al., 2008; Malik & Camm, 1995). This is attributed to the enzyme cholinesterase. The SA and AV nodes are rich in cholinesterase and acetylcholine is rapidly hydrolyzed by it. The brief latency and prompt decay of acetylcholine allow the PNS to control HR on a beat-to-beat basis. The SNS takes longer (3-5s) to elicit a change as it is mediated by norepinephrine. Norepinephrine binds to beta adrenergic receptors in the SA node to accelerate HR. This response is too slow to exert beat-by-beat control of HR (Malik & Camm, 1995; Pelosi, Tavares, Antunes-Rodrigues & Correa, 2008; Silverthorn, 2001). Autonomic Regulation of Heart Rate Hypertensive individuals experience impairment of the autonomic nervous system. Autonomic deregulation is manifested through increased sympathetic and decreased parasympathetic activity, increased vasomotor sympathetic tone, reduced spontaneous baroreflex sensitivity (SBR) and reduced heart rate variability (HRV). Sympathetic over activity is enabled by vagal withdrawal which causes acute and chronic episodes of BP elevation (Guyenet, 2006; Souza, Ballejo, Salgado, Da Silva & Salgado, 8 2001). After parasympathetic withdrawal, HR is immediately affected followed by an ensuing change in BP. This sequence of events happens because SNS activity increases either moderately or completely (Dabrowska, Dabrowski & Skrobowski, 1996; Lewis, 2005; Ohisa, Hashimoto, Yoshida, Imai & Kaku, 2005; Thayer & Lane, 2007). The distinctive increase in sympathetic drive is widespread across many organs. It is evident in the heart, the kidneys and in skeletal muscle (Julius & Majahalme, 2000). Reduced SBR sensitivity also is evident in hypertensive individuals. With increasing BP, the arterial baroreflex is strained and forced is reset to function outside of normal parameters. There is consequential diminished vagal influence and a subsequent increase in sympathetic outflow to the heart and resistance vessels (Labrova, Honzikova, Maderova, Vysocanova, Novakova, Zavodna, et al., 2005; Myredal, Gao, Friberg, Jensen, Larsson & Johansson, 2005; Prakash, Madanmohan, Sethuraman & Narayan, 2005). Aging and thickening of the carotid wall also are associated with an attenuation of the baroreflex (Parati & Lantelme, 2005). Heart Rate Variability HRV is a measure of the beat-to-beat changes in HR and a useful non-invasive tool to assess short term autonomic control. In healthy individuals, the rhythmic beating of the heart at rest is not uniform; there is oscillation in the interval between consecutive heartbeats. This oscillation can be characterized by a variability of 10% of the mean (Malik & Camm, 1995). Synergistic fluctuations in HR occur on a beat-by-beat basis, adjusted by efferent parasympathetic and sympathetic output to the sinoatrial node. HRV is a vital mechanism for achieving flexibility in cardiovascular responses to rapid and 9 unpredictable internal and external stimuli. It can be used as a predictor of mortality after cardiovascular injury since decreased HRV is linked to the incidence of cardiac arrhythmias. Loss of HRV occurs in certain pathological conditions before sudden death (Akselrod, Gordon, Madwed, Snidman, Shannon & Cohen, 1985; Akselrod, Gordon, Ubel, Shannon, Berger & Cohen, 1981; Goldberger, 1991). Measurement of Heart Rate Variability HRV can be enumerated by using an electrocardiogram (ECG) to measure beatto-beat changes in HR from one cardiac cycle to the next. The time interval between two ventricular contractions, the R-R interval, is the primary measure and can vary on a beatto-beat basis. The R-R interval provides a noninvasive quantitative method for investigating the dynamic influence of changing physiological parameters on cardiac regulation. Measurement of HRV has been standardized in order to establish consistent nomenclature/definitions, standard methods of measurement and to define physiological correlates and appropriate clinical applications (Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology (TFESCNASPE), 1996). HRV can be evaluated in two domains; time domain and frequency domain. To measure HRV in a time domain, the interval between ventricular contractions (QRS interval) is measured over time (ms) and plotted on a tachogram. The time domain method calculates the peak-to-peak value of the R-R interval directly from a time sample. Measurements are reported as a mean, standard deviation or compared at different times 10 of the day. It is commonly used for long-term recordings of HRV (24 hours) and occasionally for short-term recordings (2-5 minutes). The frequency domain method or power spectral density (PSD) illustrates how variance between R-R intervals distributes as a function of frequency. It is used for short and long term recording and has been chosen for use in this study as it is a more appropriate means for measurement of HRV (Lewis, 1995). The frequency domain method converts the R-R interval data from the time domain to the frequency domain by a Fast Fourier transform (FFT). FFT can plot the relative energy of different frequency components of HRV. It is based on the Fourier theorem which asserts that any signal can be expressed as a sum of an infinite set of sine and cosine functions. FFT breaks down periodic oscillations of R-R interval into fundamental sinusoidal components which are then transformed into a graphic format to serve as an estimation of HRV spectra. A periodogram is produced to estimate the power spectrum of a signal and is referred to as ‗‗power spectral density‘‘ (PSD). PSD describes the power content of a signal in a very narrow frequency range. The segment spectra are then averaged (Freeman, Dewey, Hadley, Myers & Froelicher, 2006; Lewis, 2005; Pichon, Roulaud, Antoine-Jonville, de Bisschop & Denjean, 2006; Yamamoto, Hughson & Peterson, 1991). There are two methods for calculating PSD, nonparametric and parametric. The nonparametric method is more widely used as it is a simple algorithm (FFT) and fast to process. Parametric tests can be used on a small sample, offer smoother spectral components which can be distinguished independently of the selected frequency bands but are complex calculations that require verification of suitability. The effect of 11 respiration, head tilt, valsalva maneuver or pharmacological intervention can be seen in both domains and methodologies (TFESCNASPE, 1996). Mathematical algorithms are then used to generate an interval tachogram which display three types of frequencies that reflect autonomic modulation on the SA node; very low frequency (VLF), low frequency (LF) and high frequency (HF) (TFESCNASPE, 1996). Frequencies are classified by a specific power spectrum and are expressed in absolute values of power (ms). VLF is characterized by less than 0.04 Hz, LF signifies 0.04-0.15 Hz and HF corresponds to 0.15-.5 Hz (TFESCNASPE, 1996). HF symbolizes parasympathetic activity and reflects vagal mediation of HR and respiratory sinus arrhythmia. HF is associated with more efficient cardiac autonomic control mechanisms (Akselrod et al., 1981; Manfrini et al., 2008). There is disagreement over the interpretation of LF; it has been argued to be a distinct indicator of sympathetic activity (Kamath, Fallen & McKelvie, 1991; Lewis, 2005; Rimoldi, Pagani, Piazza, Pagani, & Malliani, 1994) and also hypothesized to represent both sympathetic and parasympathetic contribution (Akselrod et al., 1981; Pichot, Roche, Gaspoz, Enjolras, Antoniadis, Minini, et al., 2000). The dual influence is believed to be attributable to the arterial baroreflex which triggers fluctuations in HR through vagally-mediated innervation within the range 0.08-0.12 Hz (Magosso, Biavati & Ursino, 2001). LF can be used within several ratios to gain further insight into sympatho-vagal balance. LF/HF ratio serves as an index of sympathetic activity and HF/TP (total power) is used as a measure of PNS activity. TP is mathematically equal to the sum of the variance of the spectral analysis (Milicevic, 2005; Pichot et al., 2000; TFNESCASPE, 1996). VLF component is not evaluated in this study 12 as it is a poorly understood physiological measure and not recommended for short term data recordings (TFNESCASPE, 1996). Arterial Baroreflex Healthy individuals experience BP and HR oscillations on a beat-by-beat basis (Blaber, Yamamoto & Hughson, 1995). The arterial baroreflex adjusts the short term regulation of BP through the autonomic nervous system. It is a negative feedback system to maintain arterial BP within a normal range by altering autonomic neural outflow in order to prevent excessive rise or fall and preserve homeostasis. The arterial baroreceptors are unencapsulated free nerve endings located in the aortic arch and carotid sinus which can simultaneously detect either an increase or decrease in arterial BP by sensing mechanical distension of the blood vessel walls. The autonomic nervous system responds by sending impulses via the afferent fibers to the nucleus of the tractus solitarius (NTS) and a complex wiring system ending in the nucleus ambiguus and ventrolateral in the medulla of the brain stem in order to return arterial BP to the established central nervous system operating point. An increase in BP alerts the arterial baroreflex to increase afferent neural impulses to inhibit the SNS and stimulate the PNS. Efferent autonomic nerve fibres transmit signals to the heart and blood vessels to decrease HR, cardiac output and systemic vascular resistance. A decrease in BP results in a diminution of impulses sent to the NTS causing excitation of the SNS and impedance of the PNS. This leads to an increase in HR and cardiac output (Dampney, 1994; Hainsworth, 1996; Raven, Fadel & Smith, 2002; Smit, Wieling & Karemaker, 1996). 13 The arterial baroreflex functions around a higher operating point during exercise and then is reset to its habitual level at the end of activity due to increased central blood volume (Ogoh, Fisher, Fadel & Raven, 2007). Resetting of the baroreceptors is an essential property that occurs after a sustained stimulus and is proportional to exercise intensity; the response may be acute (30 sec - 30 min) or chronic (complete resetting) and is regulated by the central nervous system. Baroreceptor resetting does not change the slope of the reflex; it shifts the curve horizontally rightward (Iellamo, Legramante, Raimondi & Peruzzi, 1997; Joyner, 2006; Raven et al., 2002). Acute resetting occurs in response to acute exercise. Chronic resetting requires prolonged pressure changes from months to years; this may be accomplished with participation in a sustained exercise program (Hainsworth, 1996; Iellamo, Legramante, Massaro, Raimondi & Galante, 2000; Shi, Schaller, Tierney, Chanthavong, Chen, Raven et al., 2008). Baroreflex failure arises when afferent baroreceptors become impaired and lose their buffering ability. There is a resultant widening of pulse pressure and labile HR. Baroreflex failure can result in hypertensive crisis, volatile hypertension, orthostatic tachycardia or malignant vagotonia (Ketch, Biaggioni, Robertson & Robertson, 2002). Measurement of Arterial Baroreflex Arterial baroreceptors are responsible for rapid reflex BP responses by adjusting HR and total peripheral resistance through the autonomic nervous system. SBR sensitivity is the degree to which a change in arterial BP elicits a response in HRV. There can be a slight time delay (lag) between a change in SBP and a subsequent variation in RR interval. The lag in baroreflex response time varies between zero and two heart beats. It 14 is assumed that SBR sensitivity is predominantly a measure of parasympathetic activity due to the beat-by-beat control it exerts on HR. SBR sensitivity is used to quantify the vagal component of the baroreflex (Blaber et al., 1995; Schrezenmaier, Singer, Swift, Sletten, Tanabe & Low, 2007). SBR sensitivity is influenced by age and gender and is significantly diminished in individuals who suffer from hypertension (Laitinen, Hartikainen, Vanninen, Niskanen, Geelen & Lansimies, 1998). There are three distinct techniques to assess SBR sensitivity; intravenous administration of vasoactive medication, direct stimulation of the carotid baroreceptors with a neck chamber device or by spontaneous baroreflex method. Vasoactive drug administration provokes the baroreceptor response by sequential intravenous bolus injections of nitroprusside (depressor) and phenylephrine (pressor) to cause an acute increase or decrease in arterial BP. This pharmacological method causes an abrupt aberrant change in the speed and intensity of the BP response that does not precisely mimic normal physiology (Parlow, Viale, Annat, Hughson & Quintin, 1995; Rudas, Crossman, Morillo, Halliwill, Tahvanainen, Kuusela et. al, 1999). Use of the noninvasive neck chamber to assess carotid baroreflex by neck suction or neck pressure is another useful tool to assess SBR sensitivity. The application of neck pressure via a rigid collar emulates a hypotensive state as it compresses the carotid baroreceptors and causes a decrease in carotid sinus transmural pressure. The application of neck suction stretches the carotid baroreceptors creating a simulated hypertensive state as carotid sinus transmural pressure increases (Fadel, Ogoh, Keller & Raven, 2003). The spontaneous baroreflex method is used to analyze parasympathetic innervation of the heart after BP fluctuation. BP and HR are two physiological variables that are interconnected by the 15 actions of the baroreflex. The spontaneous baroreflex method analyzes BP by using a computer to scan recordings of continuous finger arterial BP and ECG tracings to locate sequences in which BP spontaneously increases or decreases with parallel changes in cardiac intervals (Eckberg, 1980; Parlow et. al, 1995). Each method for testing SBR sensitivity has advantages and disadvantages for particular patient populations and study resources. The use of vasoactive medications can be advantageous as they allow investigators to discriminate between resetting of the baroreflex and changes in sensitivity. However, they are not appropriate in all clinical situations as they are fast acting potent stimuli that can cause dangerous perturbations in systolic BP and R-R interval. Another issue arises in the application of the vasoactive agent. The delivery of chemical vasopressors and vasodilators does not imitate the natural baroreflex response time accurately. Each injection is given over several seconds and the effect of the medication is influenced by the rate of administration (Eckberg, 1980; Parlow et. al, 1995). The application of neck pressure or suction can cause adverse reactions such as syncope or unsafe elevations in BP (Raine & Cable, 1999). This study deemed the spontaneous baroreflex method to be the most appropriate technique for assessing SBR sensitivity as it has several obvious advantages over other methods while producing replicable values. The spontaneous baroreflex method is non-invasive, reliable and able to measure SBR sensitivity within a normal physiological range. It allows the investigator to obtain a true steady-state assessment while the participant is studied in various conditions such as at rest, standing and during exercise (Parlow et. al, 1995). 16 The spontaneous baroreflex method generates data that can be analyzed by either the sequence method or by spectral analysis. The investigators of the present study opted to use the sequence method since it has been found to yield quantitatively similar results to spectral analysis methods (Hughson, Quintin, Annat, Yamamoto & Gharib, 1993). The sequence method detects spontaneous sequences of three or more heart beats in which systolic BP and R-R interval simultaneously change in the same direction. The sequences are then analyzed by computer software which uses linear regression to calculate the slope of each series. The mean slope is used to quantify SBR sensitivity; an increase in the baroreflex slope is associated with greater parasympathetic innervation whereas a decrease in slope is linked to reduced vagal stimulation (Blaber et al., 1995; Hughson et al., 1993; La Rovere, Bersano, Gnemmi, Specchia & Schwartz, 2002; Parlow et. al, 1995). Measuring HRV and SBR sensitivity are safe, reliable approaches to evaluating cardiac autonomic balance (Amara & Wolfe, 1998). However, these methods are susceptible to various factors which have influential effects on their measurement. These factors include hypertension, aging, gender, menopause, body posture, respiratory rate, antihypertensive medications and acute exercise. Physiological Factors Which Effect Cardiac Autonomic Function Hypertension. Impairment of the autonomic nervous system is the hallmark of essential hypertension and apparent when evaluating HRV and SBR sensitivity in hypertensive patients. Hypertension is distinguished by an imbalance of sympatho-vagal function; this is evidenced by increased sympathetic and decreased parasympathetic 17 cardiac modulation with enhanced vasomotor sympathetic innervations (Julius & Majahalme, 2000; Liao, Cai, Barnes, Tyroler, Rautaharju, Holme et al., 1996; Pagani & Lucini, 2001; Piccirillo, Germano, Vitarelli, Ragazzo, di Carlo, De Laurentis, et al., 2006; Souza et al., 2001). Power spectral analysis of ECG recordings reveals that hypertensive individuals experience low HRV (decreased R-R interval fluctuations) and prolonged QT intervals. This is attributable to increased LF power (sympathetic innervation) and reductions in HF power (parasympathetic innervation). Consequently, low to high frequency ratio, HF power and TP are also reduced (Kaftan & Kaftan, 2000; Kosch, Hausberg, Barenbrock, Kisters & Rahn, 1999; Passino, Franzoni, Gabutti, Poletti, Galetta & Emdin, 2004). Decreased vagal function is associated with an increased risk for morbidity and mortality (Thayer & Lane, 2007). In addition to this, rate-pressure product [(HR x BP) x 10-2)] is increased in hypertensive patients. Rate-pressure-product (RPP) is an estimate of myocardial oxygen consumption and gives an indication of the amount of oxygen demanded by the heart. A normal value is less than 12 ml blood /100g LV/min (Gobel, Norstrom, Nelson, Jorgensen & Wang, 1978; Pepper & Crawley, 1985; Prakash et al., 2005). The ability of the cardiovascular system to maintain BP within a normal range is further compounded by the effect of hypertension on the arterial baroreflex. The baroreflex is strained by high BP and forced to reset its sensitivity to a higher operating point. This is due to diminished vagal modulation and amplified sympathetic innervation to the heart and resistance vessels. The slope of the baroreflex decreases with increasing BP (Parati & Lantelme, 2005; Prakash et al., 2005). High BP cultivates carotid wall thickness which further decreases SBR sensitivity (Labrova et al., 2005). Autonomic 18 dysregulation is evident in the early stages of hypertension and is exaggerated as the condition worsens (Singh, Larson, Tsuji, Evans, O'Donnell & Levy, 1998). Therefore, the degree of BP elevation is proportional to the severity of autonomic impairment (Mussalo, Vanninen, Ikaheimo, Laitinen, Laakso, Lansimies et al., 2001). Aging. Increasing age hinders the autonomic nervous system in healthy normotensive and hypertensive individuals. As a function of age, the cardiovascular system gradually loses its ability to regulate HR on a beat-by-beat basis. Structural and functional changes in autonomic nerves, ganglia, heart and blood vessels are responsible for this change. There is ensuing impairment of left ventricular filling, increased afterload and diminished intotropic and chronotropic responses to catecholamines (Spina, 1999; Shimazu, Tamura & Shimazu, 2005). Laitinen, Hartikainen, Vanninen, Niskanen, Geelen & Lansimies (1998) found that plasma noepinephrine concentration increases with age. Aging cardiovascular systems demonstrate a marked reduction in parasympathetic control of HR causing decreased HRV (Jensen-Urstad, Storck, Bouvier, Ericson, Lindblad & Jensen-Urstad, 1997; Lipsitz, Mietus, Moody & Goldberger, 1990; Ryan, Goldberger, Pincus, Mietus & Lipsitz, 1994). In elderly individuals (>65yrs), there is an additional reduction in LF and HF power and HR fluctuation (Lipsitz et al., 1990; Stein, Ehsani, Domitrovich, Kleiger & Rottman, 1999). This effect is more evident during activity but can be reduced by regular endurance exercise (Arai, Saul, Albrecht, Hartley, Lilly, Cohen et al., 1989; Carter, Banister & Blaber, 2003). Goldsmith, Bigger, Bloomfield & Steinman (1997) argue that vagal modulation is fostered by physical 19 activity. Therefore, the age-related decline in parasympathetic innervation is attributed to a gradual decrease in fitness level. Aging is also associated with a reduction of maximal HR and cardiac output during exercise (Fagard, Thijs & Amery, 1993; Piccirillo et al., 2006; Stratton, Levy, Cerqueira, Schwartz & Abrass, 1994). Advancing age causes decreased compliance of arterial walls leading to reduced sensitivity of the baroreflex (Laitinen et al., 1998; Shi, Schaller, Tierney, Chanthavong, Chen, Raven & Smith, 2008). The effects of aging on arterial SBR sensitivity begin to appear in middle-aged subjects (Parati & Lantelme, 2005). The above literature highlights the influence of age on cardiac autonomic function. Gender. Cardiovascular diseases develop over time and have differential effects on men and women. The HSFC (2007) recently published a report on Canadians‘ health. This report highlighted a disparity between the cardiovascular health of men and women. Approximately 37,000 Canadian women die from cardiovascular diseases each year. Women have a higher risk of dying after a heart attack or stroke than men. For the first time in 30 years, women and men have equal mortality rates due to cardiovascular disease. More research must be directed at investigating women‘s unique cardiovascular physiology to end this phenomenon. There is a discrepancy in the literature regarding the effect of gender on the autonomic nervous system. It is argued that healthy middle-aged women have higher HF power, lower LF power and lower sympathetic indicator than healthy men (Antelmi, de Paula, Shinzato, Peres, Mansur & Grupi, 2004; Carter et al., 2003; Huikuri, Pikkujamsa, Airaksinen, Ikaheimo, Rantala, Kauma et al., 1996). Alternatively, some studies have 20 found that HRV measures are lower (TP and LF power) in women compared to men (Jensen-Urstad et al., 1997; Ramaekers, Ector, Aubert, Rubens & Van de Werf, 1998). A higher sympathetic activity has been reported in men compared to women. Franchi, Lazzeri, Villa, Barletta, Del Bene & Buzzelli (1998) noted that sympathetic control of cardiac activity is more dominant in men compared to women. Kuo, Lin, Yang, Li, Chen and Chou (1999) found that women aged 40-59 years of age showed higher parasympathetic activity in comparison to aged- matched men. Men aged 40-59 years showed greater sympathetic activity than women. There were no differences in autonomic function between men and women over the age of 60 years. These findings indicate that gender does have an effect on cardiac modulation. There are also opposing claims in the literature about gender differences and SBR sensitivity. SBR sensitivity has been found to be lower in healthy women compared to healthy men (Huikuri et al., 1996; Laitinen et al., 1998; Sevre, Lefrandt, Nordby, Os, Mulder, Gans, Rostrup & Smit, 2001). In contrast, Dougherty et al. (1999) found that SBR sensitivity was higher in middle-aged women than age-matched men in both supine and standing postures. Although ambiguous, there is a gender disparity between autonomic nervous system regulation in men and women. Menopause. Middle age is a period of transition in autonomic balance for women as they confront menopause. Menopause, or the permanent end of menstruation and fertility, is defined as 12 months of amenorrhea. The mean age at menopause is 51 years in developed countries (Greendale, Lee & Arriola, 1999). Near the onset of menopause, women experience an increased occurrence of cardiovascular disease (Davy, Willis & 21 Seals, 1997; Eaker, Chesebro, Sacks, Wenger, Whisnant, Winston, 1994). Menopausal women have a lower incidence of cardiovascular disease than postmenopausal women and age matched men. This effect may be attributed to estrogen. Estrogen demonstrates several cardio protective mechanisms which positively affect plasma lipids, carbohydrate metabolism, hemocoagulation and formation of atherosclerotic plaque. Additionally, estrogen encourages the release of nitric oxide through endothelial tissues to cause vasodilation and improve vascular tone. This causes a reduction in peripheral vascular resistance which maintains BP within a normal range. Estrogen levels decrease substantially at the onset of menopause (Rosano & Panina, 1999). The use of estrogen replacement therapy improves cardiac autonomic function, attributing gender differences in cardiac regulation to hormonal influences (Huikuri et al., 1996). Menopause is characterized by increased sympathetic and decreased parasympathetic innervation of the heart (Farag, Bardwell, Nelesen, Dimsdale & Mills, 2003; Rys, Rys, Kogut & Thor, 2006). Furthermore, R-R interval decreases and there is impairment of the baroreflex (Brockbank, Chatterjee, Bruce & Woledge, 2000). Irigoyen, Paulini, Flores, Flues, Bertagnolli, Moreira, et al. (2005) suggest that exercise conditioning can improve SBR sensitivity in postmenopausal women. Body Posture. Variations in body posture can cause alterations in HRV and arterial baroreflex (Pagani, Lombardi, Guzzetti, Rimoldi, Furlan, Pizzinelli et al., 1986; Perini, Orizio, Milesi, Biancardi, Baselli & Veicsteinas, 1993). This has been explored thoroughly through clinical cardiovascular reflex testing. HR and BP responses are evaluated after a change in position for the purpose of assessing autonomic nervous 22 system function. Changing physical posture from lying to standing (or standing to steady state exercise) disrupts sympathovagal balance which prompts a rise in sympathetic activity leading to an increase in LF power and a decrease in total HRV (Lewis, 2005; Malliani, Pagani, Lombardi, Furlan, Guzzetti & Cerutti, 1991; Pomeranz, Macaulay, Caudill, Kutz, Adam, Gordon et al., 1985). This cascade of autonomic reflexes is attributed to greater parasympathetic control of HR in the supine position compared to standing position. HR is lower when an individual is lying down due to higher vagal innervation of the heart (Pagani et al., 1986). When posture changes from supine to standing, gravity pulls blood downward so that it accumulates in the lower extremities. As blood pools in the compliant venous vessels, there is less return to the heart causing a decreased cardiac output and arterial BP. In healthy individuals, a decrease in BP is detected by arterial baroreceptors in the carotid sinus and aortic arch. The baroreceptors sense a drop in BP and react by decreasing the frequency of impulses sent to the brain stem. This causes an increase in sympathetic activity and a decrease in parasympathetic innervation of the SA node; HR, cardiac output and cardiac contractility increase to maintain an adequate BP (Kamath et al., 1991; O'Leary & Seamans, 1993). Individuals with baroreflex failure or an impaired autonomic nervous system do not have the ability to protect their BP against the excessive rise or fall experienced during a posture change. In such an event, cerebral blood flow can be compromised and dizziness or syncope can occur; this is known as orthostatic hypotension (Kappel, Fink & Batzel, 2007; Ketch et al., 2002). Respiratory Rate. An individual‘s respiratory rate influences HRV. The nucleus ambiguous is responsible for increasing parasympathetic nervous input to the heart via 23 the vagus nerve during expiration. Stimulation of the vagus nerve decreases sinoatrial node firing and slows HR. In contrast, the nucleus accumbens receives inhibitory signals during inspiration and the vagus nerve remains unstimulated as HR increases (Neff, Wang, Baxi, Evans & Mendelowitz, 2003). During inspiration, the R-R interval decreases and HR increases. For the length of expiration, the opposite occurs, the R-R interval increases and HR decreases. The parasympathetic nervous system is predominant during expiration and not involved during inspiration (Eckberg, 1980; Kollai & Mizsei, 1990; Lewis, 2005). This phenomenon is called respiratory sinus arrhythmia and reflects the changes in R-R interval during inspiration and expiration (Haggenmiller, Baumert, Adt & Frey, 1996). Respiratory sinus arrhythmia increases the HF component of HRV. This is due to respiratory-related vagal modulation of HR; the degree of change corresponds to the amount of cardiac vagal tone (Hayano, Mukai, Sakakibara, Okada, Takata & Fujinami, 1994). There is a relationship between respiratory sinus arrhythmia amplitude and breathing frequency. For breathing frequencies over .01 Hz, HF power decreases at a rate of about 20dB/decade (Hirsch & Bishop, 1981). There are several interconnected physiological mechanisms that contribute to respiratory sinus arrhythmia; the first is tidal volume. Tidal volume is the amount of air moved in and out of the lungs during a single respiration. Greater tidal volumes cause increased HRV (Brown, Beightol, Koh, & Eckbarg, 1993). This can be attributed to the Hering-Breuer reflex, stretch receptors located in the smooth muscle of the airways provide vagal feedback to slow respiration when there is over inflation or when tidal volumes exceeds 1000 mL (Taha, Simon, Dempsey, Skatrud & Iber, 1995; West, 2005). Large tidal volumes create negative intrathoracic pressure. Inspiration is accomplished by 24 the contraction or decent of the diaphragm. This creates negative intrathoracic pressure in the chest cavity which causes increased blood flow and volume into the thoracic vena cava. There is a consequent increase in HR and stroke volume due to increased venous return to the right atrium (Hayano et al., 1994). It may be assumed that conscious mental measurement of the rate and depth of breathing during HRV data collection is imperative due to the existence of the respiratory sinus arrhythmia. However, this study did not incorporate measured breathing techniques as there is no consistent recommendation in the literature regarding standardized breathing protocols to control for the effects of breathing on HRV. The literature insinuates a disagreement over the use of breathing protocols versus voluntary control of breathing. Some researchers support the use of controlled breathing as a means to enhance vagal modulation. Cooke and colleagues (1998) evaluated several breathing protocols and found that a structured pattern without strict control of inspired volume is the most efficient method to reduce the impact of respiratory sinus arrhythmia on HRV interpretation. Brown et al. (1993) argue that since respiration increases LF power spectra and decreases HRV, breathing protocols must be used in order for valid interpretation. Patwardhan, Evans, Bruce & Knapp (2001) disagree; they argue that regulated breathing is associated with a small but significant increase in mean HR and a decrease in respiratory synchronous variation in HR. They also found that HF power was similar during spontaneous versus metronomic breathing suggesting that there is no advantage to a calculated breathing regime. Further, Haggenmiller et al. (1996) advocate for voluntary control of breathing as controlled ventilation may cause participants to experience psychological stress as they attempt to counter their natural breathing pattern. This 25 conscious effort has an effect on HRV. Sufficient evidence implies that structured breathing protocols can interfere with HRV interpretation. Antihypertensive Medications. Antihypertensive therapy is initiated for the treatment of hypertension. Antihypertensive medications act by reducing systolic and diastolic BP to prevent the damaging effects of chronic elevation (Black, Elliott, Neaton, Grandits, Grambsch, Grimm, et al., 2001). There is a large variety of drugs available in the current market for reducing BP. The five most common medications can be grouped into five classes: diuretics, beta blockers, angiotension converting enzyme-inhibitors (ACE inhibitors), angiotension II receptor antagonists and calcium channel blockers (Chobanian, Bakris, Black, Cushman, Green, et al., 2003). Diuretics influence the kidneys to excrete excess salt and water from blood and tissues. Beta blockers block the action of catecholamines on β-adrenergic receptors. ACE inhibitors prevent angiotension converting enzyme from changing angiotension l into angiotension ll; a powerful vasoconstrictor. Angiotension II receptor antagonists work in the same pathway to antagonize the activation of angiotension receptors. Calcium channel blockers impede the entry of calcium into muscle cells in artery walls, inhibiting vasoconstriction (Abrams, 2004). Two-thirds of individuals suffering from hypertension will require two or more antihypertensive medications selected from different drug classes (Chobanian et al., 2003). The current literature suggests that lifestyle modification, such as exercise, plus antihypertensive therapy is the most effective multidimensional treatment to combat hypertension (Lochner, Rugge, Judkins & Saseen, 2006). 26 Beta blockers and calcium channel blockers have distinctive characteristics that allow them to manipulate the cardiac autonomic nervous system. Beta blockers reduce HR at rest and during exercise by diminishing LF power (sympathetic innervation) and LF/HF ratio. HR is further compounded by enhanced parasympathetic modulation which lengthens R-R interval by increased HF power (Pagani, 1986; Panfilov, Morris, Donnelly, Scemama & Reid, 1995). Takase, Abe, Nagata, Matsui, Hattori, Ohsuzu et al. (2005) supported these findings; they found that treatment with a beta blocker decreased BP and increased in HRV. Calcium channel blockers can interfere with the baroreceptorvagal reflex by increasing SBR sensitivity causing increased HR in some cases (Eguchi, Tomizawa, Ishikawa, Hoshide, Fukuda, Numao, Shimada, & Kario, 2007; Taylor & Kowalski, 1984). Acute Exercise. Exercise is defined as, ―any muscular activity that generates force and disrupts homeostasis‖ (ACSM, 2000). Acute exercise is defined by the performance of a short session of any aerobic exercise and has an impact on the autonomic nervous system (Maeda, Tanabe, Otsuki, Sugawara, Ajisaka & Matsuda, 2008). The current literature describes HRV indices in healthy individuals. In a resting state, the PNS is the primary influence on HR. At the onset of exercise, there is vagal withdrawal and a temporary increase in sympathetic tone. This causes HR to increase by 30-50 beats per minute. Continued activity is associated with progressive parasympathetic withdrawal and attenuation of sympathetic over-activity (Brenner, Thomas & Shephard, 1998; Chiu, Wang, Huang, Tso & Kao, 2003; Freeman et al., 2006; Nakamura, Yamamoto & Muraoka, 1993; Yamamoto, Hughson & Peterson, 1991). HR and myocardial oxygen demand increase linearly in proportion to metabolic demand during exercise. Active 27 tissues respond to the metabolic demands of exercise by local vasodilation. Increased cardiac output, decreased peripheral vascular resistance, redistribution of blood flow to active muscles, venoconstriction, and increased oxygen extraction occur at the onset of acute exercise (Silverthorn, 2001). The carotid baroreflex is reset to a higher operating point during acute exercise with no attenuation in maximal sensitivity. This is substantiated by the resulting hypotension experienced by hypertensive individuals in the post exercise period (Minami, Mori, Nagasaka, Ito, Kurosawa, Kanazawa et al., 2006; Potts, Shi & Raven, 1993; Silva, Brum, Negrao, Krieger, 1997). Effects of Exercise Conditioning on the Cardiac Autonomic Nervous System Aerobic exercise is defined as ―any activity that uses large muscle groups, can be maintained continuously and is rhythmic in nature‖ (ACSM, 2000). Regular aerobic exercise has different effects on the autonomic nervous system relative to acute aerobic exercise. Exercise conditioning is characterized as routine performance of aerobic exercise over time. Physiological responses to training include cardiac and peripheral adaptations. Pagani et al. (1988) studied a sample of 11 men and women with mild hypertension during an intensive 6 month physical training program. Training increased the resting R-R interval, decreased systemic arterial BP by 10.2 mmHg and diastolic BP by 7.1 mmHg. Resting LF power decreased and HF power increased. This signifies an increase in parasympathetic activity. Yamamoto et al. (1991) and Nakamura, Yamamoto & Muraoka (1993) found that during acute low intensity exercise, parasympathetic effects on HR are more dominant than sympathetic effects. Regular exercise conditioning 28 reduces resting and exercise HR, lowers low density lipoprotein, increases high density lipoprotein and assists with weight control (Cade, Mars, Wagemaker, Zauner, Packer, Privette et al., 1984; Malliani et al., 1991; Pagani et al., 1988). Exercise training has been found to increase the gain of the baroreflex. It appears that moderate intensity training for at least 3 months is sufficient to achieve change. Goldsmith et al., (1992) reported that parasympathetic activity is greater in aerobically trained vs. untrained normotensive men. Participation in moderate-intensity exercise has consistently lowered BP and HR in multiple populations of individuals (Campbell, Burgess, Choi, Taylor, Wilson, Cleroux et al., 1999; Fagard, 1995; Lackland, 2005). Prolonged and intense exercise training does not necessarily lead to greater enhancement of the autonomic nervous system and may not provide any added protective benefits (Iwasaki, Zhang, Zuckerman & Levine, 2003). Exercise conditioning is known to lower BP in hypertensive individuals (Davy et al., 1997; Dubbert, Martin, Cushman, Meydrech & Carroll, 1994; Ishikawa, Ohta, Zhang, Hashimoto & Tanaka, 1999; Maddens, Imam & Ashkar, 2005; Miller et al., 2002; Moreau et al., 2001; Whelton, Chin, Xin & He, 2002). Davy et al. (1997) noted a reduction in systolic and diastolic BP in post-menopausal, hypertensive women after 12 weeks of moderate-intensity aerobic exercise training. Similarly, Hagberg, Park & Brown (2000) observed that exercise training decreased BP in approximately 75% of individuals with hypertension. Systolic and diastolic BP reductions averaged approximately 11 mmHg and 8mmHg, respectively. 29 Hypertensive individuals who participate in regular exercise experience decreased total peripheral resistance and increased overall vascularization of skeletal muscle after 3 months of moderate exercise training (Iwasaki et al., 2003; Izdebska, Cybulska, Izdebskir, Makowiecka-Ciesla & Trzebski, 2004; Martin & Dubbert, 1987; O'Sullivan & Bell, 2000). There are opposing claims in the literature about the health benefits of varying intensities of exercise. Exercise is commonly recommended at high or moderateintensity to reduce high BP and restore baroreflex function (Cleroux et al., 1999; Parati & Lantelme, 2005). The problem with this prescription is that moderate and high intensity exercise increases sympathetic activity and BP. These two effects are undesirable to hypertensive individuals as they are associated with a risk for acute cardiovascular injury (Nakamura, Yamamoto & Muraoka, 1993; Yamamoto, Hughson & Peterson, 1991). In contrast, few studies have described the advantages of low intensity exercise. Low intensity exercise lowers BP and does not increase plasma catecholamines (Nakamura et al., 1993; Yamamoto et al., 1991). In a six year randomized control trial of 140 middle aged men, Tuomainen, Peuhkurinen, Kettunen and Rauramaa (2005) found that low to moderate intensity exercise has beneficial effects on the cardiac autonomic nervous system. Brown, Wolfe, Hains, Pym and Parker (1994) evaluated the effects of a 12 week low intensity vs. a moderate intensity home walking program with post operative coronary artery bypass graft patients and noted comparable cardiovascular improvements. Sugawara, Inoue, Hayashi, Yokoi and Kono (2004) reported that low intensity exercise training improves central arterial compliance in postmenopausal women. These studies support the use of low intensity exercise in cardiovascular rehabilitation programs. 30 Walking has been found to be an excellent low intensity exercise that is recommended for hypertensive individuals over other exercise regimes such as weight training (Lesniak & Dubbert, 2001; Wallace, 2003). Walking 10,000 steps per day, without regard to pace, is effective in lowering BP, increasing exercise capacity, and reducing sympathetic nerve activity in hypertensive patients (Iwane, Arita, Tomimoto, Satani, Matsumoto, Miyashita et al., 2000). A low intensity, 20 week, walking program was implemented in multiple community settings for elderly adults by Kolbe-Alexander, Lambert and Charlton (2006). They found that those who were involved in the exercise intervention had a significant decrease in systolic BP. Sakuragi and Sugiyama (2006) studied 21 healthy female subjects who underwent a four week walking program. At the end of the program, their autonomic nervous system had shifted toward parasympathetic predominance. It is recommended that postmenopausal women incorporate 30 minutes of daily walking in to their routine as it is a feasible approach to increase activity level (Asikainen, Kukkonen-Harjula & Miilunpalo, 2004). Williams (2008) assessed the relationships of walking distance and frequency to the prevalence of antihypertensive drug therapy in hypertensive individuals. He found that medication use could be substantially reduced by walking. Further, the effects of long term aerobic exercise on BP are comparable to the benefits of antihypertensive drug use (Ketelhut, Franz & Scholze, 2004; Whelton et al., 2002). Relevant work by other investigators at Queen’s University Previous research from this laboratory has laid a foundation for further investigation in the area of low intensity physical conditioning and the effect of age and 31 gender on cardiac autonomic function. Dougherty (1999) investigated the autonomic modulation of HR in healthy middle-aged men and women and was able to describe characteristics of HRV and SBR sensitivity. She tested participants in supine and standing positions but did not implement an exercise intervention. Dougherty (1999) found that gender affects HRV and SBR sensitivity as males age in a relatively stable fashion whereas females are affected by their menstrual cycle which causes autonomic imbalance during the fifth decade. Females showed higher HRV than men. Women in their fifth decade showed greater sympathetic activity compared to women in their fourth decade. Males showed a declining trend in sympathetic activity as they passed through their 4th and 5th decades. There was no difference in sympathovagal balance between men and women after 50 years of age. Myslivecek, Brown and Wolfe (2002) studied the effect of low-intensity exercise on HRV and spontaneous baroreflex function in 32 normotensive middle-aged women. They were specifically interested in investigating the differences between menopausal and postmenopausal women. Participants were placed into one of two hormonal groups: menopausal (n= 16) and postmenopausal (n=16) and then randomly assigned to either a 12-week, low-intensity exercise training group or to a non-exercise control group. The exercise group was required to walk 3 days /week. Myslivecek et al. (2002) found that menopausal and postmenopausal women in the exercise group experienced higher vagal modulation, lower sympathetic innervation and longer R-R intervals than the sedentary control group. 32 Hua (2006) examined the effects of low-intensity exercise conditioning on BP, HR and cardiac autonomic function in men and women with mild hypertension. Forty participants were separated according to their gender and then randomized into either a 12 week low-intensity exercise program or delegated to a control group. Participants in the exercise group were required to walk 3 days/week. Hua (press) found that the 12 week walking program reduced diastolic BP and increased R-R interval during exercise testing in hypertensive men and women. A reduction in men‘s resting HR was also noted. These results suggest that an exercise conditioning effect had been achieved. It has not been determined if a low intensity exercise program, performed five days/week, would reduce HR, systolic/diastolic BP and improve autonomic balance in women with hypertension. This investigation will not be a replication of previous studies but will utilize earlier findings to guide the hypothesis and study design. Further research directed towards women‘s unique cardiovascular physiology has been identified by Dougherty (1999). The present study aimed to achieve cardiovascular and autonomic adaption through low-intensity exercise by applying a Myslivecek et al. (2002) finding‘s to a population of hypertensive women. Addtionally, Hua et al. (in press) recommended that the quantity of low-intesity exercise be increased from 3 days/ week in order to achieve autonomic adaption. These recommendations were incorporated into the current research design; participants were required to walk 5 days/week. Exercise Adherence Compliance poses the largest obstacle to successful participation in an exercise regime. Compliance and adherence are two words that are often used interchangeably in 33 the literature but are defined slightly differently. This paper will use both terms but favors the use of adherence because it requires patient agreement to the recommendations; this seems appropriate due to the voluntary nature of the study. Compliance will be used because of its wide spread acceptance in the literature. Adherence is defined as, ―the extent to which a persons‘ behavior – taking medications and/or executing lifestyle changes, corresponds with agreed recommendations from a health care provider‖ (Sabaté, 2003). Efficacy of exercise is determined by an individual‘s adherence rate to it. Two thirds of patients are non-adherence with exercise programs. The problem is further complicated as it is difficult to assess compliance rates when noncompliance is not readily admitted and there are extremes of compliance to a regimen (Sluijs, Kok & van der Zee, 1993). Adherence is quantitatively defined as the percentage of sessions completed relative to the number of session prescribed (Cox, Burke, Morton, Gillam, Beilin, & Puddey, 2001). An individual‘s level of self-efficacy is the strongest predictor of adherence to regular exercise (Egan, 2006; McAuley et al, 2003; Sears & Stanton, 2001). Lee, Avis & Arthur (2007) found that self efficacy was directly associated with success in a community based walking program. The Cleveland Clinic, the United States national leader in cardiovascular rehabilitation links personal factors (perceived seriousness of their health problem, feeling of control over their health situation and their level of self-efficacy) to exercise adherence (Egan, 2006). Compliance to an exercise regime is quantified by a simple numeric rating system; high compliance is defined as participation in 67% of prescribed exercise sessions; moderate compliance is associated with 33-66% involvement; low compliance is less than 33% (Hawkins & Hackett, 1982). This study defined adherence to the 34 exercise regime as a minimum of three out of five walks per week at the prescribed distance. Participants were required to complete the entire 12 week protocol. This is consistent with other studies done with similar populations. A minimum of three exercise sessions per week is necessary to produce a conditioning effect (Cleroux, Feldman & Petrella, 1999; Cox et al., 2001; Hua, 2006; Hua et al., in press; Myslivecek et al., 2002). Rationale and Hypothesis Rationale. Hypertension is a well known precursor to stroke and heart disease and has been identified as one of the leading risk factors for death in developed countries (WHO, 2002). Hypertensive individuals experience impairment of the autonomic nervous system. Autonomic deregulation is manifested through increased sympathetic and decreased parasympathetic activity, increased vasomotor sympathetic tone, reduced SBR sensitivity and reduced HRV. The risk of developing hypertension increases with age. More women suffer from hypertension than men (Corrao, Becker, Ockene & Hamilton, 1990). Physical inactivity is a major risk factor which contributes to the development of hypertension. Exercise conditioning is known to lower BP in hypertensive women and reverse some effects of autonomic dysregulation (Davy, Willis & Seals, 1997; Whelton, Chin, Xin & He, 2002). Exercise is commonly recommended at high- or moderateintensity to reduce high BP and restore baroreflex function (Cleroux, Feldman & Petrella, 1999; Parati & Lantelme, 2005). However, moderate-intensity exercise can be harmful as it increases sympathetic activity and BP which could result in cardiovascular injury. Low intensity exercise may offer comparable cardiovascular benefits without increasing plasma catecholamines (Brown et al., 1994; Nakamura et al., 1993; Yamamoto et al., 35 1991). Walking has been found to be a suitable low intensity exercise that is recommended for hypertensive individuals (Lesniak & Dubbert, 2001). Currently, there are is no available literature which describes the effect of a low intensity exercise conditioning program on BP, HR and cardiac autonomic function in middle-aged women diagnosed with hypertension. The purpose of this study is to determine the effects of a 12 week low intensity exercise conditioning program on BP, RPP, HR and cardiac autonomic function in women with hypertension. Additionally, the influence of menopausal state will be evaluated to determine its influence on the outcome variables. Hypothesis. Compared with hypertensive women in a non exercising comparison group, those in a 12 week low intensity home walking program will demonstrate the following: 1) Cardiovascular adaptation (decreased systolic BP, diastolic BP, HR and RPP at rest, standing and at a given sub maximal exercise) 2) Autonomic adaptation (increased parasympathetic modulation of HR and decreased sympathetic indicator at rest, standing and at a given submaximal exercise). Additionally, menopausal state (menopausal, postmenopausal) will influence HRV and SBR sensitivity such that postmenopausal women will demonstrate increased sympathetic and decreased parasympathetic innervation of the heart and decreased spontaneous baroreflex sensitivity compared to menopausal women. 36 CHAPTER THREE Method Participants Fifty sedentary, non-smoking women, diagnosed with hypertension by a physician (BP ≥ 140/90 mmHg) (Canadian Hypertension Education Program (CHEP), 2007), aged 45-65 years, were invited to participate in this study. Consistent with the American College of Sports Medicine (ACSM) (2006) guidelines, sedentary was defined as performance of fewer than two sessions per week of regular aerobic exercise. Nonsmoking status was defined as self reported abstinence from cigarette smoking for a period of three months prior to the study. Participants were required to read and write the English language and give informed consent in order to volunteer for this study (Appendix A). Physician approval had to be obtained for women who answered ―yes‖ to at least one of seven questions on the Physical Activity Readiness Questionnaire (PARQ) (Canadian Society for Exercise Physiology, 2002) (Appendix B). Individuals were excluded from the study for the following reasons: 1) currently participating in more than two aerobic physical activity sessions per week; 2) co-morbid conditions that limited ability to participate in exercise or exercise testing; 3) taking hormone replacement therapy; 4) diagnosed with stroke, heart failure, ischemic heart disease, myocardial infarction, renal disease or vascular disease; 5) tobacco/ marijuana smoking; 6) family physician disapproval. Four eligible women withdrew from the study due to illness (n= 1) 37 and loss to follow up (n= 3). See Appendix O for a summary of the study sample and reasons for attrition. Antihypertensive medications are prescribed by family physicians in this region as standard practice for the treatment of hypertension. Consequently, BP medications were accounted for in the data analysis. Participants were eliminated from the study if they underwent a change of medication type or dose during the study. Recruitment was carried out in Kingston, Ontario from September 2007 to March 2008. Potential participants were solicited through community newspapers, internet advertisements and through flyers distributed at local hospitals, family physician‘s offices, post secondary institutions and public notice boards. A convenience sample was utilized; 150 interested women responded to advertisements and were screened for preliminary eligibility by telephone or e-mail. Women who failed to meet the inclusion criteria were excluded from the study. Eligible women were then invited to the Exercise Research Laboratory in the Hotel Dieu Hospital (Kingston, Ontario) in order to confirm eligibility, provide written informed consent and perform the initial HR and BP testing. Participants were counterbalanced within the exercise and control group according to classification of BP medications (beta blocker or no beta blocker). Blinding was not possible as participants in the exercise group had to actively engage in a walking program and the control group maintained their sedentary lifestyle. To decrease contamination, the control group was specifically asked to maintain their current lifestyle (exercise/nutrition) for the duration of the experiment. 38 The sample size was calculated using systolic BP as the primary outcome measure and based on previous findings in women. Hua, Brown, Hains, Godwin, and Parlow (in press) used a sample of 20 women divided into two groups (control/exercise) in order to demonstrate a reduction in BP due to low intensity exercise performed over 12 weeks. Using the systolic BP values obtained from women in the exercise group (Week 1136mmHg, Week 12- 129 mmHg, SD 12, alpha .05, desired power .80) the sample size for this study was calculated to be 37. Ethics approval was obtained from the Queen‘s University Research Ethics Board and the Affiliated Teaching Hospitals Health Sciences Human Research Ethics Board (Kingston, ON). Permission was granted for all previously developed tools used within this study. Equipment and Instruments The PAR-Q (CSEP, 2002) was used to screen interested women for eligibility before they came to the Exercise Physiology Laboratory at Hotel Dieu Hospital for initial testing. The PAR-Q consists of seven ―yes‖ or ―no‖ questions which are designed to identify adults for whom physical activity may be inappropriate. If a participant answered ―yes‖ to one or more questions, their Family physician was notified and written approval was obtained. If a participant answered ―no‖ to all questions, she proceeded through the study design and did not require permission from her family physician. This procedure was established in consultation with the medical supervisor of this research project. Permission to use the PAR-Q was granted by the Canadian Society for Exercise Physiology. 39 The Human Activity Profile (HAP) (Daughton, Fix, Kass, Bell & Patil, 1982) is an instrument that was used to measure regular physical activity. The HAP consists of 94 common daily activities ranked in order from least to most amount of energy expenditure. These activities cover a wide range and represent self care tasks (taking a bath), personal/household work (carrying out the garbage), entertainment /social activities (golfing 18 holes without riding a cart) and independent activities. Participants indicated if they are currently able, unable or have never been able to perform the activity. The Maximum Activity Score (MAS) and the Adjusted Activity Score (AAS) are calculated from participant responses. Higher MAS and AAS scores signify activities which require more energy to perform. Low scores indicate difficulty with activity levels. The HAP takes about ten minutes to complete and is a valid and reliable measure of physical activity (Bilek, Venema, Camp, Lyden & Meza, 2005; Davidson & de Morton, 2007). Participant‘s weight and height were measured with a Seca 700 scale (Seca Corporation, Hanover, MD); measurements were used to calculate body mass index (kg/m2). Waist circumference was measured with a soft plastic measuring tape while the participant stood upright. The measuring tape was placed around the participant‘s waist, parallel to the floor, between the bottom of the rib cage and the top of the hipbones. The BpTRU (Model BPM-300, VSM Medtech Ltd. Coqitlam, BC) is an automated non invasive BP monitor that was used to measure systolic and diastolic BP and HR via an inflatable arm cuff, at rest, standing and at peak exercise. The BpTRU has been shown to be an accurate non-invasive BP monitoring device for individuals aged 383 years (Mattu, Heran & Wright, 2004) 40 The Finapres® 2300 (Ohmeda, Englewood, CO) is a digital automated BP monitor which was used during testing to measure and record spontaneous changes in beat-by-beat finger arterial BP. This is a photoplethysmographic measure. The reliability of the Finapres® 2300 in detecting changes in systolic BP has been demonstrated by several studies (Iellamo, Legramante, Raimondi, Castrucci, Massaro & Peruzzi, 1996; Imholz, van Montfrans, Settels, van der Hoeven, Karmaker & Weiling, 1988; Imholz, Wieling, van Montfrans, Wesseling, 1998). A computer software program developed by Blaber, Yamamoto & Hughson (1995) was used for spontaneous baroreflex analysis. The Spacelab 521T Cardiac Monitor with QRS detector (Squibb Vitatek Inc., Hillsboro, USA) was used to collect HRV data (R-R interval). Standard surface electrocardiographic (ECG) electrodes were used with the monitor. The cardiac monitor was interfaced with a personal computer by means of an eight-channel analog/digital convertor (DAS-16, Metrabyte Corp., Multitest Electronics, Scarborough, ON). The DAS-16 provides an R-R interval accuracy of 1 ms at a sampling rate of 1000Hz (Parlow, Viale, Annat, Hughson & Quintin, 1995). The digital R-R interval output was stored on a password protected personal laptop computer (Dell Inspiron 9400). Hughson and Yamamoto (1993) computer software program was used for spectral analysis of HRV. Each participant performed steady-state exercise on the Ergometrics er800s cycle ergometer (Ergoline GmbH, Lindenstrabe, Germany). This is an electronic, computerized, stationary ergometer that is self regulated. Borg‘s Rating of Perceived Exertion (Borg, 1982) was used by participants during steady-state exercise testing and by the exercise group during the 12 week walking 41 program. It is a 6-20 point descriptive scale where 6 represents, "no exertion at all" and 20 represents "maximal exertion." Participants in the exercise group were told to aim for a perceived exertion level of 11-13 (light - somewhat hard) as 12-14 (somewhat hard – hard) is associated with a moderate intensity level of intensity. The scale is based on physical sensations experienced during activity; increased HR, increased respiration, increased sweating and muscle fatigue. Although this is a subjective measure, exertion rating is indicative of HR during physical activity (Borg, 1998). Borg‘s Rating of Perceived Exertion scale has been shown to be a valid measure of exercise intensity (Robertson & Noble, 1997). A log was provided to participants in both groups. The exercise log for the exercise group contained instructions on how to measure radial/carotid pulse (Appendix C), Borg‘s Rating of Perceived Exertion (Appendix D), a 12 week low-intensity walking protocol (Brown, Laschinger, Hains & Parry, 1992; Brown, Wolfe, Hains, Pym & Parker, 1994) (Appendix E), and a log to measure compliance to the exercise regime: distance, duration of exercise, HR, perceived exertion, reasons for not exercising and additional physical activity (Appendix F). The control group received an activity log which contained a 12 week log to record daily physical activity (Appendix G). 42 Eligible Sample N=50 Inclusion Criteria; Female Age >44 yrs Diagnosed with Hypertension (BP >140/90) Sedentary (<2 exercise sessions/week) Approval of physician or pass PAR-Q Time N = 12 weeks Assignment to Groups Control N=23 Exercise N=27 Week 1- Baseline Telephone call every three weeks Week 12 – Follow-up Figure 1. Study design Procedure Prior to testing, participants were screened through telephone interviews based on the inclusion and exclusion criteria. During the initial telephone screening, participants verbally completed the PAR-Q questionnaire (CSEP, 2002). Responses were documented and evaluated for entrance into the study. Physician‘s written approval was granted for women who answered ―yes‖ to one or more of the PAR-Q questions. After telephone screening, potential participants were invited to the Exercise Physiology Laboratory at Hotel Dieu Hospital and asked to refrain from consuming alcohol or caffeine 12 hours before testing (Daniels, Mole, Shaffrath & Stebbins, 1998; Richardson, Rozkovec, Thomas, Ryder, Meckes & Kerr, 2004). Participants were also asked to avoid eating a large meal two hours in advance and refrain from strenuous physical activity for 24 hours prior to testing. During the initial visit, the researcher explained the study in detail and answered participants‘ questions. Eligible participants provided written informed consent, 43 following which demographic data was collected to determine if there were any confounding influences on the outcome measures. Demographic data included age, education level, marital status, occupation, cardiovascular medical history/medications and menopausal state. Participants completed the HAP (Daughton et al., 1982) before height, weight and waist circumference were measured with the shoes removed. Body mass index (BMI) was calculated by dividing body weight by height squared (kg/m2). The physiological data that were collected included arterial BP in the brachial artery and autonomic data (HRV [R-R interval data] and beat-by-beat finger arterial BP) in three conditions (supine, standing, exercise). Arterial BP, using a BpTRU automatic BP monitor on the left arm, was taken in two postures (supine, standing) and at the end (peak) of low intensity exercise. The lower edge of the BpTRU BP cuff was placed approximately 2.5 cm above the site of the brachial artery (determined by palpation of the left arm). Autonomic data were measured and recorded continuously for 10 min, after 35 min equilibration, in each condition, for a minimum of 512 cardiac cycles. R-R interval data were obtained using an ECG recording, with 3 latex-free, standard surface ECG electrodes in a Lead II configuration (right arm, left arm and left leg). Beat-by-beat arterial BP data were measured using the Finapres 2300 automated BP monitor. A finger cuff was placed on the middle phalanx of the third digit on the left hand and connected to a transducer that is positioned on top of the left hand. The left hand was elevated to the level of the phlebostatic axis of the heart by placing it on an adjustable side table. In the supine position, arterial BP (BpTRU) was measured in a quiet, lightattenuated room after a 3 min equilibration period. Autonomic data (HRV, beat-by-beat 44 arterial BP) were then recorded continuously for 10 min. Participants were advised to relax and refrain from speaking or moving during data recording (Brown, Wolfe, Haines, Ropchan & Parlow, 2003). Electrocardiogram electrodes were placed in a Lead II configuration in order to obtain R-R interval data. A finger cuff was placed on the participant‘s middle finger in order to obtain arterial BP. Participants then stood upright for a 3-5 min equilibration period (Kamath, Fallen & McKelvie, 1991). After the equilibration period, arterial BP (BpTRU) was taken in the left arm. Subsequently, R-R interval and beat-by-beat arterial BP data were collected for 10 min in the free standing position. The 512 cardiac cycles recorded was used for analyses of HRV and SBR sensitivity (Brown et al., 2003; Hughson, Northey, Xing, Dietrich, & Cochrane, 1991). HRV and arterial BP were measured with the same electrocardiogram electrode configuration and finger cuff placement as the supine position. Subjects were reminded to remain as still as possible and not to talk during data collection. The participants were advised to notify the researcher immediately if they experienced signs of orthostatic hypotension: dizziness, light-headedness, shortness of breath, weakness or palpitations. If they experienced any of these symptoms, the testing was discontinued. Participants then performed low-intensity, steady-state exercise at a constant work rate on a cycle ergometer (Brown et al., 2003; Hua et al., in press; Myslivecek et al., 2002). Each participant sat upright on the cycle ergometer with the seat, handle bars and foot straps adjusted to suit them comfortably. The finger cuff was maintained at the level of the heart by elevating the hand/transducer parallel to the participant‘s body with an 45 adjustable stainless steel side table. After a 3-5 min equilibration period, autonomic data were collected for 512 cardiac cycles during steady-state exercise and was used for analyses of HRV and SBR sensitivity. At peak exercise, arterial BP (BpTRU) was taken in the left arm. Steady state is reached when HR remains constant at the desired work intensity. A four minute warm-up at 20 watts was followed by a ramp increase in work rate within 30 seconds to a work rate equivalent to 40% of the maximal HR reserve (HRR). The Karvonen method was used to determine participants target HR (40% of maximum HRR) (Miller, Wayne, Wallace & Eggert, 1993; Myslivecek, Brown & Wolfe, 2002; Stejskal, Rechbergova, Salinger, Slachta & Elfmark, 2001). A participant‘s maximum HR, resting HR (recorded by BpTru) and the percentage of desired exercise intensity (40% HRR) are used in the formula below to determine target HR: Target HR= (40%) (HR max - HR rest) + HR rest Steady state exercise intensity was determined by measuring HR. HR rises exponentially during the first minutes of exercise as it eventually reaches a plateau. After this initial period, it remains relatively stable for the duration of the effort (McArdle, Katch & Katch, 2007). A participant‘s HR was monitored and steady state was recognized as a HR which was no longer increasing at the target work rate. After the initial testing, women were counterbalanced between one of two groups, exercise (n=27) or control (n=23). The exercise group was given verbal and written instructions for a 12 week, low-intensity progressive walking program, an exercise log (to record exercise sessions, HR, level of perceived exertion and reasons for not exercising), 46 Borg‘s rating of perceived exertion scale (Borg, 1982; Borg, 1998) and instructions to measure HR. Participants were taught how to monitor HR by radial palpation, use the walking protocol, record their walking sessions and use Borg‘s Rating of Perceived Exertion. Their understanding was verified by having them demonstrate each task prior to leaving the laboratory. Compliance rates were to be recorded in the log, a participant was considered compliant if they completed a minimum of three exercise sessions per week (Cleroux, Feldman & Petrella, 1999; Lesniak & Dubbert, 2001; Wallace, 2003). The women in the exercise group were asked to refrain from making any dietary changes during the study. They were advised not to walk within two hours of consuming a large meal, alcohol or caffeine and encouraged to stretch and drink adequate fluids before and after each walking session. In the event of an adverse reaction to exercise (shortness of breath, dizziness, chest pain or any musculoskeletal injury), participants were told to contact their family physician. See Figure 1 for study design. Participants were told to notify the primary investigator in the event of illness or injury. They were instructed to continue to record daily activity regardless of inactivity and to resume the walking program from the point where they initially left off. These periods were analyzed at the end of the 12 week walking program. Participants who were sick for >3 weeks were encouraged to see their family physician and were excluded from the study. The exercise conditioning protocol was a 12-week progressive, low-intensity (40% maximum RR), walking program, which was validated by Brown et al. (1992; 1994), Hua et al. (in press) and Myslivecek et al. (2002). Participants in the exercise group were 47 instructed to walk five times per week at a prescribed distance. The walking program started at .08 km/day for the first two weeks and then gradually increased in increments of 400 meters (1.2 km/day, 1.6km/day, 2 km/day) every week to a maximum distance of 4.8 km/day. See Appendix E for exercise conditioning protocol. The control group was given verbal instructions to record daily physical activity in the activity log provided. They were also asked to maintain their current level of activity and refrain from making dietary changes during the 12 week study. Exercise and control groups were given telephone calls or sent e-mails from the primary investigator every three weeks to answer questions and monitor progress. The testing procedures were repeated at the end of the 12-week study period. The initial testing lasted approximately 2 hours to complete while the follow-up after 12 weeks took 1 hr. Exercise/activity logs were collected at the follow-up visit to measure compliance. Data Analysis Analysis of Heart Rate Variability. HRV is a measure of beat-to-beat variations in HR and was analyzed by power spectral analysis using the frequency domain method (TFESCNASPE, 1996). R-R interval data from electrocardiogram recordings were converted into a tachogram. The tachogram was then subjected to Fast Fourier Transformation and converted into a frequency spectrum, separated into LF and HF power. The variables for analysis of HRV are HF, LF and TP, the ratio of HF to TP (parasympathetic indicator) and the ratio of LF to HF power (sympathetic indicator). The editing process was guided by the methods used by Hua, Brown, Hains, Godwin & 48 Parlow (in press) and Hughson, Quintin, Annat, Yammamoto & Gharib (1993). See Appendix J for a description of the editing process. Analysis of Baroreflex Sensitivity. The arterial baroreceptor reflex is a homeostatic mechanism which adjusts the short term, beat-by-beat, regulation of arterial BP. Measuring the sensitivity of the arterial baroreflex serves as an index of cardiac autonomic control (Kardos, Watterich, de Menezes, Csanády, Casadei & Rudas, 2008). SBR sensitivity was evaluated using the sequence method. The sequence method detects spontaneous sequences of three or more heart beats in which systolic BP and R-R interval simultaneously change in the same direction. SBR sensitivity is quantified by an R-R interval response to a 1 mmHg change in systolic BP (Brown, et al., 2003). The sequences are then analyzed by computer software which uses linear regression to calculate the slope of each series. The mean slope is used to quantify SBR sensitivity; an increase in the baroreflex slope is associated with greater parasympathetic innervation whereas a decrease in slope is linked to reduced vagal stimulation (Hughson et al., 1993; Blaber et al., 1995; La Rovere, Bersano, Gnemmi, Specchia & Schwartz, 2002; Parlow et. al, 1995). The variables for analysis of SBR sensitivity include mean baroreceptor slope, systolic BP and R-R interval. R-R interval data from the electrocardiogram and arterial BP from the Finapres were collected and edited (Hua et al., 2006; Blaber, Yammamoto & Hughson, 1995). The methods used for editing can be found in Appendix K. 49 Statistical Analysis Descriptive statistics were used to determine the means, frequencies and standard deviations for the demographic, physiological and lifestyle data collected. Demographic variables that were analyzed included: age, education level (years), marital status, menopausal state (pre vs. post), antihypertensive medications, height, weight, body mass index and waist circumference. Physiological data included: HR, systolic BP, diastolic BP, HRV and SBR sensitivity in three conditions (supine, standing, steady state exercise). A numeric activity profile was used to determine lifestyle data. All variables were evaluated at the beginning and the end of the exercise program. Student t-statistics were used to determine if the two groups differed from each other in these variables at week 1 and 12. Repeated measures analysis of variance (ANOVA), with time (two levels: week 1, week 2) and condition (rest, standing, exercise) as the within-subjects factors, group (two levels: exercise, control) and menopausal state (two levels: menopausal, postmenopausal) as the between-subjects factors, was done to determine if there were any significant differences between means at week 12. Several repeated measures ANOVA‘s were performed using two-between factors (Group- exercise, control; Menopausal state- pre, post) and two-within factors (Timeweek 1, week 12; Condition- resting, standing, exercise) to evaluate HR, BP and cardiac autonomic function. The following were analyzed using this method: BP, HR, RPP, HRV (R-R interval, HF power, LF power, TP, parasympathetic indicator, sympathetic indicator) and SBR sensitivity (slope, systolic BP, R-R interval). All data analysis was conducted with SPSS version 16.0. Compliance rates were determined by calculating 50 average number of walking sessions completed per week. Mean number of walking sessions were calculated and compared between groups. Differences for all analysis will be significant if p<.05. 51 CHAPTER FOUR Results Descriptive statistics were used to determine the means, frequencies and standard deviations for the demographic, physiological and lifestyle data. Independent t-tests were used to determine if there were any significant differences between the two groups. Fifty hypertensive women enrolled in this study. Forty-six participants completed the 12-week study. The means (±SD) at week1 for participants‘ age, education level, body mass index (BMI), waist circumference, maximum activity score, adjusted activity score, BpTRU resting systolic and diastolic blood pressure, BpTRU resting heart rate and resting ratepressure-product are shown in Table 1. There were 18 menopausal and 32 postmenopausal women in the study sample. The control group consisted of 39% menopausal and 61% postmenopausal women. The exercise group included 33% menopausal and 67% postmenopausal women. At week 1, there was no significant difference between the two groups. At week 12, BMI was lower in the Exercise group compared to the control group (see page 62). See Appendix O for study sample and reasons for attrition, Appendix P for other demographic data (marital status, employment status) and Appendix Q for demographic, physiological and lifestyle Chisquared/ANOVA summary tables. 52 Table 1. Means (±SD) at week 1 for demographic, physiological and lifestyle measures in both control and exercise group separately. Measure Control Group Exercise Group (n = 23) (n = 27) Age (years) 51.9 (5.8) 55.0 (7.2) Education (years) 13.3 (2.5) 13.1 (2.4) Body Mass Index (kg/m2) 34.9 (6.8) 32.6 (5.7) Waist Circumference (inches) 41.9 (5.3) 40.8 (5.4) Mean Activity Score 79.9 (5.9) 78.3 (6.8) Adjusted Activity Score 68 (10.2) 63.7 (17.7) Resting Systolic BP (mmHg) 130 (17) 137 (21) Resting Diastolic BP (beats/min) 81 (10) 86 (13) Resting HR (beats/min) 67(7) 67(10) Resting Rate-Pressure-Product 9 (1) 9 (2) ((HR x systolic BP) x10-2) Note. BP taken using BpTRU automated BP monitor. BP = blood pressure; HR = heart rate; min = minute 53 Antihypertensive Medications The majority of participants were taking at least one antihypertensive medication during the 12 week study. Twenty of twenty-three women in the control group were on antihypertensive medications; similarly 23 out of 27 in the exercise group were using antihypertensive drugs. The exercise and control groups were counterbalanced by medication type (beta blocker or no beta blocker). At week 1, there was no difference between the two groups. See Table 2 for antihypertensive medication classification. Table 2. Antihypertensive medication classification for both control and exercise group separately. Antihypertensive Medication Control Group Exercise Group Classifications (n = 23) (n = 27) Diuretics 1 1 Ace-Inhibitors 2 4 Angiotensin II Receptor Antagonist 3 2 Calcium Channel Blockers 1 0 Beta Blockers 5 3 Combination of ≥ 2 BP Medications 8 13 No BP Medications 3 4 Total: 23 27 Note. BP = blood pressure 54 BpTRU Blood Pressure and Heart Rate Measures over Time BpTRU systolic BP, diastolic BP, heart rate (HR) and rate-pressure-product (RPP) means (±SD) are shown at week 1 in Table 1. To test for the effects of exercise conditioning, repeated measures ANOVA with two-between (Group– control, exercise; Menopausal state- pre, post) and two-within (Time- week 1, week 12; Condition – rest, standing, exercise) were performed to analyze changes in BpTRU BP, HR and RPP between groups over the 12 week study period. See Appendix Q for ANOVA summary tables for BpTRU BP, HR and RPP measures. BpTRU Systolic BP. In the ANOVA performed on systolic BP data, there was a significant main effect of Time, F(1,42) = 8.07, p<.01 and Condition, F(2, 84) = 51.79, p<.001. The main effect of Time was qualified by a significant Time X Group interaction, F(1,42) = 4.30, p<.05. See Figure 2 for the linear Time X Group interaction; the exercise group experienced a significant reduction in systolic BP. See Figure 3 for the linear main effect of Condition; when compared to rest, there was an increase in systolic BP during standing and exercise. No other effects were found. 55 Figure 2. Mean systolic blood pressure as a function of time for the control and exercise group separately. Figure 3. Mean systolic blood pressure in three conditions for the control and exercise group over time. 56 BpTRU Diastolic BP. In the ANOVA performed on diastolic BP data, there was a significant Time X Group interaction, F(1, 42) = 7.97, p<.01 and a main effect of Condition, F(2, 84) = 30.07, p<.001. See Figure 4 for the linear Time X Group interaction; the Control group experienced a significant increase in diastolic BP over time while the Exercise group experienced a significant decrease in diastolic BP over time. See Figure 5 for the quadratic main effect of Condition; compared to rest, there was an increase in diastolic BP during standing and exercise. No other effects were found. 57 Figure 4. Mean diastolic blood pressure as a function of time for the control and exercise group separately. Figure 5. Mean diastolic blood pressure in three conditions for the control and exercise group separately. 58 BpTRU HR. In the ANOVA performed on HR data, there was a main effect of Condition, F(2, 84) = 164.21, p<.001. The effect of condition which was qualified by a Time X Condition interaction, F(2, 84) = 3.33, p<.05. See Figure 6 for the linear Time X Condition interaction; compared to rest, there was an increase in HR during standing and exercise. HR increased over time during standing compared with rest. No other effects were found. Figure 6. Mean heart rate in three conditions for week 1 and week 12. 59 BpTRU RPP. In the ANOVA performed on RPP data, there was a significant Time X Group interaction, F(1, 42) = 5.71, p<.05 and a main effect of Condition, F(2, 84) = 152.27, p<.001. See Figure 7 for the linear Time X Group interaction; the exercise group experienced a significant decrease in RPP over time. See Figure 8 for the linear main effect of Condition; compared to rest, there was a significant increase in RPP during standing and exercise. No other effects were found. 60 Figure 7. Mean Rate-Pressure-Product as a function of time for the control and exercise group separately. Figure 8. Mean Rate-Pressure-Product in three conditions for the control and exercise group separately. 61 There was no correlation between BMI and BpTRU measures (systolic BP, diastolic BP, HR and RPP). BMI (week 1, week 12) was examined by bivariate correlation with the outcome measures. Further, age and menopausal state did not affect any of the BpTRU measures (systolic BP, diastolic BP, HR and RPP). Age was examined as a covariate and menopausal state was examined as a between-subjects factor. 62 Comparison of Body Mass Index and Waist Circumference over Time Repeated measures ANOVA with one-between (Group– control, exercise) and one-within (Time- week 1, week 12) were performed to examine BMI and waist circumference. BMI measures demonstrated a significant Time X Group, F(1,44) = 9.34, p<.01, interaction. See Figure 9 for linear Time X Group interaction. No significant effects were found for waist circumference. At week 1, the control group had a mean waist circumference of 41.9 (SD± 5.3) inches and the exercise group had a mean waist circumference of 40.8 (SD±5.4) inches. At week 12, the control group had a mean waist circumference of 42.5 (SD± 5.5) inches and the exercise group had a mean waist circumference of 40.0 (SD±5.1) inches. No other effects were found. Figure 9. Mean body mass index as a function of time for the control and exercise group 63 Heart Rate Variability Measures Eleven out of 294 raw data files collected were missing when heart rate variability (HRV) analysis was performed (4% of total). Five files corresponded to participants in the control group and seven belonged to participants in the exercise group. Due to skewness, outliers and unequal variation that existed in the raw HRV data, log transformations were performed on low frequency (LF) power, high frequency (HF) power, total power (TP), parasympathetic nervous system (PNS) indicator and sympathetic nervous system (SNS) indicator to minimize the effect of extreme values. Log transformed data was used for all HRV statistical analyses. Independent t-tests determined that there were no significant differences between the two groups at week 1. See Table 3 for HRV means (±SD) at week 1. Repeated measures ANOVA with two-between factors (Group- exercise, control; Menopausal state- pre, post) and two-within factors (Time- week 1, week 12; Conditionresting, standing, exercise) were performed on each HRV measure (LF, HF, TP, PNS indicator and SNS indicator). See Appendix Q for ANOVA summary tables for all HRV measures. 64 Table 3. Means (±SD) for log transformed heart rate variability measures for both control and exercise group at week 1. Time Week 1 Group Control Exercise (n=23) (n=27) Resting 1.94 (.37) 1.99 (.48) Standing 2.07 (.37) 2.05 (.41) Exercise 1.50 (.64) 1.43 (.73) Resting 1.78 (.43) 1.81 (.52) Standing 1.45 (.33) 1.42 (.53) Exercise 1.33 (.69) 1.27 (.70) Resting 2.57 (.32) 2.55 (.46) Standing 2.56 (.30) 2.51 (.40) Exercise 2.28 (.58) 2.41 (.66) Low Frequency Power (ms2/Hz) High Frequency Power (ms2/Hz) Total Power (ms2/Hz) PNS Indicator (HF/TP) Resting -.79 (.26) -.74 (.24) Standing -1.11(.24) -1.09 (.35) Exercise -.95 (.36) -1.13 (.30) Resting .16 (.37) .18 (.33) Standing .62 (.30) .63 (.36) Exercise .17 (.23) .16 (.20) SNS Indicator (LF/HF) Note. SNS = sympathetic nervous system; PNS = parasympathetic nervous system; ms = milliseconds; m2/Hz = milliseconds squared per hertz; HF/TP = high frequency/ total power; LF/HF = low frequency/ high frequency 65 Low Frequency Power. In the ANOVA performed on LF data, there was a significant main effect of Condition, F(2, 72) = 16.57, p<.001, which was qualified by a Time X Condition, F(2, 72) = 5.28, p<.01 interaction. There was also a significant main effect of Menopause, F(1, 36) = 6.43, p<.05, between subjects. See Figure 10 for the quadratic Time X Condition interaction; compared to rest, there was a significant increase in LF power during standing and a decrease during exercise. LF power increased over time during standing compared to rest. See Figure 11 for the linear main effect of Menopause; LF power was lower in postmenopausal than menopausal women. No other effects were found. 66 Figure 10. Mean of the log transformed low frequency power in three conditions as a function of time. Figure 11. Mean of the log transformed low frequency power as a function of menopausal state. 67 High Frequency Power. In the ANOVA performed on HF data, there was a significant main effect of Condition, F(2, 72) = 11.34, p<.001 and a Menopause X Group interaction, F(1, 36) = 5.20, p<.05 between subjects. See Figure 12 for the quadratic main effect of Condition; compared to rest, there was a significant decrease of HF power during standing and exercise. See Figure 13 for the linear Menopause X Group interaction; HF power was lower in the postmenopausal exercise group than the postmenopausal control group. No other effects were found. 68 Figure 12. Mean of the log transformed high frequency power in three conditions for the control and exercise group separately. Figure 13. Mean of the log transformed high frequency power as a function of menopausal state for the control and exercise group separately. 69 Total Power. In the ANOVA performed on TP data, there was a main effect of Menopause, F(1, 36) = 4.28, p<.05, between subjects. See Figure 14 for the linear main effect of Menopause; TP was lower in postmenopausal than Menopausal women. No other effects were found. Figure 14. Mean of the log transformed total power as a function of menopausal state. 70 PNS Indicator. In the ANOVA performed on PNS Indicator data, there was a significant main effect of Condition, F(2, 72) = 33.34, p<.001, which was qualified by Condition X Group interaction, F(2, 72) = 5.55, p<.01, and a Condition X Menopause interaction, F(2, 72) = 3.94, p<.05, within subjects. See Figure 15 for the quadratic Condition X Group interaction; the Exercise group experienced a decreased PNS indicator compared to the Control group during steady-state exercise. See Figure 16 for the quadratic Condition X Menopause interaction; postmenopausal women had lower PNS indicator during rest and standing compared to menopausal women. No other effects were found. 71 Figure 15. Mean of the log transformed PNS Indicator in three conditions for the control and exercise group separately. Figure 16. Mean of the log transformed PNS Indicator in three conditions for menopausal and postmenopausal women separately. 72 SNS Indicator. In the ANOVA performed on SNS Indicator data, there was a significant main effect of Condition, F(2, 72) = 50.29, p<.001 and a Condition X Menopause X Group interaction, F(2, 72) = 5.24, p<.01, within subjects. See Figure 17 for the quadratic main effect of Condition; compared to rest, SNS indicator increased during standing. See Figure 18 for the quadratic Condition X Menopause X Group interaction. Postmenopausal women in control group had decreased SNS indicator during rest and steady-state exercise compared to menopausal women in the control group. Menopausal women in the exercise group demonstrated decreased SNS indicator during rest compared to postmenopausal women in the exercise group. Figure 17. Mean of the log transformed SNS Indicator in three conditions for the control and exercise group separately. 73 To sort out the Condition X Menopause X Group interaction, a simple effects analysis was conducted by separating the groups (Group- Exercise, Control; Menopausal State- pre, post) and then repeating the analysis. For menopausal women in the Control group, F(1, 7) = 8.44, p<.05, and postmenopausal women in the Control, F(1, 11) = 29.85, p<.001 and Exercise group, , F(1, 13) = 11.67, p<.01, there was a significant increase in SNS indicator during standing. For menopausal women in the Exercise group, there was a significant increase in SNS indicator during standing, F(1, 5) = 17.02, p<.01 and exercise, F(1, 5) = 19.22, p<.01. No other effects were found 74 a) Control Group b) Exercise Group Figure 18. Mean of the log transformed SNS Indicator in 3 conditions as a function of menopausal state for a) control group and b) exercise group. 75 There was no correlation between BMI and HRV measures (LF, HF, TP, PNS indicator, SNS indicator). BMI (week 1, week 12) was examined by bivariate correlation with the outcome measures. Further, Age did not affect any of the BpTRU measures (systolic BP, diastolic BP, HR and RPP). Age was examined as a covariate. 76 Baroreflex Measures Eleven out of 294 raw data files collected were missing when HRV and spontaneous baroreflex sensitivity analysis was performed (4% of total). Five files corresponded to participants in the control group and seven belonged to participants in the exercise group. Independent t-tests determined that there were no significant differences between the Exercise and Control group at week 1. The means (±SD) for spontaneous baroreflex sensitivity measures at week 1 are shown in Table 4. Repeated measures ANOVA with two-between (Group- Exercise, Control; Menopausal state- menopausal and postmenopausal) and two-within (Time- week 1, week 12; Condition- resting, standing, exercise) were performed to examine the effects of exercise conditioning on spontaneous baroreflex measures (slope, systolic BP, R-R interval) between groups, over time. 77 Table 4. Means (±SD) for spontaneous baroreflex measures for in both control and exercise group at week 1. Time Week 1 Group Control Exercise (n=23) (n=27) Resting 6.38 (3.88) 6.55 (3.37) Standing 3.16 (1.59) 3.12 (2.01) Exercise 5.57 (5.13) 6.38 (4.70) Resting 108 (36) 122 (28) Standing 147 (27) 140 (25) Exercise 157 (39) 169 (42) Resting 882 (91) 897 (119) Standing 776 (95) 764 (101) Exercise 518 (99) 530 (74) Baroreflex Slope (ms/mmHg) Systolic Finapres arterial BP (mmHg) R-R Interval (ms) Note. BP = blood pressure; ms = milliseconds; mmHg = millimeters of mercury 78 Baroreflex Slope. In the ANOVA performed on baroreflex slope data, there was a significant main effect of Condition, F(2, 72) = 12.16, p<.001. See Figure 19 for the quadratic main effect of Condition; compared to rest, there was a decrease in baroreflex slope during standing. No other effects were found. Figure 19. Mean baroreflex slope in three conditions for the control and exercise group separately. 79 Systolic Finapres Arterial BP. In the ANOVA performed on systolic BP data, there was a significant main effect of Condition, F(2, 72) = 36.61, p<.001, which can be qualified by a Time X Condition interaction, F(2, 72) = 4.87, p<.05 and a Condition X Group interaction, F(2, 72) = 5.63, p<.01. See Figure 20 for the linear Time X Condition interaction; compared to rest, there was a significant increase in systolic BP during standing and steady-state exercise. Systolic BP decreased over time during standing and steady-state exercise compared to rest. See Figure 21 for the quadratic Condition X Group interaction; the Exercise group experienced a significant increase in systolic BP during steady-state exercise compared to rest. No other effects were found. 80 Figure 20. Mean systolic Finapres arterial blood pressure in three conditions as a function of time. Figure 21. Mean systolic Finapres arterial blood pressure in three conditions for the control and exercise group separately. 81 R-R Interval. In the ANOVA performed on R-R interval data, there was a significant main effect of Condition, F(2, 72) = 372.49, p<. 001, and a there was a Time X Condition X Menopause interaction, F(2, 72) = 3.31, p<.05. See Figure 22 for the linear main effect of Condition; compared to rest, there was a decrease in R-R interval during standing and steady-state exercise. See Figure 23 for the linear Time X Condition X Menopause interaction; over time, R-R interval decreased significantly in postmenopausal women during exercise compared with rest. Figure 22. Mean R-R Interval in three conditions for the control and exercise group separately. 82 To sort out the Time X Condition X Menopause interaction, a simple effects analysis was conducted by separating the groups by menopausal state (menopausal, postmenopausal) and then repeating the analysis. For menopausal women, there was a significant decrease in R-R interval during standing, F(1, 12) = 93.03, p<.001, and exercise, F(1, 12) = 269.95, p<.001, vs. rest. For postmenopausal women, there was a significant decrease in R-R interval during standing, F(1, 24) = 194.69, p<.001, and during exercise, F(1, 24) = 338.57, p<.001, vs. rest. Over time, there was a significant Time X Condition interaction found during exercise in the postmenopausal group, F(1, 24) = 15.18, p<.001. R-R interval decreased during exercise compared with rest. No other effects were found. 83 a) Menopausal Women b) Postmenopausal Women Figure 23. Mean R-R interval in 3 conditions as a function time for a) menopausal women and b) postmenopausal women separately. 84 There was no correlation between BMI or age and spontaneous baroreflex sensitivity (slope, systolic Finapres BP, R-R interval). BMI (week 1, week 12) was examined by bivariate correlation. Age was examined as a covariate with the outcome measures. R-R interval decreased over time during exercise compared with rest. No effects were found. Exercise Compliance Volunteers for this study were required to be sedentary at week 1 (<2 exercise sessions per week). Participants who were assigned to the exercise group were given a 12 week low-intensity walking program and asked to perform 5 sessions of structured low intensity walking per week. Those who were assigned to the control group were asked to maintain their current activity level for the 12 week study. Compliance to these requirements was monitored with self report log books which were distributed at the beginning of the study and collected at the end. There was a significant difference between activity levels in the two groups; the exercise group participated in an average of 4.06 (±SD 1.55) walking sessions per week while the control group averaged 0.63 (±SD 1.06) walking sessions per week. 85 CHAPTER FIVE Discussion The purpose of this study was to test the effects of a low-intensity exercise conditioning intervention on HR, BP, RPP, HRV and SBR sensitivity in hypertensive women. Our results confirm that the low-intensity walking program lowers systolic and diastolic BP and RPP in hypertensive women. Additionally, the low intensity exercise conditioning program attenuated the physiological response to stress. This was evidenced by decreased systolic and diastolic BP and RPP in the exercise group and increased diastolic BP in the control group. These findings suggest that a conditioning effect was achieved and can be attributed to the exercise intervention as there was an 81% compliance rate among participants. This is the first study to report and statistically account for the effects of a low-intensity exercise conditioning program on menopausal and postmenopausal hypertensive women. The results of this study support the hypothesis that a low-intensity exercise conditioning program reduces systolic and diastolic BP and RPP in hypertensive women. As expected, mean systolic and diastolic BP and RPP decreased after 12 weeks of lowintensity exercise. Women in the exercise group experienced a mean systolic BP reduction of 10 mmHg, mean diastolic BP reduction of 5 mmHg and mean RPP reduction of .96 . In contrast, women in the control group had a mean diastolic BP increase of 5 mmHg. This degree of BP and RPP reduction is statistically significant and clinically relevant as it has been shown to decrease the incidence of coronary heart disease and stroke (Cook, Cohen, Hebert, Taylor & Hennekens, 1995). 86 This degree of systolic BP reduction is consistent with previous findings for hypertensive populations. Hua, Brown, Hains, Godwin & Parlow (in press) implemented a similar exercise intervention with analogous methods of testing and analysis in the same laboratory as the present study. After 40 men and women completed the 12 week low intensity exercise program, they noted an 11 mmHg reduction in systolic BP. Davy et al. (1997) studied eight sedentary postmenopausal women with either high normal BP or hypertension as they participated in a 12 week moderate-intensity exercise program and found a systolic BP reduction of 8 mmHg. Likewise, Moreau, et al. (2001) followed 24 postmenopausal hypertensive women through a 12 week moderate-intensity walking program and revealed a 6 mmHg decrease in systolic BP with no change in diastolic BP. By 24 weeks, systolic BP had decreased by an additional 5 mmHg. Hagberg, Park & Brown (2000) reported analogous findings with low-to-moderate-intensity exercise, describing a systolic BP reduction of 11 mmHg. Similarly, Ishikawa et al. (1999) asserted comparable reductions in systolic (10 mmHg) BP in women aged 50-69 years after eight weeks of low-intensity exercise. Slight variation exists among the above findings as differences in the intensity and duration of exercise vary along with sample size. There was no difference in systolic BP reduction between menopausal and postmenopausal women. This is in contrast to a study done by Staessen, Bulpitt, Fagard, Lijnen & Amery (1989) where a random sample (n=430) of normotensive and hypertensive women revealed that postmenopausal women had higher systolic BP compared to menopausal women. The present study may have not found comparable findings due to antihypertensive medication use and homogenous hypertensive sample. 87 This degree of diastolic BP reduction is consistent with previous findings for hypertensive populations. Hua et al. (in press) also found that a similar 12 week walking program reduced diastolic BP by 5mmHg. Davy et al. (1997) found a similar reduction in diastolic (5 mmHg) BP. Likewise, Hagberg et al. (2000) reported a diastolic BP reduction of 8 mmHg and Ishikawa et al. (1999) asserted a diastolic reduction of 6 mmHg. This magnitude of diastolic BP reduction has clinical implications for hypertensive women. Cook et al. (1995) found that a 2 mmHg diastolic BP reduction produced a 6% decrease in the incidence of coronary heart disease and a 15% decrease in the incidence of stroke. Stamler, Stamler, Gosch, Civinelli, Fishman, McKeever et al. (1989) performed a five year prospective study with men and women with high normal BP and found that the incidence of hypertension could be decreased by 20-30% with a 1-3 mmHg reduction of diastolic BP. These findings suggest that low-intensity exercise training is an essential component of primary prevention of cardiovascular disease. The results clearly illustrate the importance of physical activity in the treatment of hypertension. A number of studies using moderate-to-high intensity exercise claim smaller reductions in systolic BP than low-intensity regimes (Hagberg et al., 2000). Kelley (1999) performed a meta-analysis of 10 randomized trials (n= 732 hypertensive women) in which moderate intensity exercise lasting between 10-52 weeks reduced resting systolic BP by 2% (~3 mmHg). Fagard (1995) performed a meta-analysis of 36 studies evaluating moderate-to-high intensity exercise and reported a reduction of 5.3 mmHg for systolic BP. This is consistent with the findings of Whelton et al. (2002). They reviewed 54 randomized controlled trials to evaluate the effect of moderate-to-high aerobic exercise on BP and found an average decrease of 4 mmHg systolic BP. Cox, Burke, 88 Morton, Gillam, Beilin and Puddey (2001) found remarkably similar results in a normotensive population. 126 normotensive women participated in an 18 month moderate intensity exercise intervention and experienced a 2.81 mmHg reduction in systolic BP. In the present study, the exercise group showed a significant reduction in RPP. RPP is an estimate of myocardial work load and gives an accurate indication of myocardial oxygen consumption (Laaksonen, Kalliokoski, Luotolahti, Kemppainen, Teras, Kyrolainen, et al., 2007). These findings suggest that low-intensity exercise training decreases RPP and is consistent with previous findings (Nagpal, Walia, Lata, Sood & Ahuja, 2007; Prakash et al., 2005). Jarrell, Hains, Kisilevsky & Brown (2005) examined hemodynamic responses to exercise in men and women after early recovery from myocardial infarction and documented decreased RPP in both genders. Kokkinos, Andreas, Coutoulakis, Colleran, Narayan and Dotson (2002) found that unfit, hypertensive women had a higher RPP than aerobically fit hypertensive women. The literature does not specify a normative decrease in RPP for hypertensive women after an exercise intervention. RPP is negatively affected by gender (female), increasing age and BMI (Hui, Jackson & Wier, 2000). Previous exercise conditioning studies done with men and women have reported reductions in resting HR and increased R-R interval which indicate improved parasympathetic modulation of the heart (Amano, Kanda, Ue & Moritani, 2001; Antelmi, et al., 2004). The present study did not find a significant change in HR or R-R interval between the Exercise and Control group. This could be attributed to gender differences 89 which were not detected in earlier studies. This study focused on women exclusively and the results reflect previous research. Hua et al. (in press) implemented the same lowintensity walking program with a sample of hypertensive men and women. They reported a decrease in resting HR in men but not women and an increased R-R interval in both sexes. Davy et al. (1997) studied eight women with either high BP or hypertension and found a comparable BP reduction and no change in resting HR or R-R interval. Similarly, Ramaekers et al. (1998) studied a sample of 276 normotensive men and women and found that R-R interval was lower in women compared to men. This is further supported by Gregoire, Tuck, Yamamoto and Hughson (1996) and Ueno & Moritani, (2003), who affirm that men experience a significantly greater mean R-R interval than women after an exercise conditioning program. However, these studies are in contrast to those that report greater parasympathetic activity in normotensive women compared to men (Carter et al., 2003; Kuo et al., 1999). There were no significant differences in HF power, TP, parasympathetic indicator, sympathetic indicator, baroreflex slope or R-R interval between the exercise and control group. Consistent with the literature, both groups experienced progressive withdrawal of parasympathetic innervation in response to standing and submaximal steady-state exercise (Macor, Fagard & Amery, 1996). However, the results of this study indicate that participation in the low-intensity exercise conditioning program attenuated physiological responses to stress in hypertensive women. This was demonstrated by a significant decrease in systolic and diastolic BP and RPP in the exercise group and a significant increase in diastolic BP in the control group during standing and at a given low submaximal steady-state exercise test at week 12. These findings are consistent with 90 previous research which supports the use of exercise conditioning to suppress sympathetic modulation induced by stress (Morimoto, Tan, Nishiyasu, Sone & Murakami, 2000; Pagani, Somers, Furlan, Dell'Orto, Conway, Baselli et al., 1988). It remains unclear as to what mechanism is responsible for the significant systolic and diastolic BP reduction found in this study. Since HRV and SBR measures did not change significantly, which would have been a clear indication of autonomic adaptation, interpretation of the BP reduction can only be considered speculation. Sowers & Lester (2000) suggest that hypertension and aging instigate structural and functional changes in the peripheral vasculature causing increased peripheral vascular resistance and enhanced vascular reactivity. These changes decrease beta-adrenergic responses to catecholamines while leaving alpha-adrenergic responses intact, creating vasoconstriction of peripheral vessels. Structural alteration of resistance arteries occur first, followed by endothelial dysfunction and in some cases cardiac hypertrophy (Park & Schiffrin, 2001). Sivertsson (1987) proposes that in addition to changes in vessel caliber, hypertension causes thickening of the arterial walls. Furthermore, menopause appears to impair endothelial vasodilation in normotensive and hypertensive women which potentiates increased systolic BP (Staessen, Celis & Fagard, 1998; Taddei, Virdis, Ghiadoni, Mattei, Sudano, Bernini, et al., 1996). Therefore, increased total peripheral resistance may contribute to the etiology of hypertension. Increased peripheral vascular resistance appears to decline with participation in exercise. Support for this theory comes from Iwasaki et al. (2003). They calculated total peripheral resistance through similutaneous measurement of HR and BP 91 (electrosphygmomanometry) at baseline and then at three, six, nine and twelve months of moderate-intensity exercise. After three months, they credited a 10 mmHg decrease in systolic BP to a 136 dynes x s x cm-5 reduction in total peripheral resistance. Exercise conditioning also has been linked to increased vascularization of skeletal muscle, peripheral vasodilation and increased tissue perfusion (Halliwill, Taylor, Hartwig & Eckberg, 1996; Lesniak & Dubbert, 2001; Martin, Montgomery, Snell, Corbett, Sokolov, Buckey, et al., 1987). These findings are noteworthy as they may be the mechanisms which contributed to the systolic and diastolic BP reduction found in this study. Eighteen menopausal and thirty-two postmenopausal women were involved in this study. Counter-balanced allocation to either exercise or control group resulted in equal distribution of menopausal women. There was a difference between menopausal women and postmenopausal women in regard to HRV measures. Consistent with the literature, postmenopausal women demonstrated decreased HF power and TP in comparison to menopausal women. This is consistent with studies done with normotensive menopausal and postmenopausal women. Our findings were remarkably similar to those found by Farag, Bardwell, Nelesen, Dimsdale and Mills (2003). They studied 18 menopausal women and 34 postmenopausal women without subjecting them to an exercise program and found that postmenopausal women have increased sympathetic, decreased parasympathetic activity and decreased R-R interval. However, their findings were no longer significant when age was used as a covariate. Age did not affect the findings of the present study. Brockbank, Chatterjee, Bruce and Woledge (2000) and Rys, Kogut and Thor (2006) also documented decreased parasympathetic innervation of HR and significant reductions in R-R interval in postmenopausal women. 92 The present study found that postmenopausal women showed lower LF power in comparison to menopausal women. LF power has been hypothesized to be jointly mediated by both the sympathetic and parasympathetic nervous system (Akselrod, Gordon, Madwed, Snidman, Shannon & Cohen, 1985). It is possible to speculate that the low-intensity exercise conditioning program caused a non significant decrease in sympathetic activity in postmenopausal women as seen by lower LF power. These findings may suggest that postmenopausal hypertensive women experience greater benefits than menopausal women with a low-intensity exercise regime. There were no significant differences in HRV or SBR sensitivity measures between the exercise and control group. These findings do not support the hypothesis that the low-intensity exercise conditioning program improves autonomic adaptation (increased parasympathetic modulation of HR and decreased sympathetic indicator at rest, standing and during submaximal steady-state exercise) in hypertensive women. Previous low and moderate-intensity exercise conditioning studies done with normotensive and hypertensive populations have also resulted in non-significant changes in HRV and BRS sensitivity (Davy et al., 1997; Hua et al., in press; Loimaala, Huikuri, Oja, Pasanen and Vuori, 2000; Reiling & Seals, 1988). Conversely, other studies have demonstrated differences in HRV and SBR sensitivity after a low-moderate-intensity exercise program (Amano et al., 2001; Malliani, Pagani, Lombardi, Furlan, Guzzetti & Cerutti, 1991). Myslivecek et al. (2002) studied the effect of moderate-intensity exercise on HRV and SBR function between pre and post menopausal normotensive women. They found that pre and post menopausal women in the exercise group experienced higher vagal modulation, lower sympathetic innervation and longer R-R intervals than the 93 sedentary control group. O'Sullivan and Bell (2000) demonstrated that chronic moderateintensity exercise training reduced sympathetic activity and increased the slope of the arterial baroreflex. Iwasaki, Zhang, Zuckerman and Levine (2003) found that three months of physical training increased HRV and SBR sensitivity in sedentary participants. The quantity of exercise conditioning may have contributed to the non-significant differences in HRV and SBR sensitivity between groups. The present study used previous findings from Hua et al. (in press) in order to design a 12-week low-intensity exercise conditioning program which could affect HRV and SBR sensitivity. Hua et al. (in press) used the same low-intensity walking program as the present study but required that participants perform 4 sessions of walking per week. After finding no significant differences in HRV between the exercise and control group, they concluded that hypertensive individuals may require a higher quantity of exercise to achieve a significant difference between groups. However, they did find a significant increase in R-R interval during submaximal steady-state exercise in men and women. The present study required participants to complete five walking sessions per week in an attempt to document a change in HRV and SBR sensitivity. This higher quantity of low-intensity exercise conditioning did not produce the significant difference in HRV or SBR sensitivity between the exercise and control group. Previous studies which have demonstrated an improvement in cardiac autonomic function have implemented a moderate-intensity exercise conditioning program (Davy et al., 1997; Myslivecek et al., 2002; Tuomainen et al., 2005). 94 Participants in this study demonstrated an 81% compliance rate. Hawkins and Hackett (1982) define a high compliance rate as participation in 67% of prescribed exercise sessions. Women in the exercise group were asked to perform 5 sessions of structured low-intensity walking per week. Participants recorded their exercise sessions in a log book. The exercise group participated in an average of 4.06 (±SD 1.55) walking sessions per week while the control group averaged 0.63 (±SD 1.06) walking sessions per week. The significant reduction in systolic BP and RPP combined with a high compliance rate suggests that the low-intensity walking program is an effective means for reducing systolic BP and RPP. Conclusions This is the first study to report and statistically account for the influence of a lowintensity exercise conditioning program on cardiac and autonomic function in menopausal and postmenopausal hypertensive women. The results of this study indicate that a low-intensity exercise conditioning program lasting three months is sufficient to reduce systolic and diastolic BP and RPP, but not adequate to influence cardiac autonomic function in hypertensive women. Additionally, the low-intensity exercise conditioning program attenuated the physiological response to stress. This was evidenced by decreased systolic and diastolic BP and RPP in the exercise group and increased diastolic BP in the control group. It was evident that menopausal and postmenopausal women differ from each other in regard to cardiac autonomic function. Postmenopausal women demonstrated greater sympathetic activity in comparison to menopausal women. Postmenopausal women had decreased HF power and TP. However, postmenopausal 95 women demonstrated a significant reduction in LF power compared to menopausal women. This may indicate that the low-intensity exercise program fosters autonomic adaption in postmenopausal women. 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Journal 130 of Applied Physiology, 71(3), 1136-42. 131 Appendix A Queen’s University RESEARCH INFORMATION CONSENT FORM Title of Project: Effects of low intensity exercise conditioning on blood pressure, heart rate, rate-pressure-product and cardiac autonomic modulation in hypertensive women Background Information: You are being invited to participate in a research study directed by Dr. Ann Brown, RN, Ph.D, to evaluate the effects of a 12 week walking program on high blood pressure. Catherine Baines, BScN, RN MSc (c), will read through this consent form with you and describe procedures in detail and answer any questions you may have. Details of the Study: Aim of the study: The aim of this study is to determine the extent to which low intensity exercise conditioning will decrease your blood pressure. You will be considered eligible to participate in the study if you are a woman with hypertension (as diagnosed by your family physician), are a non smoker, do not perform regular physical exercise more than twice per week, are between 45-65 years of age, not taking hormone replacement therapy and not diagnosed with stroke or heart disease. You may be assigned to either an exercise group or a non-exercise group. Description of visits and tests to be performed as part of the study: The study involves your participation for two sessions in a research laboratory at Hotel Dieu Hospital, at the beginning and at the end of the 12 week study period. Your blood pressure will be measured while you are resting on a cot for 10 minutes, while you stand for 10 minutes and while you are performing light exercise on an exercise bike for 5 minutes. The first session will take an hour and a half and the second session will last 45 mins. If you are assigned to the 12 week walking program, we will provide you with an explanation, written instructions and materials for the low intensity walking program. If you are assigned to the control group, you will be asked to avoid changing your current level of activity for the duration of the study. At the end of 12 weeks, you will be provided with an explanation, written instructions and materials to carry out the walking program. 132 All participants will be asked to refrain from making dietary changes or changes in exercise that differ from the study‘s guidelines for 12 weeks. The principal investigator will be calling you every three weeks to monitor progress and answer questions. Risks/Side Effects: Risks: There are unlikely to be any physical risks associated with the walking program or the low intensity exercise testing protocol. Nevertheless, all volunteers will have to complete the Physical Activity Readiness Questionnaire (PAR-Q) as a condition of eligibility for participation in the study. Physician approval must be obtained for participants if they answered ―yes‖ to one of seven questions on the PAR-Q. Participants will have blood pressure and heart rate monitored continuously during the testing and will be taught to take their own pulse during exercise. It is possible that this level of exercise will not reduce your blood pressure. Similarly, patients in the non-exercise group will not be using this form of lifestyle change to reduce blood pressure for the study duration. However, at the end of the 12 weeks of their participation, they will be provided with the same information given to the exercise group. Emergency contact persons: If any untoward symptoms occur during exercise, please contact your family physician or local emergency department to obtain the appropriate treatment advice. Please contact the study investigators (either Catherine Baines (613544-3400 ext. 2473) or Dr Ann Brown, School of Nursing, 613-533-4480, ext 74763) to inform them of your symptoms. Benefits: For participants in the exercise group, there may be a reduction in your blood pressure by the end of 12 weeks. For those in the non exercise group, there may be no direct benefits. Indirect benefits for each group include contributing to the knowledge base that could benefit themselves or other people with high blood pressure in the future. Confidentiality: All information obtained during the course of this study is strictly confidential and your anonymity will be protected at all times. All of the information collected will be identified using a coding system. All data will be stored in locked files and will be available only to Catherine Baines and Dr Ann Brown. There is a possibility that your medical record, including identifying information, may be inspected by regulatory agencies in the course of carrying out regular government functions. You will not be identified in any publications or reports. 133 Alternative Therapies: At this time, your Family Physician has recommended lifestyle change and/or medication as methods of reducing your blood pressure. Exercise is one of the lifestyle changes that are normally recommended. Other lifestyle changes may include changes in your diet or a decrease in your stress level. Voluntary nature of study/Freedom to withdraw or participate: Your participation in this study is voluntary. You may withdraw from this study at any time, for any reason. Your withdrawal will not affect your present/future medical care with your Family Physician or at Hotel Dieu Hospital. Withdrawal of subject by principle investigator: The study investigators may decide to withdraw you from this study if your Family Physician wishes to change your medical treatment or if you experience symptoms during exercise or during testing. Liability: In the event that you are injured as a result of the study procedures, medical care will be provided to you until resolution of the medical problem. By signing this consent form, you do not waive your legal rights nor release the investigator(s) and sponsors from their legal and professional responsibilities. 134 SUBJECT STATEMENT AND SIGNATURE SECTION: I have read and understand the consent form for this study. I have had purposes, procedures and technical language of this study explained to me. I have been given sufficient time to consider the above information and seek advice if I chose to do so. I have had the opportunity to ask questions which have been answered to my satisfaction. I am voluntarily signing this form. I will receive a copy of this consent form for my information. The results of my tests may be made available to my family physician. My family physician may also be contacted if there are any significant health related issues that occur during the study. If at any time I have further questions, problems or adverse events, I can contact Principal Investigator: Catherine Baines, BScN, RN, MSc (c) at 613-544-3400 ext 2473 or Dr Ann Brown PhD, Queen‘s School of Nursing at 613-533-6000 ext 74763 Or Department Head: Dr. C. Baker, Director, Queen‘s School of Nursing at 613-533-2668 or If I have questions regarding my rights as a research subject I can contact Dr. Albert Clark, Chair, Research Ethics Board at 613-533-6081 By signing this consent form, I am indicating that I agree to participate in this study. ------------------------------ ----------------------------------- Signature of Participant Date Statement of Investigator: I have carefully explained to the subject the nature of the above research study. I certify that, to the best of my knowledge, the subject understands clearly the nature of the study and demands, benefits, and risks involved to participants in this study. ------------------------------------------- ------------------------------------------- Signature of Principal Investigator Date 135 Appendix B Physical Activity Readiness Questionnaire Regular physical activity is fun and healthy, and increasingly more people are starting to become more active every day. Being more active is very safe for most people. However, some people should check with their doctor before they start becoming much more physically active. If you are planning to become much more physically active than you are now, start by answering the seven questions in the box below. If you are between the ages of 15 and 69, the PAR-Q will tell you if you should check with your doctor before you start. If you are over 69 years of age, and you are not used to being very active, check with your doctor. Common sense is your best guide when you answer these questions. Please read the questions carefully and answer each one honestly: check YES or NO. 1. Has your doctor ever said that you have a heart condition and that you should only do physical activity recommended by a doctor? 2. Do you feel pain in your chest when you do physical activity? 3. In the past month, have you had chest pain when you were not doing physical activity? 4. Do you lose your balance because of dizziness or do you ever lose consciousness? 5. Do you have a bone or joint problem (for example, back, knee or hip) that could be made worse by a change in your physical activity? 6. Is your doctor currently prescribing drugs (for example, water pills) for your blood pressure or heart condition? 7. Do you know of any other reason why you should not do physical activity? If answered YES to any of the above questions, tell your fitness or health professional. Ask whether you should change your physical activity plan. Talk with your doctor by phone or in person BEFORE you start becoming much more physically active or BEFORE you have a fitness appraisal. Tell your doctor about the PAR-Q and which questions you answered YES. You may be able to do any activity you want — as long as you start slowly and build up gradually. Or, you may need to restrict your activities to those which are safe for you. Talk with your doctor about the kinds of activities you wish to participate in and follow his/her advice. 136 If you answered NO honestly to all PAR-Q questions, you can be reasonably sure that you can: start becoming much more physically active; begin slowly and build up gradually. This is the safest and easiest way to go. Take part in a fitness appraisal, this is an excellent way to determine your basic fitness so that you can plan the best way for you to live actively. It is also highly recommended that you have your blood pressure evaluated. If your reading is over 144/94, talk with your doctor before you start becoming much more physically active. DELAY BECOMING MUCH MORE ACTIVE; if you are not feeling well because of a temporary illness such as a cold or a fever, wait until you feel better; or if you are or may be pregnant, talk to your doctor before you start becoming more active. PLEASE NOTE: If your health changes so that you then answer YES to any of the above questions, tell you fitness or health professional. Ask whether you should change your physical activity plan. Informed Use of the PAR-Q: The Canadian Society for Exercise Physiology, Health Canada, and their agents assume no liability for persons who undertake physical activity, and if in doubt after completing this questionnaire, consult your doctor prior to physical activity. ―I have read, understood and completed this questionnaire. Any questions I had were answered to my full satisfaction." NAME: _________________________________________________________________ SIGNATURE:____________________________________________________________ DATE:__________________________________________________________________ SIGNATURE OF PARENT WITNESS or GUARDIAN (for participants under the age of majority):________________________________________________________________ WITNESS ______________________________________________________________ l questions Note: This physical activity clearance is valid for a maximum of 12 months from the date it is completed and becomes invalid if your condition changes so that you would answer YES to any of the seven questions. © Canadian Society for Exercise Physiology Supported by: HealthCanadaSantéCanada Source: Physical Activity Readiness Questionnaire (PAR-Q) © 2002. Reprinted with permission from the Canadian Society for Exercise Physiology. http://www.csep.ca/forms.asp 137 Appendix C Measuring Your Pulse and Your Target Heart Rate What is your pulse? Your pulse is your heart rate, or the number of times your heart beats in one minute. Pulse rates vary from person to person. Your pulse is lower when you are at rest and increases when you exercise (because more oxygen-rich blood is needed by the body when you exercise). Knowing how to take your pulse can help you evaluate your exercise program. How to take your pulse 1. Place the tips of your index, second, and third fingers on the palm side of your other wrist, below the base of the thumb. Or, place the tips of your index and second fingers on your lower neck, on either side of your windpipe. (See the illustrations below.) 2. Press lightly with your fingers until you feel the blood pulsing beneath your fingers. You might need to move your fingers around slightly up or down until you feel the pulsing. 3. Use a watch with a second hand, or look at a clock with a second hand. 4. Count the beats you feel for 10 seconds. Multiply this number by six to get your heart rate (pulse) per minute. Check your pulse: _______________ x 6 = ________________ (beats in 10 seconds) (your pulse) 138 Appendix D Borg Rating of Perceived Exertion (RPE) Scale While doing physical activity, we want you to rate your perception of exertion. This feeling should reflect how heavy and strenuous the exercise feels to you, combining all sensations and feelings of physical stress, effort, and fatigue. Do not concern yourself with any one factor such as leg pain or shortness of breath, but try to focus on your total feeling of exertion. Look at the rating scale below while you are engaging in an activity; it ranges from 6 to 20, where 6 means "no exertion at all" and 20 means "maximal exertion." Choose the number from below that best describes your level of exertion. This will give you a good idea of the intensity level of your activity, and you can use this information to speed up or slow down your movements to reach your desired range. Try to appraise your feeling of exertion as honestly as possible, without thinking about what the actual physical load is. Your own feeling of effort and exertion is important, not how it compares to other people. Look at the scales and the expressions and then give a number. 6 No exertion at all 7 Extremely light (7.5) 8 9 Very light 10 11 Light 12 13 Somewhat hard 14 15 Hard (heavy) 16 17 Very hard 18 19 Extremely hard 20 Maximal exertion 139 Appendix E Walking Protocol Week Distance (km/day) Distance (mile/day) 1 .8 km /day .50 mile/day 2 .8 km /day .50 mile/day 3 1.2 km /day .74 mile/day 4 1.6 km /day 1.0 mile/day 5 2.0 km /day 1.2 mile/day 6 2.4 km /day 1.5 mile/day 7 2.8 km /day 1.7 mile/day 8 3.2 km /day 2.0 mile/day 9 3.6 km /day 2.2 mile/day 10 4.0 km /day 2.5 mile/day 11 4.4 km /day 2.7 mile/day 12 4.8 km /day 3.0 mile/day * Adopted from Brown et al. (1992; 1994), Myslivecek et al. (2002) and Hua et al. (2006) 140 Appendix F Exercise Log ID_________________ Age________________ Start Date___________ End Date ___________ Wk Day Distance (km/mile) Duration (min) Heart Rate Borg‘s (beats/min) Perceived Exertion # 1 Before Exercise: After Exercise: 2 Pre: Post: 3 Pre: Post: 4 Pre: Post: 5 Pre: Post: 6 Pre: Post: 7 Pre: Post: Reason (s) for stopping Other physical activity 141 Appendix G Activity Log ID_________ Age______ Start Date_________________________ End Date ___________________________ Week Day Physical Activities 1 2 3 4 5 6 7 Week Day 1 2 3 4 5 6 7 Physical Activities 142 Appendix H Study Advertisement 143 Appendix I Demographic and Data Form ID : Group: Age: yrs Address: Education: Phone #: Marital Status: Occupation: Menopausal State: Blood Pressure Medications: Time 1 Height: Weight: Waist Circumference: Time 2 Height: Weight: Waist Circumference: Time #1 Time #2 Date: Date: Supine Supine BP BP HR HR Standing Standing BP BP HR HR Exercise Exercise HR MAX 40% HR BP Peak BP Peak HR Peak HR Peak 144 Appendix J Editing Heart Rate Variability Data HRV data files were collected using a Spacelab 521T Cardiac Monitor with QRS detector (Squibb Vitatek Inc., Hillsboro, USA) which was interfaced with a personal computer by means of an eight-channel analog/digital convertor (DAS-16, Metrabyte Corp., Multitest Electronics, Scarborough, ON). After raw binary data files were accrued, they were converted into RR files by exporting them to an ASCII text format and assigning them an extension (‗.RR‖) based on the original binary file name. These RR files, which contained HR, systolic BP, diastolic BP and R-R interval data, were imported into a general spectral analysis computer software program (Hughson and Yamamoto, 1993). This program used RR files to generate an R-R interval time series graph. The graph was manually edited as described below and then saved to a separate file containing the edited data (―.GSA‖). Editing of the time series graph was accomplished by examining each data point of a series. Obvious outliers or artifacts which deviated by more than 30% from the previous data point were deleted. This was accomplished by use of a toggle which was maneuvered from the beginning to the end of the data set; touching each data point separately. Editing outliers or artifacts was a step-wise process; the toggle was moved directly over the start and end points of the outlying data with the right and left arrow keys; the ENTER key was pressed to highlight each point; the DELETE key was then pressed to eliminate the line connecting the start and end points of the outlier data. After removing outliers, the time series graph was subjected to Fast Fourier Transform analysis converting the edited data into a power frequency spectrum. The 145 summary of the power frequency spectrum was saved for separately for analysis. The original raw HRV data files were maintained during this process. 146 Appendix K Editing Baroreflex Sensitivity Data BRS data files were collected using R-R interval data from the Spacelab 521T Cardiac Monitor with QRS detector (Squibb Vitatek Inc., Hillsboro, USA) and the Finapres® 2300 (Ohmeda, Englewood, CO) which were interfaced with a personal computer by means of an eight-channel analog/digital convertor (DAS-16, Metrabyte Corp., Multitest Electronics, Scarborough, ON). After raw binary data files were accrued, they were converted into RR files by exporting them to an ASCII text format and assigning them an extension (‗.RR‖) based on the original binary file name. RR files were imported into the Spontaneous Baroreflex Analysis program developed by Andrew Blaber of Cambridge, Ontario, Canada and the summary data generated by this program as described below was saved to a separate file with the extension ―.SBR‖. This program detects spontaneous sequences of three or more heart beats in which systolic BP and R-R interval simultaneously change in the same direction. It then uses linear regression to calculate the slope of each sequence. Editing for outliers or artifacts was accomplished automatically by using the ―fl‖ command-line parameter when executing the program for each RR file. 147 Appendix L Means (±SD) for BpTRU Systolic and Diastolic Blood Pressure, Heart Rate and RatePressure-Product in Both Control and Exercise Group at Week 1 and Week 12 Time Week 1 Week 12 Group Control Exercise Control Exercise Systolic Blood Pressurea, b, c (n=23) (n=27) (n=23) (n=27) Resting 130 (17) 137 (21) 128 (16) 131.3 (22) Standing 140 (25) 146 (21) 140 (25) 133.0 (20) Exercise 154 (20) 160 (25) 153 (24) 148.8 (28) Resting 81 (10) 86 (13) 81 (10) 81 (13) Standing 91 (17) 99 (14) 99 (19) 92 (13) Exercise 90 (16) 98 (18) 97 (10) 93 (20) Resting 67.0 (7.3) 67.1 (10.4) 70.2 (8.6) 66.6 (8.9) Standing 76.7 (10.3) 78.5 (11.0) 80.2 (10.2) 79.1 (12.4) Exercise 92.2 (10.3) 89.2 (13.4) 91.3 (12.8) 87.3 (14.5) Resting 8.7 (1.3) 9.2 (2.0) 8.9 (1.4) 8.7 (1.7) Standing 10.8 (2.5) 11.4 (2.0) 11.2 (2.4) 10.5 (2.0) Exercise 14.2 (2.2) 14.24 (3.0) 13.91 (2.68) 13.0 (3.6) (mmHg) Diastolic Blood Pressureb, c (mmHg) Heart Rate (beats/min)c Rate-Pressure- Productb, c ((HR x systolic BP) x10-2) Note. BP and HR taken using BpTRU automated BP monitor. BP = blood pressure; HR = heart rate; min = minute; ms = milliseconds a c significant Time effect , p.<.05 bsignificant Time X Group interaction, p<.05 significant Condition effect, p<.001 148 Appendix M Means (±SD) for Log Transformed Heart Rate Variability Measures for Both Control and Exercise Group at Week 1 and Week 12 Time Week 1 Group Week 12 Control Exercise Control (n=23) (n=27) (n=23) Exercise (n=27) Low Frequency Powera, b, d (ms2/Hz) Resting 1.94 (.37) 1.99 (.48) 1.82 (.43) 1.90 (.53) Standing 2.07 (.37) 2.05 (.41) 2.10 (.32) 2.0 (.43) Exercise 1.50 (.64) 1.43 (.73) 1.86 (.67) 1.42 (.62) Resting 1.78 (.43) 1.81 (.52) 1.71 (.51) 1.75 (.70) Standing 1.45 (.33) 1.42 (.53) 1.50 (.34) 1.45 (.55) Exercise 1.33 (.69) 1.27 (.70) 1.57 (.78) 1.20 (.68) Resting 2.57 (.32) 2.55 (.46) 2.48 (.38) 2.54 (.46) Standing 2.56 (.30) 2.51 (.40) 2.58 (.29) 2.60 (.41) Exercise 2.28 (.58) 2.41 (.66) 2.61 (.62) 2.34 (.48) Resting -.79 (.26) -.74 (.24) -.77 (.25) Standing -1.11(.24) -1.09 (.35) -1.08 (.24) -1.15 (.26) Exercise -.95 (.36) -1.13 (.30) -1.03 (.28) -1.13 (.50) High Frequency Powera, e (ms2/Hz) Total Powerd (ms2/Hz) PNS Indicatora, c, f (HF/TP) -.79 (.34) 149 SNS Indicatora, g (LF/HF) Resting .16 (.37) .18 (.33) .11 (.32) .15 (.31) Standing .62 (.30) .63 (.36) .60 (.25) .55 (.29) Exercise .17 (.23) .16 (.20) .29 (.28) .22 (.29) Note. SNS = sympathetic nervous system; PNS = parasympathetic nervous system; ms = milliseconds; m2/Hz = milliseconds squared per hertz; HF/TP = high frequency/ total power; LF/HF = low frequency/ high frequency a significant Condition effect , p.<.001 b c significant Condition X Time interaction, p<.05 significant Condition X Group interaction, p<.01 d significant Menopause effect, p<.05 e significant Menopause X Group interaction, p<.05 f significant Condition X Menopause interaction, p<.05 g significant Condition X Menopause X Group interaction, p<.01 150 Appendix N Means (±SD) for Spontaneous Baroreflex Measures for Both Control and Exercise Group at Week 1 and Week 12 Time Week 1 Group Week 12 Control Exercise Control (n=23) (n=27) (n=23) Exercise (n=27) Baroreflex Slopea (ms/mmHg) Resting 6.38 (3.88) 6.55 (3.37) 5.80 (3.43) 6.19 (5.39) Standing 3.16 (1.59) 3.12 (2.01) 3.41 (1.61) 3.23 (2.15) Exercise 5.57 (5.13) 6.38 (4.70) 8.27 (6.56) 4.22 (4.60) Resting 108 (36) 122 (28) 126 (26) 143 (23) Standing 147 (27) 140 (25) 143 (31) 135(30) Exercise 157 (39) 169 (42) 150 (38) 165 (40) Resting 882 (91) 897 (119) 852 (97) 894 (147) Standing 776 (95) 764 (101) 759 (110) 783(114) Exercise 518 (99) 530 (74) 530 (92) 590 (103) Systolic Finapres arterial BP (mmHg)a, b R-R Interval (ms)a, c Note. BP = blood pressure; ms = milliseconds; mmHg = millimeters of mercury a significant effect of Condition , p.<.001 b c significant Condition X Group interaction, p<.05 significant Time X Condition X Menopause, p<.05 151 Appendix O Summary of Study Sample and Reasons for Attrition Participants Control Exercise Total # completed the study Menopausal 9 9 ** 18 Post menopausal 14 18 ** 32 Total (n=) 23 27 50 # Loss to follow-up 0 4 Total # completed the study 23 27 50 Note. ** = two lost to follow up 4 participants lost to follow up due to illness (n=1) or unable to contact after initial testing (n=3) 152 Appendix P Other demographic data at baseline testing Measure Control Group Exercise Group (n = 23) (n = 27) Marital Status Married/Common Law 18 (78.3%) 22 (81.5%) Single 5 (21.7 %) 5 (18.5%) Total: 23 (100%) 27 (100%) Working 17 (73.9%) 18 (66.7%) Not working 2 (8.7%) 3 (11.1%) Retired 4 (17.4%) 6 (22.2%) Total: 23 (100%) 27 (100%) Employment Status 153 Appendix Q Chi-squared Summary Tables Demographic, Physiological and Lifestyle Measures Participant‘s Age at Baseline Testing Chi-Square Tests Pearson Chi-Square Likelihood Ratio Linear-by-Linear Association N of Valid Cases Value 20.612 27.213 df 17 17 Asymp. Sig. .244 .055 2.735 1 .098 50 Participant‘s Education Level at Baseline Testing Chi-Square Tests Pearson Chi-Square Likelihood Ratio Linear-by-Linear Association N of Valid Cases Value .028 .028 df 2 2 Asymp. Sig. .986 .986 .014 1 .907 50 Participant‘s Maximum Activity Level at Baseline Testing Chi-Square Tests Pearson Chi-Square Likelihood Ratio Linear-by-Linear Association N of Valid Cases Value 21.964 29.951 df 21 21 Asymp. Sig. .402 .093 .757 1 .384 50 Participant‘s Menopausal State at Baseline Testing Chi-Square Tests Pearson Chi-Square Likelihood Ratio Linear-by-Linear Association N of Valid Cases Value .181 .181 df 1 1 Asymp. Sig. .670 .671 .178 1 .673 50 154 Participant‘s Body Mass Index at Baseline Testing Chi-Square Tests Pearson Chi-Square Likelihood Ratio Linear-by-Linear Association N of Valid Cases Value 50.000 68.994 df 49 49 Asymp. Sig. .433 .031 1.670 1 .196 50 Participant‘s Resting Systolic Blood Pressure at Baseline Testing Chi-Square Tests Pearson Chi-Square Likelihood Ratio Linear-by-Linear Association N of Valid Cases Value 27.053 36.631 df 29 29 Asymp. Sig. .569 .156 1.847 1 .174 50 Participant‘s Resting Diastolic Blood Pressure at Baseline Testing Chi-Square Tests Pearson Chi-Square Likelihood Ratio Linear-by-Linear Association N of Valid Cases Value 33.561 45.767 df 26 26 Asymp. Sig. .146 .010 1.689 1 .194 50 Participant‘s Resting HR at Baseline Testing Chi-Square Tests Pearson Chi-Square Likelihood Ratio Linear-by-Linear Association N of Valid Cases Value 33.561 45.767 df 25 25 Asymp. Sig. .118 .007 .001 1 .977 50 Participant‘s Resting Rate-Pressure-Product at Baseline Testing Chi-Square Tests Pearson Chi-Square Likelihood Ratio Linear-by-Linear Association N of Valid Cases Value 47.987 66.222 df 47 47 Asymp. Sig. .433 .034 1.177 1 .278 50 155 Appendix Q ANOVA Summary Tables BpTRU Systolic Blood Pressure (SBP) Descriptive Statistics Group SBPrest1 DBPstand1 SBPexer1 SBPrest12 Std. Deviation Control 129.8261 16.94282 Exercise 138.3478 21.26373 Total 134.0870 19.49225 Control 90.6087 16.71890 Exercise 97.3478 13.02309 Total 93.9783 15.20452 Control 154.3043 20.24494 Exercise 161.6957 26.36188 Total 158.0000 23.53909 Control 127.4783 15.68980 Exercise 131.3043 22.36156 Total 129.3913 19.19778 139.9565 25.25052 Exercise 132.9565 20.34359 Total 136.4565 22.94700 Control 152.5652 23.45756 Exercise 148.4783 28.15843 Total 150.5217 25.70840 SBPstand12 Control SBPexer12 Mean Tests of Within-Subjects Effects Source Time (T) T X Group (Gr) T X Menopause (M) T X Gr X M Error (T) Condition (C) CXG CXM C X Gr X M Error (C) TYPE III SS 2260.666 1205.310 .921 51.653 11773.560 20275.207 557.204 663.499 60.755 16443.893 Df 1 1 1 1 42 2 2 2 2 84 MS 2260.666 1205.310 .921 51.653 280.323 10137.603 278.602 331.749 30.377 195.761 F 8.065 4.300 .003 .184 Sig. .007* .044* .955 .670 51.786 1.423 1.695 .155 .000* .247 .190 .857 156 TXC T X C X Gr TXCXM T X C X Gr X M Error (T X C) 52.366 138.296 6.542 613.164 9666.041 Tests of Between-Subjects Effects Source Type III SS Intercept 4964910.356 Gr 207.022 M 57.039 Gr X M 80.976 Error 94424.166 2 2 2 2 84 df 1 1 1 1 42 26.183 69.148 3.271 306.582 115.072 MS 4964910.356 207.022 57.039 80.976 2248.194 .228 .601 .028 2.664 F 2208.399 .092 .025 .036 .797 .551 .972 .076 Sig. .000 .763 .874 .850 BpTRU Systolic Blood Pressure (SBP) for the Exercise Group Tests of Within-Subjects Contrasts Condition T Error (T) C S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R Error (T X C) S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 940177.394 Error 16861.106 TYPE III SS 1333.452 2646.382 793.065 18883.130 6402.435 9746.870 287.500 438.348 2254.000 8045.652 df 1 22 MS 940177.394 766.414 df 1 22 1 1 22 22 1 1 22 22 MS 1333.452 120.290 793.065 18883.130 291.020 443.040 287.500 438.348 102.455 365.711 F 1226.723 F 11.085 Sig. .003* 2.725 42.622 .113 .000* 2.806 1.199 .108 .285 Sig. .000 BpTRU Systolic Blood Pressure (SBP) for the Control Group Tests of Within-Subjects Contrasts Source Condition T Error (T) C S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R Type III SS 22.727 1295.995 5946.283 28252.174 8836.217 5502.826 56.543 4.261 Df 1 22 1 1 22 22 1 1 MS 22.727 58.909 5946.283 28252.174 401.646 250.128 56.543 4.261 F .386 Sig. .541 14.805 112.951 .001* .000* .325 .022 .574 .884 157 Error (T X C) S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 910676.060 Error 14657.106 3827.957 4306.739 df 1 22 MS 910676.060 666.232 22 22 F 1366.905 173.998 195.761 Sig. .000 158 Appendix Q ANOVA Summary Tables BpTRU Diastolic Blood Pressure (DBP) Descriptive Statistics DBPrest1 Group Mean Control 81.2609 10.42382 Exercise 85.3913 12.64817 Total 83.3261 11.64866 90.6087 16.71890 Exercise 97.3478 13.02309 Total 93.9783 15.20452 Control 89.6522 16.16846 Exercise 97.5217 20.04511 Total 93.5870 18.44099 Control 80.5652 10.23286 Exercise 81.2174 13.31765 Total 80.8913 11.74777 98.7826 18.86304 Exercise 92.4348 13.03082 Total 95.6087 16.34826 97.2609 10.02369 Exercise 93.4348 20.32649 Total 95.3478 15.96415 DBPstand1 Control DBPexer1 DBPrest12 DBPstand12 Control DBPexer12 Control Std. Deviation Tests of Within-Subjects Effects T T X Gr TXM T X Gr X M Error (T) C C X Gr TYPE III SS 14.393 950.659 3.078 437.963 5007.614 8702.208 81.589 df 1 1 1 1 42 2 2 MS 14.393 950.659 3.078 437.963 119.229 4351.104 40.795 F .121 7.973 .026 3.673 Sig. .730 .007* .873 .062 30.074 .282 .000* .755 159 CXM C X Gr X M Error (C) TXC T X C X Gr TXCXM T X C X Gr X M Error(T X C) 102.505 10.909 12153.131 286.604 326.418 17.559 644.855 9199.590 Tests of Between-Subjects Effects Source Type III SS Intercept 2064045.528 Gr 156.669 M 2337.743 Gr X M 153.559 Error 29305.952 2 2 84 2 2 2 2 84 df 1 1 1 1 42 51.252 5.454 144.680 143.302 163.209 8.780 322.427 109.519 MS 2064045.528 156.669 2337.743 153.559 697.761 .354 .038 .703 .963 1.308 1.490 .080 2.944 .276 .231 .923 .058 F 2958.099 .225 3.350 .220 Sig. .000 .638 .074 .641 BpTRU Diastolic Blood Pressure (DBP) for the Exercise Group Tests of Within-Subjects Contrasts Source Condition T Error (T) C S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R Error (T X C) S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS df Intercept 382808.988 1 Error 6155.957 22 Type III SS 221.761 838.739 6175.848 6817.391 4719.652 8632.609 6.283 .087 2247.217 6657.913 MS 382808.988 279.816 Df 1 22 1 1 22 22 1 1 22 22 MS 221.761 38.125 6175.848 6817.391 214.530 392.391 6.283 .087 102.146 302.632 F 1368.073 Sig. .000 F 5.817 Sig. .025* 28.788 17.374 .000* .000* .062 .000 .806 .987 160 BpTRU Diastolic Blood Pressure (DBP) for the Control Group Source T Error (T) C Error (C) TXC Error (T X C) Condition Type III SS 290.843 979.435 8738.174 7237.587 7020.826 3968.913 904.696 793.065 5748.304 2839.435 S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 370024.466 Error 4469.589 df 1 22 MS 370024.466 203.163 Df 1 22 1 1 22 22 1 1 22 22 MS 290.843 44.520 8738.174 7237.587 319.128 180.405 904.696 793.065 261.287 129.065 F 1821.317 Sig. .000 F 6.533 Sig. .018* 27.381 40.119 .000* .000* 3.462 6.145 .076 .021* 161 Appendix Q ANOVA Summary Tables BpTRU Heart Rate (HR) Descriptive Statistics HRrest1 HRstand1 HRexer1 HRrest12 Group Mean Control 67.0000 7.28635 Exercise 67.4348 10.36527 Total 67.2174 8.86169 Control 76.6522 10.34236 Exercise 78.1739 11.61759 Total 77.4130 10.90275 Control 92.2174 10.32630 Exercise 89.3478 13.71664 Total 90.7826 12.09208 Control 70.2174 8.75399 Exercise 66.5652 8.89242 Total 68.3913 8.91809 80.2174 10.23344 Exercise 79.0870 12.40203 Total 79.6522 11.25703 Control 91.3913 12.78756 Exercise 87.2609 14.50460 Total 89.3261 13.68057 HRstand12 Control HRexer12 Std. Deviation Tests of Within-Subjects Effects TYPE III SS T T X Gr TXM T X Gr X M Error (T) C C X Gr CXM 16.635 125.336 9.230 2.122 3944.116 20406.064 107.831 64.847 df 1 1 1 1 42 2 2 2 MS 16.635 125.336 9.230 2.122 93.908 10203.032 53.916 32.423 F Sig. .177 1.335 .098 .023 .676 .255 .755 .881 164.212 .868 .522 .000* .424 .595 162 C X Gr X M Error (C) TXC T X C X Gr TXCXM T X C X Group X M Error (T X C) 69.028 5219.192 186.890 5.924 19.577 32.132 2360.627 Tests of Between-Subjects Effects Source Type III SS Intercept 1534599.445 Gr 322.643 M 4.975 Gr X M 300.335 Error 20643.646 2 84 2 2 2 2 84 df 1 1 1 1 42 MS 1534599.445 322.643 4.975 300.335 491.515 34.514 62.133 93.445 2.962 9.789 16.066 28.103 F 3122.180 .656 .010 .611 .555 .576 3.325 .105 .348 .572 .041* .900 .707 .567 Sig. .000 .422 .920 .439 163 Appendix Q ANOVA Summary Tables BpTRU Rate-Pressure-Product (RPP) Descriptive Statistics RPPrest1 RPPstand1 RPPexer1 RPPrest12 Group Mean Control 8.6807 1.30891 Exercise 9.3183 1.96001 Total 8.9995 1.67917 Control 10.7719 2.48239 Exercise 11.2790 1.99892 Total 11.0255 2.24317 Control 14.1952 2.17364 Exercise 14.4223 3.08878 Total 14.3088 2.64335 Control 8.9350 1.44423 Exercise 8.7029 1.69586 Total 8.8190 1.56190 11.1988 2.37558 Exercise 10.4525 1.96167 Total 10.8256 2.18693 Control 13.9108 2.68465 Exercise 12.9988 3.59233 Total 13.4548 3.16941 RPPstand12 Control RPPexer12 Std. Deviation Tests of Within-Subjects Effects Source Type III SS T 11.471 T X Gr 17.911 8T X M .341 T X Gr X M .098 Error (T) 131.665 C 1003.863 C X Gr 2.301 CXM 12.245 C X Gr X M 3.810 Df 1 1 1 1 42 2 2 2 2 MS 11.471 17.911 .341 .098 3.135 501.932 1.151 6.123 1.905 F 3.659 5.713 .109 .031 Sig. .063 .021* .743 .860 152.266 .349 1.857 .578 .000* .706 .162 .563 164 Error (C) TXC T X C X Gr TXCXM T X C X Gr X M Error(T X C) 276.899 7.007 .633 .962 1.721 175.023 84 2 2 2 2 84 Tests of Between-Subjects Effects Source Type III SS Intercept 31167.215 Gr 2.398 M .004 Gr X M 8.050 Error 808.153 df 1 1 1 1 42 3.296 3.503 .317 .481 .860 2.084 MS 31167.215 2.398 .004 8.050 19.242 1.681 .152 .231 .413 F 1619.772 .125 .000 .418 .192 .859 .794 .663 Sig. .000 .726 .989 .521 BpTRU Rate-Pressure-Product (RPP) for the Control Group Tests of Within Subjects Contrasts Source T TXM Error (T) C CXM Error (C) TXC TXCXM Error (T X C) Condition S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Type III SS .126 .143 16.617 224.002 1160.568 6.440 9.115 75.959 109.518 .374 4.767 .035 3.388 34.471 91.373 df 1 1 21 1 1 1 1 21 21 1 1 1 1 21 21 MS .126 .143 .791 224.002 1160.568 6.440 9.115 3.617 5.215 .374 4.767 .035 3.388 1.641 4.351 Tests of Between-Subjects Effects Source Intercept M Error Type III SS 5616.444 1.366 111.216 df 1 1 21 MS 5616.444 1.366 5.296 F 1060.504 .258 Sig. .000 .617 F .160 .180 Sig. .693 .675 61.929 222.538 1.780 1.748 .000* .000* .196 .200 .228 1.096 .021 .779 .638 .307 .886 .388 165 BpTRU Rate-Pressure-Product (RPP) for the Exercise Group Tests of Within Subjects Contrasts Source T TXM Error (T) C CXM Error (C) T XC TXCXM Error (T X C) Condition S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Type III SS 9.137 .012 27.271 146.357 855.351 1.758 .051 71.864 200.970 .889 6.600 .527 .015 19.294 132.606 Df 1 1 21 1 1 1 1 21 21 1 1 1 1 21 21 MS 9.137 .012 1.299 146.357 855.351 1.758 .051 3.422 9.570 .889 6.600 .527 .015 .919 6.315 F 7.036 .009 Sig. .015* .926 42.768 89.378 .514 .005 .000* .000* .481 .942 .968 1.045 .574 .002 .336 .318 .457 .962 Tests of Between-Subjects Effects Intercept Menopause Error 4820.261 1.321 158.168 1 1 21 4820.261 1.321 7.532 639.988 .175 .000 .680 166 Appendix Q ANOVA Summary Tables Log Transformed Low Frequency (LgLF) Power LgLFrest1 Group Control Exercise Total LgLFstand1 Control Exercise Total LgLFexer1 Control Exercise Total LgLFrest12 Control Exercise Total Menopause Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Mean 2.1299 1.8395 1.9557 2.1422 1.8802 1.9588 2.1352 1.8614 1.9572 2.0673 2.0895 2.0806 2.3976 1.8556 2.0182 2.2089 1.9636 2.0494 1.4810 1.5581 1.5273 1.6041 1.2258 1.3393 1.5338 1.3792 1.4333 2.0002 1.7144 1.8287 2.1440 1.7494 1.8678 2.0618 1.7333 1.8483 Std. Deviation .29837 .38760 .37560 .47023 .42025 .44068 .36472 .39796 .40416 .35092 .43023 .39071 .16238 .41920 .43830 .32439 .43239 .41105 .66384 .66970 .65078 .60655 .55912 .58511 .61870 .62326 .61820 .37532 .48489 .45678 .46000 .55618 .54933 .40335 .51441 .49905 167 LgLFstand12 Control Exercise Total LgLFexer12 Control Exercise Total Tests of Within-Subjects Effects Source T T X Gr TXM T X Gr X M Error (T) C C X Gr CXM C X Gr X M Error (C) TXC T X C X Gr TXCXM T X C X Gr X M Error (T X C) Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Type III SS .063 .167 .036 .004 5.282 9.030 1.084 .080 .633 19.624 1.276 .336 .144 .036 8.698 Tests of Within-Subjects Contrasts Source Condition T T X Gr TXM 2.0406 2.0893 2.0698 2.2392 1.8328 1.9547 2.1257 1.9512 2.0123 1.9595 1.9007 1.9242 1.7986 1.2127 1.3884 1.8905 1.5302 1.6563 Df 1 1 1 1 36 2 2 2 2 72 2 2 2 2 72 Type III SS .021 .056 .012 .32463 .34221 .32745 .25174 .39683 .40117 .30252 .38785 .36612 .57142 .75113 .66919 .58781 .61759 .65405 .56173 .75428 .70723 MS .063 .167 .036 .004 .147 4.515 .542 .040 .317 .273 .638 .168 .072 .018 .121 Df 1 1 1 MS .021 .056 .012 F .429 1.137 .244 .025 Sig. .517 .293 .624 .874 16.565 1.989 .146 1.162 .000* .144 .864 .319 5.281 1.391 .597 .151 .007* .255 .553 .860 F .429 1.137 .244 Sig. .517 .293 .624 168 T X Gr X M Error (T) C C X Gr CXM C X Gr X M Error (C) TXC T X C X Gr TXCXM T X C X Gr X M Error (T X C) S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 754.398 Group .232 M 3.487 Gr X M 1.619 Error 19.530 .001 1.761 1.147 9.156 .042 1.864 .141 .092 .987 .911 6.768 27.424 .035 2.152 .088 .656 .094 .052 .068 .005 2.759 11.741 df 1 1 1 1 36 1 36 1 1 1 1 1 1 1 1 36 36 1 1 1 1 1 1 1 1 36 36 .001 .049 1.147 9.156 .042 1.864 .141 .092 .987 .911 .188 .762 .035 2.152 .088 .656 .094 .052 .068 .005 .077 .326 MS 754.398 .232 3.487 1.619 .542 F 1390.617 .427 6.428 2.984 .025 .874 6.102 12.020 .223 2.447 .752 .121 5.250 1.196 .018* .001* .640 .127 .392 .730 .028* .281 .451 6.599 1.147 2.013 1.229 .159 .887 .015 .506 .014* .291 .165 .275 .692 .353 .904 Sig. .000 .518 .016* .093 Log Transformed Low Frequency (LgLF) Power for the Control Group Tests of Within-Subjects Contrasts Source Condition T TXM Error (T) C S vs. R E vs. R CX M S vs. R E vs. R Type III SS .078 .003 1.229 .872 1.477 1.005 .848 Df 1 1 18 1 1 1 1 MS .078 .003 .068 .872 1.477 1.005 .848 F 1.137 .043 Sig. .300 .838 5.466 3.064 6.297 1.759 .031* .097 .022* .201 169 Error (C) TXC TXCXM Error (T X C) S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 139.477 M .063 Error 3.670 2.872 8.680 .125 2.778 .001 .047 1.183 7.370 df 1 1 18 18 18 1 1 1 1 18 18 MS 139.477 .063 .204 .160 .482 .125 2.778 .001 .047 .066 .409 F 684.087 .310 1.898 6.785 .017 .116 .185 .018* .896 .738 Sig. .000 .585 Log Transformed Low Frequency (LgLF) Power for the Exercise Group Tests of Within-Subjects Contrasts Source Condition T TXM Error (T) C S vs. R E vs. R CXM S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R TXCXM S vs. R E vs. R Error (T X C) S vs. R E vs. R Type III SS .004 .010 .532 .352 9.039 .179 .199 3.897 18.744 .006 .202 .151 .012 1.577 4.370 Tests of Between-Subjects Effects Source Type III SS df Intercept 113.779 1 M 1.540 1 Error 2.840 18 MS 113.779 1.540 .158 Df 1 1 18 1 1 1 1 18 18 1 1 1 1 18 18 MS .004 .010 .030 .352 9.039 .179 .199 .216 1.041 .006 .202 .151 .012 .088 .243 F 721.158 9.763 Sig. .000 .006* F .131 .331 Sig. .721 .572 1.625 8.680 .826 .191 .219 .009* .375 .667 .066 .833 1.724 .049 .801 .374 .206 .828 170 Appendix Q ANOVA Summary Tables Log Transformed High Frequency (lgHF) Power Descriptive Statistics LgHFrest1 Group Control Exercise Total LgHFstand1 Control Exercise Total LgHFexer1 Control Exercise Total LgHFrest12 Control Exercise Total Menopause Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Mean 1.7943 1.7080 1.7425 2.1253 1.6259 1.7757 1.9362 1.6638 1.7591 1.4240 1.4217 1.4226 1.7691 1.2625 1.4145 1.5719 1.3360 1.4185 1.2162 1.4262 1.3422 1.2840 1.1431 1.1854 1.2453 1.2738 1.2638 1.7167 1.6672 1.6870 2.2514 1.4496 1.6901 1.9459 Std. Deviation .26337 .44411 .37634 .48270 .46962 .51704 .39478 .45078 .44668 .17704 .41743 .33530 .64428 .49712 .57883 .45599 .46013 .46692 .70666 .72066 .70414 .62607 .53345 .54977 .64874 .63025 .62857 .51889 .53492 .51524 .43762 .63633 .68526 .54227 171 LgHFstand12 Control Exercise Total LgHFexer12 Control Exercise Total Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Tests of Within-Subjects Effects Source T T X Gr TXM T X Gr X M Error (T) C C X Gr CXM C X Gr X M Error (C) TXC T X C X Gr TXCXM T X C X Gr X M Error (T X C) Tests of Within-Subjects Contrasts Source Condition T T X Gr TX M Type III SS .119 .128 .193 .147 6.985 7.208 1.346 .627 .022 22.880 .567 .175 .192 .100 10.404 Type III SS .040 .043 .064 1.5500 1.6885 1.4503 1.4634 1.4581 1.6953 1.2390 1.3759 1.5553 1.3426 1.4170 1.5784 1.6904 1.6456 1.5628 1.0017 1.1700 1.5717 1.3196 1.4078 Df 1 1 1 1 36 2 2 2 2 72 2 2 2 2 72 Df 1 1 1 .59050 .59842 .22383 .38556 .32337 .50213 .47379 .51571 .37387 .44175 .42690 .84635 .77102 .78182 .74505 .64406 .70674 .77413 .77450 .77402 MS .119 .128 .193 .147 .194 3.604 .673 .314 .011 .318 .283 .088 .096 .050 .145 MS .040 .043 .064 F .616 .661 .992 .755 Sig. .438 .422 .326 .391 11.341 2.117 .987 .035 .000* .128 .378 .966 1.960 .607 .665 .346 .148 .548 .518 .709 F .616 .661 .992 Sig. .438 .422 .326 172 T X Gr X M Error (T) C C X Gr CXM C X Gr X M Error (C) TXC T X C X Gr TXCXM T X C X Gr X M Error (T X C) S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Type III Source SS Intercept 510.164 Gr .008 M 2.863 Gr X M 3.735 Error 25.849 .049 2.328 7.648 13.219 .145 2.472 .263 1.252 .041 .022 7.053 31.960 .022 .974 .061 .348 .123 .071 .157 .000 2.993 15.005 1 36 1 1 1 1 1 1 1 1 36 36 1 1 1 1 1 1 1 1 36 36 Df MS 510.164 .008 2.863 3.735 .718 1 1 1 1 36 .049 .065 7.648 13.219 .145 2.472 .263 1.252 .041 .022 .196 .888 .022 .974 .061 .348 .123 .071 .157 .000 .083 .417 .755 .391 39.035 14.890 .739 2.784 1.345 1.410 .210 .025 .000* .000* .396 .104 .254 .243 .649 .875 .262 2.336 .734 .834 1.480 .171 1.886 .001 .612 .135 .397 .367 .232 .681 .178 .978 F 710.500 .011 3.987 5.202 Sig. .000 .916 .053 .029 Log Transformed High Frequency (LgHF) Power for the Control Group Tests of Within-Subjects Contrasts Source Condition T TXM Error (T) C S vs. R E vs. R CXM S vs. R E vs. R Type III SS .088 .001 1.569 3.047 2.281 .052 .503 Df 1 1 18 1 1 1 1 MS .088 .001 .087 3.047 2.281 .052 .503 F 1.015 .006 Sig. .327 .937 15.515 3.238 .262 .714 .0* .089 .615 .409 173 Error (C) TXC TXCXM Error (T X C) S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 91.826 M .010 Error 3.861 3.535 12.682 .083 1.331 .001 .044 1.697 10.665 df 1 1 18 18 18 1 1 1 1 18 18 MS 91.826 .010 .215 .196 .705 .083 1.331 .001 .044 .094 .593 F 428.060 .048 .884 2.247 .012 .074 .359 .151 .915 .789 F .001 2.500 Sig. .981 .131 23.738 11.871 1.231 .704 .000* .003* .282 .412 .064 .307 3.631 .121 .802 .587 .073 .733 Sig. .000 .829 Log Transformed High Frequency (LgHF) Power for the Exercise Group Tests of Within-Subjects Contrasts Source Condition T TXM Error (T) C S vs. R E vs. R CXM S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R TXCXM S vs. R E vs. R Error (T X C) S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS df Intercept 79.081 1 M 2.053 1 Error 4.755 18 Type III SS 2.385E-5 .105 .759 4.639 12.714 .241 .754 3.518 19.278 .005 .074 .261 .029 1.296 4.339 MS 79.081 2.053 .264 Df 1 1 18 1 1 1 1 18 18 1 1 1 1 18 18 MS 2.385E-5 .105 .042 4.639 12.714 .241 .754 .195 1.071 .005 .074 .261 .029 .072 .241 F 299.353 7.770 Sig. .000 .012* 174 Appendix Q ANOVA Summary Tables Log Transformed Total Power (LgTP) Descriptive Statistics LgTPrest1 Group Control Exercise Total LgTPstand1 Control Exercise Total LgTPexer1 Control Exercise Total LgTPrest12 Control Exercise Total Menopause Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Mean 2.6316 2.4995 2.5523 2.6563 2.4526 2.5137 2.6421 2.4742 2.5330 2.5300 2.5721 2.5553 2.7983 2.3553 2.4882 2.6450 2.4553 2.5217 2.3545 2.2130 2.2696 2.4560 2.3265 2.3654 2.3980 2.2741 2.3175 2.5975 2.3994 2.4786 2.7332 2.3850 2.4894 2.6557 Std. Deviation .26199 .35534 .32062 .40692 .43379 .42602 .31750 .39240 .37267 .26304 .36219 .31919 .17946 .42363 .41793 .26197 .40397 .36862 .63470 .58569 .59336 .54657 .60174 .57452 .57839 .58528 .57851 .38602 .40855 .40181 .46465 .43263 .46010 .41004 175 LgTPstand12 Control Exercise Total LgTPexer12 Control Exercise Total Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total 2.3916 2.4840 2.5528 2.5480 2.5500 2.6718 2.4847 2.5408 2.6038 2.5139 2.5454 2.6362 2.6370 2.6367 2.7357 2.1726 2.3415 2.6789 2.3869 2.4891 .41331 .42640 .18950 .35237 .29176 .35617 .40889 .39436 .26807 .37764 .34243 .61368 .69544 .64711 .69912 .27951 .50218 .62721 .55604 .59094 MS .187 .070 .032 .046 .169 .311 .024 .027 .060 .191 .302 .165 .081 .217 .112 F .107 .412 .190 .273 Sig. .300 .525 .666 .605 1.631 .125 .141 .314 .203 .882 .869 .731 2.704 1.475 .723 1.945 .074 .236 .489 .150 Tests of Within-Subjects Effects Source Type III SS T .187 T X Gr .070 TX M .032 T X Gr X M .046 Error (T) 6.092 C .622 C X Gr .048 CX M .054 C X Gr X M .120 Error (C) 13.728 TXC .605 T X C X Gr .330 TXCXM .162 T X C X Gr X M .435 Error(T X C) 8.051 df 1 1 1 1 36 2 2 2 2 72 2 2 2 2 72 Tests of Within-Subjects Contrasts Source Condition T T X Gr TX M Type III SS .062 .023 .011 Df 1 1 1 MS .062 .023 .011 F 1.107 .412 .190 Sig. .300 .525 .666 176 T X Gr X M Error (T) C C X Gr CXM C X Gr X M Error (C) TXC T X C X Gr TXCXM T X C X Gr X M Error (T X C) S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 453.986 Gr .000 M .663 Gr X M .258 Error 5.574 .015 2.031 .028 .759 6.968E-5 .069 .094 .003 .223 .122 4.090 21.769 .018 1.024 .022 .586 .197 .007 .163 .277 2.284 10.381 df 1 1 1 1 36 1 36 1 1 1 1 1 1 1 1 36 36 1 1 1 1 1 1 1 1 36 36 MS 453.986 .000 .663 .258 .155 .015 .056 .028 .759 6.968E-5 .069 .094 .003 .223 .122 .114 .605 .018 1.024 .022 .586 .197 .007 .163 .277 .063 .288 .273 .605 .246 1.256 .001 .115 .825 .004 1.959 .202 .623 .270 .980 .737 .370 .947 .170 .656 .282 3.553 .343 2.032 3.111 .025 2.568 .961 .598 .068 .562 .163 .086 .874 .118 .334 F 2932.180 .003 4.283 1.669 Sig. .000 .960 .046* .205 MS .087 .000 .072 .014 .198 .324 .086 .111 .371 F 1.197 .003 Sig. .288 .956 .122 .533 2.913 .232 .731 .475 .105 .636 Log Transformed Total Power (LgTP) for the Control Group Tests of Within-Subjects Contrasts Source Condition T TXM Error (T) C S vs. R E vs. R CX M S vs. R E vs. R Error (C) S vs. R E vs. R Type III SS .087 .000 1.305 .014 .198 .324 .086 2.003 6.686 Df 1 1 18 1 1 1 1 18 18 177 TXC TXCXM Error (T X C) S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 242.754 M .050 Error 3.001 .042 1.693 .001 .104 .920 7.314 df 1 1 18 1 1 1 1 18 18 MS 242.754 .050 .167 .042 1.693 .001 .104 .051 .406 F 1456.224 .301 .829 4.167 .017 .256 .375 .056 .897 .619 Sig. .000 .590 Log Transformed Total Power (LgTP) for the Exercise Group Tests of Within-Subjects Contrasts Source Condition T TX M Error (T) C S vs. R E vs. R CX M S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R TXCXM S vs. R E vs. R Error (T X C) S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS df Intercept 213.202 1 M .820 1 Error 2.573 18 Type III SS .004 .024 .726 .014 .604 .013 .042 2.086 15.083 8.665E-5 .029 .337 .176 1.364 3.067 MS 213.202 .820 .143 Df 1 1 18 1 1 1 1 18 18 1 1 1 1 18 18 F 1491.379 5.737 MS .004 .024 .040 .014 .604 .013 .042 .116 .838 8.665E-5 .029 .337 .176 .076 .170 Sig. .000 .028* F .110 .601 Sig. .744 .448 .125 .721 .111 .050 .728 .407 .743 .826 .001 .167 4.447 1.030 .973 .687 .049 .324 178 Appendix Q ANOVA Summary Tables Log Transformed PNS Indicator (LgPNSI) Descriptive Statistics LgPNSIrest1 Group Control Exercise Total LgPNSIstand1 Control Exercise Total LgPNSIexer1 Control Exercise Total LgPNSIrest12 Control Exercise Menopause Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Mean -.8372 -.7915 -.8098 -.5310 -.8267 -.7380 -.7060 -.8104 -.7739 -1.1060 -1.1505 -1.1327 -1.0292 -1.0927 -1.0737 -1.0731 -1.1194 -1.1032 -1.1383 -.7868 -.9274 -1.1719 -1.1834 -1.1800 -1.1527 -1.0003 -1.0537 -.8809 -.7322 -.7917 -.4818 -.9354 -.7993 Std. Deviation .28688 .19770 .23125 .12971 .26407 .26734 .27482 .23191 .24939 .23235 .24446 .23450 .49941 .31307 .36549 .35574 .27951 .30457 .40474 .25284 .35858 .25254 .31063 .28781 .33621 .34491 .34548 .26468 .22161 .24459 .06025 .29217 .32380 179 Total LgPNSIstand12 Control Exercise Total LgPNSIexer12 Control Exercise Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Menopausal Post Menopausal Total Tests of Within-Subjects Effects Source T T X Gr TXM T X Gr X M Error (T) C C X Gr CXM C X Gr X M Error (C) TXC T X C X Gr TXCXM T X C X Gr X M Error (T X C) -.7098 -.8416 -.7955 -1.1026 -1.0847 -1.0918 -.9765 -1.2456 -1.1649 -1.0485 -1.1713 -1.1284 -1.0579 -.9466 -.9911 -1.1729 -1.1708 -1.1715 -1.1072 -1.0673 -1.0813 Type III SS .008 .009 .067 .028 2.523 5.423 .903 .640 .245 5.856 .001 .039 .017 .201 3.842 df 1 1 1 1 36 2 2 2 2 72 2 2 2 2 72 Tests of Within-Subjects Contrasts Source Condition Type III SS Df T .003 1 T X Gr .003 1 .28481 .27689 .28327 .20423 .22167 .20951 .19445 .24025 .25584 .20296 .24152 .23375 .31581 .17795 .24126 .54697 .52567 .51749 .41505 .41306 .40885 MS .008 .009 .067 .028 .070 2.712 .452 .320 .123 .081 .000 .019 .008 .100 .053 MS .003 .003 F .108 .126 .962 .403 Sig. .744 .725 .333 .530 33.341 5.553 3.937 1.507 .000* .006* .024* .228 .007 .365 .155 1.879 .993 .696 .857 .160 F .108 .126 Sig. .744 .725 180 TXM T X Gr X M Error (T) C C X Gr CXM C X Gr X M Error (C) TXC T X C X Gr TXCXM T X C X Gr X M Error (T X C) Tests of Between-Subjects Effects Source Intercept Gr M Gr X M Error S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R .022 .009 .841 8.601 7.641 .151 1.712 .043 1.139 .455 .249 4.605 7.311 .000 .001 .010 .031 .009 .033 5.742E-5 .297 1.927 4.501 Type III SS 68.334 .005 .026 .369 2.274 1 1 36 1 1 1 1 1 1 1 1 36 36 1 1 1 1 1 1 1 1 36 36 Df 1 1 1 1 36 .022 .009 .023 8.601 7.641 .151 1.712 .043 1.139 .455 .249 .128 .203 .000 .001 .010 .031 .009 .033 5.742E-5 .297 .054 .125 MS 68.334 .005 .026 .369 .063 .962 .403 .333 .530 67.230 37.627 1.182 8.433 .335 5.607 3.560 1.227 .000* .000* .284 .006* .566 .023* .067 .275 .003 .005 .185 .248 .163 .264 .001 2.373 .953 .943 .669 .622 .689 .610 .974 .132 F 1081.990 .081 .418 5.842 Sig. .000 .777 .522 .021* Log Transformed PNS Indicator (LgPNSI) for the Control Group Tests of Within-Subjects Contrasts Source Condition T TXM Error (T) C S vs. R E vs. R CX M S vs. R E vs. R Type III SS 8.014E-6 .001 .347 3.467 1.135 .117 .173 Df 1 1 18 1 1 1 1 MS 8.014E-6 .001 .019 3.467 1.135 .117 .173 F .000 .078 Sig. .984 .783 40.938 8.436 1.384 1.284 .000* .009* .255 .272 181 Error (C) TXC TXCXM Error (T X C) S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 35.976 M .106 Error .694 1.524 2.422 .007 .022 .004 .283 1.184 1.362 df 1 1 18 18 18 1 1 1 1 18 18 MS 35.976 .106 .039 .085 .135 .007 .022 .004 .283 .066 .076 F 933.492 2.751 .104 .287 .060 3.735 .750 .599 .809 .069 Sig. .000 .115 Log Transformed PNS Indicator (LgPNSI) for the Exercise Group Tests of Within-Subjects Contrasts Source Condition T TXM Error (T) C S vs. R E vs. R CXM S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R TXCXM S vs. R E vs. R Error (T X C) S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 32.589 M .278 Error 1.580 Type III SS .005 .029 .494 5.171 7.776 .365 1.150 3.081 4.888 .003 .011 .005 .062 .743 3.138 df 1 1 18 MS 32.589 .278 .088 Df 1 1 18 1 1 1 1 18 18 1 1 1 1 18 18 MS .005 .029 .027 5.171 7.776 .365 1.150 .171 .272 .003 .011 .005 .062 .041 .174 F 371.289 3.166 F .186 1.041 Sig. .671 .321 30.212 28.631 2.130 4.234 .000* .000* .162 .054 .084 .061 .116 .354 .775 .808 .737 .559 Sig. .000 .092 182 Log Transformed PNS Indicator (LgPNSI) for Menopausal Women in the Control Group Tests of Within-Subjects Contrasts Source Condition T Error (T) C S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R Error (T X C) S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 16.661 Error .593 Type III SS .001 .154 .962 .914 .279 1.199 .009 .062 .362 .393 df 1 7 df 1 7 1 1 7 7 1 1 7 7 MS .001 .022 .962 .914 .040 .171 .009 .062 .052 .056 MS 16.661 .085 F .033 Sig. .862 24.171 5.335 .002* .054 .171 1.097 .691 .330 F 196.786 Sig. .000 Log Transformed PNS Indicator (LgPNSI) for Postmenopausal Women in the Control Group Tests of Within-Subjects Contrasts Source Condition T Error (T) C S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R Error (T X C) S vs. R E vs. R Type III SS .001 .193 3.037 .264 1.246 1.223 .000 .288 .823 .970 Tests of Between-Subjects Effects Source Type III SS Df Intercept 20.110 1 Error .101 11 MS 20.110 .009 df 1 11 1 1 11 11 1 1 11 11 MS .001 .018 3.037 .264 .113 .111 .000 .288 .075 .088 F 2189.675 F .046 Sig. .834 26.816 2.373 .000* .152 .003 3.269 .955 .098 Sig. .000 183 Log Transformed PNS Indicator (LgPNSI) for Menopausal Women in the Exercise Group Tests of Within-Subjects Contrasts Source Condition T Error (T) C S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R Error (T X C) S vs. R E vs. R Type III SS .003 .052 2.958 5.323 1.070 1.632 3.790E-5 .008 .150 .478 Tests of Between-Subjects Effects Source Type III SS Df Intercept 9.589 1 Error .427 5 MS 9.589 .085 df 1 5 1 1 5 5 1 1 5 5 MS .003 .010 2.958 5.323 .214 .326 3.790E-5 .008 .030 .096 F 112.347 F .325 Sig. .593 13.828 16.305 .014* .010* .001 .079 .973 .790 Sig. .000 Log Transformed PNS Indicator (LgPNSI) for Postmenopausal Women in the Exercise Group Tests of Within-Subjects Contrasts Source Condition T Error (T) C S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R Error (T X C) S vs. R E vs. R Type III SS .048 .442 2.325 2.454 2.012 3.256 .014 .103 .593 2.660 Tests of Between-Subjects Effects Source Type III SS df Intercept 32.405 1 Error 1.153 13 MS 32.405 .089 df 1 13 1 1 13 13 1 1 13 13 MS .048 .034 2.325 2.454 .155 .250 .014 .103 .046 .205 F 365.308 F 1.419 Sig. .255 15.024 9.800 .002* .008* .300 .503 .593 .491 Sig. .000 184 Appendix Q ANOVA Summary Tables Log Transformed SNS Indicator (LgSNSI) Descriptive Statistics LgSNSIrest1 Menopause Menopausal Post Menopausal Total LgSNSIstand1 Menopausal Post Menopausal Total LgSNSIexer1 Menopausal Post Menopausal Total LgSNSIrest12 Menopausal Post Menopausal Total Group Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Mean .3356 .0169 .1990 .1315 .2543 .1976 .2131 .1831 .1981 .6433 .6285 .6370 .6678 .5931 .6276 .6580 .6037 .6309 .2648 .3201 .2885 .1319 .0827 .1054 .1851 .1539 .1695 .2835 -.1074 .1160 .0473 .2998 .1833 .1418 .1777 Std. Deviation .37815 .25567 .35905 .23069 .37242 .31533 .30661 .35292 .32667 .32345 .49982 .39048 .27174 .33201 .30208 .28539 .37608 .33067 .23735 .23336 .22822 .21034 .16168 .18354 .22546 .21136 .21628 .30738 .15884 .31761 .27497 .26307 .29282 .30444 .30108 185 LgSNSIstand12 Menopausal Post Menopausal Total LgSNSIexer12 Menopausal Post Menopausal Total Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Tests of Within-Subjects Effects Source Type III SS T .009 TXM .062 T X Gr .003 TXMX G .104 Error (T) 1.565 C 8.501 CXM .381 C X Gr .025 C X M X Gr .886 Error (C) 6.086 TXC .142 TXCXM .003 T X C X Gr .027 T X C X M X Gr .019 Error(T X C) 2.787 Tests of Within-Subjects Contrasts Source Condition T TXM T X Gr T X M X Gr Error (T) .1597 .5903 .5439 .5705 .6259 .5937 .6086 .6117 .5788 .5952 .3812 .2358 .3188 .2103 .2109 .2107 .2787 .2184 .2485 df 1 1 1 1 36 2 2 2 2 72 2 2 2 2 72 Type III SS .003 .021 .001 .035 .522 .29941 .23310 .30367 .25553 .27043 .30249 .28289 .25035 .29567 .27093 .37321 .26652 .32848 .21376 .31377 .26702 .29179 .29358 .29052 MS .009 .062 .003 .104 .043 4.250 .190 .012 .443 .085 .071 .002 .013 .009 .039 Df 1 1 1 1 36 MS .003 .021 .001 .035 .014 F .207 1.434 .058 2.383 Sig. .652 .239 .810 .131 50.285 2.253 .147 5.244 .000* .112 .863 .007* 1.840 .045 .346 .240 .166 .956 .709 .787 F .207 1.434 .058 2.383 Sig. .652 .239 .810 .131 186 C CXM C X Gr C X M X Gr Error (C) TXC TXCXM T X C X Gr T X C X M X Gr Error(T X C) S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 7.936 M .010 Gr .051 M X Gr .145 Error 2.488 14.719 .372 .019 .665 .031 .043 1.432 1.219 8.528 3.478 .001 .231 .002 .002 .002 .049 .018 .003 2.141 3.255 df 1 1 1 1 36 1 1 1 1 1 1 1 1 36 36 1 1 1 1 1 1 1 1 36 36 14.719 .372 .019 .665 .031 .043 1.432 1.219 .237 .097 .001 .231 .002 .002 .002 .049 .018 .003 .059 .090 MS 7.936 .010 .051 .145 .069 62.133 3.849 .080 6.879 .130 .443 6.044 12.619 .000 .058 .779 .013 .720 .510 .019* .001* .025 2.551 .032 .017 .041 .538 .308 .029 .876 .119 .858 .897 .840 .468 .582 .866 F 114.816 .148 .740 2.102 Sig. .000 .702 .395 .156 Log Transformed SNS Indicator (LgSNSI) for Menopausal Women in the Control Group Tests of Within-Subjects Contrasts Source Condition T TXM T X Gr T X M X Gr Error (T) C S vs. R E vs. R CXM S vs. R E vs. R C X Gr S vs. R Type III SS 5.732E-5 .000 .000 .000 .067 1.511 .003 .000 .000 .000 Df 1 0 0 0 7 1 1 0 0 0 MS 5.732E-5 F .006 Sig. .940 .010 1.511 .003 8.441 .023* .019 .893 187 C X M X Gr Error (C) TXC TXCXM T X C X Gr T X C X M X Gr Error(T X C) E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 2.775 M .000 Gr .000 M X Gr .000 Error .706 .000 .000 .000 1.253 1.047 2.843E-6 .113 .000 .000 .000 .000 .000 .000 .457 1.036 df 1 0 0 0 7 0 0 0 7 7 1 1 0 0 0 0 0 0 7 7 MS 2.775 .179 .150 2.843E-6 .113 .000 .766 .995 .410 .065 .148 F 27.528 Sig. .001 .101 Log Transformed SNS Indicator (LgSNSI) for Postmenopausal Women in the Control Group Tests of Within-Subjects Contrasts Source Condition T TXM T X Gr T X M X Gr Error (T) C S vs. R E vs. R CXM S vs. R E vs. R C X Gr S vs. R E vs. R C X M X Gr S vs. R E vs. R Error (C) S vs. R E vs. R Type III SS .002 .000 .000 .000 .248 7.459 .160 .000 .000 .000 .000 .000 .000 2.748 .564 Df 1 0 0 0 11 1 1 0 0 0 0 0 0 11 11 MS .002 F .067 .023 7.459 .160 29.854 .000* 3.128 .105 .250 .051 Sig. .800 188 TXC TXCXM T X C X Gr T X C X M X Gr Error (T X C) S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 2.196 M .000 Gr .000 M X Gr .000 Error .319 .011 .159 .000 .000 .000 .000 .000 .000 .337 .673 df 1 0 0 0 11 1 1 0 0 0 0 0 0 11 11 MS 2.196 .011 .159 .351 .565 2.597 .135 .031 .061 F 75.680 Sig. .000 .029 Log Transformed SNS Indicator (LgSNSI) for Menopausal Women in the Exercise Group Tests of Within-Subjects Contrasts Source Condition T TXM T X Gr T X M X Gr Error (T) C S vs. R E vs. R CXM S vs. R E vs. R C X Gr S vs. R E vs. R C X M X Gr S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R TXCXM S vs. R E vs. R T X C X Gr S vs. R Type III SS .029 .000 .000 .000 .048 4.785 1.253 .000 .000 .000 .000 .000 .000 1.406 .326 .005 .005 .000 .000 .000 Df 1 0 0 0 5 1 1 0 0 0 0 0 0 5 5 1 1 0 0 0 MS .029 F Sig. 2.979 .145 .010 4.785 1.253 17.018 .009* 19.224 .007* .281 .065 .005 .005 .059 .060 .818 .817 189 T X C X M X Gr Error (T X C) E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept .894 M .000 Gr .000 M X Gr .000 Error .439 .000 .000 .000 .403 .403 df 1 0 0 0 5 0 0 0 5 5 MS .894 .081 .081 F 10.185 Sig. .024 .088 Log Transformed SNS Indicator (LgSNSI) for Postmenopausal Women in the Exercise Group Tests of Within-Subjects Contrasts Source Condition T TXM T X Gr T X M X Gr Error (T) C S vs. R E vs. R CXM S vs. R E vs. R C X Gr S vs. R E vs. R C X M X Gr S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R TXCXM S vs. R E vs. R T X C X Gr S vs. R E vs. R T X C X M X Gr S vs. R E vs. R Error (T X C) S vs. R E vs. R Type III SS .024 .000 .000 .000 .159 2.802 .475 .000 .000 .000 .000 .000 .000 3.121 1.542 .014 .048 .000 .000 .000 .000 .000 .000 .944 1.143 Df 1 0 0 0 13 1 1 0 0 0 0 0 0 13 13 1 1 0 0 0 0 0 0 13 13 MS .024 F Sig. 1.936 .187 .012 2.802 .475 11.672 .005* 4.004 .067 .240 .119 .014 .048 .195 .544 .073 .088 .666 .474 190 Tests of Between-Subjects Effects Source Type III SS Intercept 3.220 M .000 Gr .000 M X Gr .000 Error 1.025 df 1 0 0 0 13 MS 3.220 .079 F 40.847 Sig. .000 191 Appendix Q ANOVA Summary Tables Baroreflex Slope (BSLOPE) Descriptive Statistics BSLOPErest1 Menopause Menopausal Post Menopausal Total BSLOPEstand1 Menopausal Post Menopausal Total BSLOPEexer1 Menopausal Post Menopausal Total BSLOPErest12 Menopausal Post Menopausal Total Group Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Mean 6.6193 8.8679 7.5830 5.5978 5.1201 5.3406 6.0064 6.2444 6.1254 2.8873 4.5621 3.6050 3.1848 2.4832 2.8070 3.0658 3.1068 3.0863 5.4825 5.8156 5.6253 5.9920 5.9837 5.9875 5.7882 5.9333 5.8607 5.7710 7.4161 6.4760 5.6259 4.4648 5.0007 5.6840 Std. Deviation 3.19693 4.33135 3.74865 3.19380 2.40681 2.74943 3.15190 3.46487 3.27157 .62491 2.94747 2.07157 2.05674 1.53367 1.79210 1.61718 2.20248 1.90730 4.91715 5.56402 4.99554 5.52858 3.80426 4.57977 5.16420 4.24916 4.66842 2.90354 2.85097 2.89472 3.59153 3.26227 3.39972 3.25257 192 BSLOPEstand12 Menopausal Post Menopausal Total BSLOPEexer12 Menopausal Post Menopausal Total Tests of Within-Subjects Effects Source T TXM T X Gr T X M X Gr Error (T) C CXM C X Gr C X M X Gr Error (C) TXC TXCXM T X C X Gr T X C X M X Gr Error(T X C) Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Type III SS 1.103 1.043 43.321 .086 433.125 421.914 20.726 78.732 14.068 1248.913 30.259 14.625 50.009 .013 698.890 5.3502 5.5171 3.0217 4.5493 3.6764 3.4022 2.3884 2.8563 3.2500 3.0367 3.1433 9.6170 5.5545 7.8759 8.5711 3.9327 6.0735 8.9895 4.4193 6.7044 Df 1 1 1 1 36 2 2 2 2 72 2 2 2 2 72 3.36838 3.27262 .58814 2.79998 1.95371 2.09959 1.25605 1.73944 1.64808 2.04322 1.83542 7.73857 5.03729 6.80867 5.75465 4.86587 5.69593 6.44296 4.84342 6.08341 MS 1.103 1.043 43.321 .086 12.031 210.957 10.363 39.366 7.034 17.346 15.129 7.312 25.004 .007 9.707 F .092 .087 3.601 .007 Sig. .764 .770 .066 .933 12.162 .597 2.269 .406 .000* .553 .111 .668 1.559 .753 2.576 .001 .217 .474 .083 .999 193 Tests of Within-Subjects Contrasts Source Condition T TX M T X Gr T X M X Gr Error (T) C S vs. R E vs. R CXM S vs. R E vs. R C X Gr S vs. R E vs. R C X M X Gr S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R TXCXM S vs. R E vs. R T X C X Gr S vs. R E vs. R T X C X M X Gr S vs. R E vs. R Error (T X C) S vs. R E vs. R Type III SS .368 .348 14.440 .029 144.375 592.686 2.408 20.746 38.665 .660 126.580 .423 23.856 363.887 1929.392 11.265 60.155 3.131 28.203 .767 67.072 .008 .027 122.256 1092.437 Tests of Between-Subjects Effects Source Type III SS Intercept 2004.346 M 22.404 Gr 2.673 M X Gr 16.080 Error 217.421 df 1 1 1 1 36 df 1 1 1 1 36 1 1 1 1 1 1 1 1 36 36 1 1 1 1 1 1 1 1 36 36 MS 2004.346 22.404 2.673 16.080 6.039 MS .368 .348 14.440 .029 4.010 592.686 2.408 20.746 38.665 .660 126.580 .423 23.856 10.108 53.594 11.265 60.155 3.131 28.203 .767 67.072 .008 .027 3.396 30.345 F 331.874 3.710 .443 2.663 F .092 .087 3.601 .007 Sig. .764 .770 .066 .933 58.636 .045 2.052 .721 .065 2.362 .042 .445 .000* .833 .161 .401 .800 .133 .839 .509 3.317 1.982 .922 .929 .226 2.210 .002 .001 .077 .168 .343 .341 .637 .146 .961 .976 Sig. .000 .062 .510 .111 194 Appendix Q ANOVA Summary Tables Systolic Finapres Arterial Blood Pressure (ABP) Descriptive Statistics ABPrest1 Menopause Menopausal Post Menopausal Total ABPstand1 Menopausal Post Menopausal Total ABPexer1 Menopausal Post Menopausal Total ABPrest12 Menopausal Post Menopausal Total Group Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Mean 107.4879 124.1400 114.6245 101.2255 121.3368 112.0547 103.7304 122.1778 112.9541 155.6149 132.5202 145.7171 138.3213 143.8478 141.2971 145.2388 140.4495 142.8441 166.9878 161.9130 164.8129 145.8618 171.3493 159.5858 154.3121 168.5184 161.4153 141.2592 140.2733 140.8367 116.2907 143.9591 131.1890 126.2781 Std. Deviation 39.39609 16.81488 31.89982 33.94152 34.67261 35.16488 35.33665 29.97822 33.66620 27.05537 34.56587 31.53341 21.38058 22.52484 21.74540 24.69593 26.26656 25.28097 46.00835 61.95207 51.21295 30.49683 31.39523 33.01013 37.82945 41.28072 39.73835 28.26807 9.79785 21.62070 19.67023 26.69295 27.17745 25.99813 195 ABPstand12 Menopausal Post Menopausal Total ABPexer12 Menopausal Post Menopausal Total Tests of Within-Subjects Effects Source T TXM T X Gr T X M X Gr Error (T) C CXM C X Gr C X M X Gr Error (C) TXC TXCXM T X C X Gr T X C X M X Gr Error (T X C) Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Type III SS 554.871 35.337 .216 39.083 40176.897 40809.424 152.835 6277.436 143.488 40130.055 9395.469 168.632 197.427 1512.637 69495.979 Tests of Within-Subjects Contrasts Source Condition T TXM T X Gr T X M X Gr Type III SS 184.957 11.779 .072 13.028 142.8533 134.5657 148.0385 130.2258 140.4045 134.3718 135.3135 134.8788 139.8384 133.7872 136.8128 150.4952 162.5120 155.6453 144.7000 161.7190 153.8641 147.0181 161.9569 154.4875 df 1 1 1 1 36 2 2 2 2 72 2 2 2 2 72 22.71067 25.51483 26.64428 19.21771 24.65747 30.64824 36.36133 33.18198 29.19844 31.74174 30.25864 38.52393 41.69193 38.80408 36.60486 41.31436 39.39545 36.48283 40.31659 38.69796 MS 554.871 35.337 .216 39.083 1116.025 20404.712 76.418 3138.718 71.744 557.362 4697.734 84.316 98.713 756.319 965.222 Df 1 1 1 1 MS 184.957 11.779 .072 13.028 F .497 .032 .000 .035 Sig. .485 .860 .989 .853 36.609 .137 5.631 .129 .000* .872 .005* .879 4.867 .087 .102 .784 .010* .916 .903 .461 F .497 .032 .000 .035 Sig. .485 .860 .989 .853 196 Error (T) C CXM C X Gr C X M X Gr Error (C) TXC TXCXM T X C X Gr T X C X M X Gr Error (T X C) S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R 13392.299 16747.032 81385.458 279.718 163.180 10731.266 219.437 260.883 13.339 32487.225 57019.004 13538.879 14626.519 103.307 335.931 130.111 391.816 1376.858 2885.221 53642.561 96532.189 36 1 1 1 1 1 1 1 1 36 36 1 1 1 1 1 1 1 1 36 36 372.008 16747.032 81385.458 279.718 163.180 10731.266 219.437 260.883 13.339 902.423 1583.861 13538.879 14626.519 103.307 335.931 130.111 391.816 1376.858 2885.221 1490.071 2681.450 18.558 51.384 .310 .103 11.892 .139 .289 .008 .000* .000* .581 .750 .001* .712 .594 .927 9.086 5.455 .069 .125 .087 .146 .924 1.076 .005* .025* .794 .725 .769 .705 .343 .307 Tests of Between-Subjects Effects Source Intercept M Gr M X Gr Error Type III SS 1421504.805 496.611 765.984 1647.312 26828.965 Df 1 1 1 1 36 MS 1421504.805 496.611 765.984 1647.312 745.249 F 1907.423 .666 1.028 2.210 Sig. .000 .420 .317 .146 Systolic Finapres Arterial Blood Pressure (ABP) for the Control Group Tests of Within-Subjects Contrasts Source Condition T TXM Error (T) C S vs. R E vs. R CXM S vs. R E vs. R Error (C) S vs. R E vs. R Type III SS 103.032 .017 6449.251 29083.929 48244.757 .176 44.577 23853.558 32214.193 Df 1 1 18 1 1 1 1 18 18 MS 103.032 .017 358.292 29083.929 48244.757 .176 44.577 1325.198 1789.677 F .288 .000 Sig. .598 .995 21.947 26.957 .000 .025 .000* .000* .991 .876 197 TXC TXCXM Error (T X C) S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 726576.074 M 2117.610 Error 10707.806 8744.715 10610.461 1197.031 2780.435 27167.225 47807.967 df 1 1 18 1 1 1 1 18 18 MS 726576.074 2117.610 594.878 8744.715 10610.461 1197.031 2780.435 1509.290 2655.998 F 1221.386 3.560 5.794 3.995 .793 1.047 .027* .061 .385 .320 F .216 .060 Sig. .648 .809 .651 24.883 1.056 .092 .430 .000* .318 .765 3.510 1.772 .231 .217 .077 .200 .636 .647 Sig. .000 .075 Systolic Finapres Arterial Blood Pressure (ABP) for the Exercise Group Tests of Within-Subjects Contrasts Source Condition T TXM Error (T) C S vs. R E vs. R CXM S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R TXCXM S vs. R E vs. R Error (T X C) S vs. R E vs. R Type III SS 83.311 23.241 6943.048 312.466 34290.427 506.660 126.482 8633.667 24804.811 5163.053 4795.535 340.253 586.949 26475.336 48724.222 Df 1 1 18 1 1 1 1 18 18 1 1 1 1 18 18 Tests of Between-Subjects Effects Source Type III SS df Intercept 697624.799 1 M 157.019 1 Error 16121.159 18 MS 697624.799 157.019 895.620 F 778.930 .175 MS 83.311 23.241 385.725 312.466 34290.427 506.660 126.482 479.648 1378.045 5163.053 4795.535 340.253 586.949 1470.852 2706.901 Sig. .000 .680 198 Appendix Q ANOVA Summary Tables R-R Interval (RRI) Descriptive Statistics RRIrest1 Menopause Menopausal Post Menopausal Total RRIstand1 Menopausal Post Menopausal Total RRIexer1 Menopausal Post Menopausal Total RRIrest12 Menopausal Post Menopausal Group Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Mean 830.7290 884.0470 853.5796 901.6607 869.2388 884.2027 873.2880 873.6812 873.4846 729.9809 757.1833 741.6391 785.7792 754.9782 769.1940 763.4598 755.6398 759.5498 499.7738 544.2400 518.8307 517.3518 544.8580 532.1628 510.3206 544.6726 527.4966 833.0479 906.8267 864.6674 862.4817 846.2444 Std. Deviation 50.13143 73.05291 64.46379 101.63311 116.50396 108.97076 90.42722 103.63293 95.99973 70.34136 102.26987 82.95876 96.86768 109.11620 102.78704 89.67683 104.40270 96.14450 54.73911 70.99132 63.82221 115.45238 73.04380 93.99376 94.33410 70.54696 84.03917 75.79177 125.24953 102.77337 106.19357 127.90775 199 Total RRIstand12 Menopausal Post Menopausal Total RRIexer12 Menopausal Post Menopausal Total Tests of Within-Subjects Effects Source T TXM T X Gr T X M X Gr Error (T) C CXM C X Gr C X M X Gr Error (C) TXC TXCXM T X C X Gr T X C X M X Gr Error(T X C) Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Control Exercise Total Type III SS 1875.673 3747.443 4423.919 137.513 289530.260 3985739.034 2398.208 8591.132 12295.560 385212.381 11394.505 12508.205 537.944 222.804 136054.769 Tests of Within-Subjects Contrasts Source Condition T Type III SS 625.224 853.7385 850.7081 864.4191 857.5636 730.4174 792.0498 756.8313 762.4317 748.8001 755.0916 749.6260 761.7750 755.7005 507.7736 561.3735 530.7450 550.1352 589.1197 571.1269 533.1906 580.7959 556.9932 Df 1 1 1 1 36 2 2 2 2 72 2 2 2 2 72 Df 1 116.35059 94.14911 127.01787 110.57358 67.85807 121.05543 95.48610 108.21297 98.47355 101.20725 93.46069 104.42571 98.00955 82.85149 121.71967 100.75831 103.80690 102.66821 103.03100 96.02599 106.21271 102.80715 MS 1875.673 3747.443 4423.919 137.513 8042.507 1992869.517 1199.104 4295.566 6147.780 5350.172 5697.253 6254.102 268.972 111.402 1889.650 MS 625.224 F .233 .466 .550 .017 Sig. .632 .499 .463 .897 372.487 .224 .803 1.149 .000* .800 .452 .323 3.015 3.310 .142 .059 .055 .042* .868 .943 F .233 Sig. .632 200 TXM T X Gr T X M X Gr Error (T) C CXM C X Gr C X M X Gr Error (C) TXC TXCXM T X C X Gr T X C X M X Gr Error (T X C) S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R 1249.148 1474.640 45.838 96510.087 852910.762 7686076.083 338.423 4491.828 1297.399 8306.490 2021.914 23282.575 116625.927 511278.863 2056.679 21718.488 564.151 21696.763 250.459 287.920 188.825 49.097 46635.259 173413.383 1 1 1 36 1 1 1 1 1 1 1 1 36 36 1 1 1 1 1 1 1 1 36 36 1249.148 1474.640 45.838 2680.836 852910.762 7686076.083 338.423 4491.828 1297.399 8306.490 2021.914 23282.575 3239.609 14202.191 2056.679 21718.488 564.151 21696.763 250.459 287.920 188.825 49.097 1295.424 4817.038 .466 .550 .017 .499 .463 .897 263.276 541.189 .104 .316 .400 .585 .624 1.639 .000* .000* .748 .577 .531 .449 .435 .209 1.588 4.509 .435 4.504 .193 .060 .146 .010 .216 .041* .514 .041 .663 .808 .705 .920 Tests of Between-Subjects Effects Source Intercept M Gr M X Gr Error Type III SS 3.729E7 3014.388 10278.728 14436.500 441362.989 Df 1 1 1 1 36 MS 3.729E7 3014.388 10278.728 14436.500 12260.083 F 3041.602 .246 .838 1.178 Sig. .000 .623 .366 .285 R-R Interval (RRI) for the Menopausal Group Tests of Within-Subjects Contrasts Source Condition T T X Gr Error (T) C S vs. R E vs. R Type III SS 1393.566 780.786 46461.226 339500.608 3085019.187 Df 1 1 12 1 1 MS 1393.566 780.786 3871.769 339500.608 3085019.187 F .360 .202 Sig. .560 .661 93.025 .000* 269.951 .000* 201 C X Gr Error (C) TXC T X C X Gr Error(T X C) S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 1.401E7 Group 18779.931 Error 66843.044 2509.665 1444.765 43794.726 137136.703 178.510 .002 334.524 219.951 13226.358 74439.665 df 1 1 12 1 1 12 12 1 1 1 1 12 12 MS 1.401E7 18779.931 5570.254 F 2515.831 3.371 2509.665 1444.765 3649.561 11428.059 178.510 .002 334.524 219.951 1102.197 6203.305 .688 .126 .423 .728 .162 .000 .304 .035 .694 1.000 .592 .854 Sig. .000 .091 R-R Interval (RRI) for the Postmenopausal Group Tests of Within-Subjects Contrasts Source Condition T T X Gr Error (T) C S vs. R E vs. R C X Gr S vs. R E vs. R Error (C) S vs. R E vs. R TXC S vs. R E vs. R T X C X Gr S vs. R E vs. R Error(T X C) S vs. R E vs. R Tests of Between-Subjects Effects Source Type III SS Intercept 2.738E7 Group 254.016 Error 374519.945 df 1 1 24 Type III SS 77.085 721.515 50048.860 590819.792 5278090.635 57.718 42838.324 72831.201 374142.160 3443.621 62618.147 3.134 71.558 33408.901 98973.718 MS 2.738E7 254.016 15604.998 Df 1 1 24 1 1 1 1 24 24 1 1 1 1 24 24 F 1754.424 .016 MS 77.085 721.515 2085.369 590819.792 5278090.635 57.718 42838.324 3034.633 15589.257 3443.621 62618.147 3.134 71.558 1392.038 4123.905 Sig. .000 .900 F .037 .346 Sig. .849 .562 194.692 338.572 .019 2.748 .000* .000* .891 .110 2.474 15.184 .002 .017 .129 .001* .963 .896