Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Left ventricular twist mechanics during exercise in trained and untrained men By Samuel Cooke A report submitted in partial fulfilment of the requirements for the Degree of Master of Science Physical Activity and Health Cardiff School of Sport Cardiff Metropolitan University March 2016 This report has been produced as a ‘Journal Article Format’. The target Journal is ‘Journal of Applied Physiology’. The word count is: 5640 not including abstract and references. Samuel Cooke Left ventricular twist mechanics during exercise in trained and untrained men. Left ventricular twist mechanics during exercise in trained and untrained men. Samuel Cooke1 1Department of Physiology & Health, Cardiff School of Sport, Cardiff Metropolitan University, Cardiff, Wales, United Kingdom. Running title: Cooke et al. LV twist mechanics during exercise. Cooke et al. LV twist mechanics during exercise. Abstract Introduction: Left ventricular (LV) twist and untwisting rate (LV twist mechanics) play a crucial role during myocardial deformation. It is suggested that exercise training alters resting LV twist mechanics. However, it is unknown whether LV twist mechanics respond differently during exercise in trained and untrained individuals. Aim: To compare LV twist mechanics in trained and untrained individuals at rest and during exercise. Methodology: 11 trained male runners (Peak oxygen uptake (VO2peak): 46.2 ± 6.1 ml.kg-1.min-1 SD) and 13 untrained healthy males (VO2peak: 36.4 ± 6.4 ml.kg-1.min-1 SD) were examined at rest and during supine cycling exercise at 30%, 40%, and 50% peak power output (PPO). Blood pressure and heart rate (HR) were measured continuously using photoplethysmography. Echocardiographical images were collected at rest and during the last 3 minutes of each exercise stage. Speckle tracking technology was used post-hoc to quantify LV twist mechanics. Results: There were no significant differences between the two cohorts in HR, blood pressure, end-systolicvolume (ESV), cardiac output (CO), LV twist or circumferential strain at rest or during exercise (P > 0.05). However, the trained cohort had a significantly lower LV untwisting rate and sphericity index during exercise, as well as a greater end-diastolicvolume (EDV) and stroke volume (SV) (P < 0.05). Conclusion: In trained and untrained individuals LV twist and circumferential strain are similar at rest and respond similarly to exercise. The lower LV untwisting rate during exercise in trained individuals may reflect a more efficient diastolic function when the cardiovascular system is challenged. 2 New and Noteworthy This is the first study to investigate LV twist mechanics in trained and untrained males in response to progressive submaximal exercise. The novel data in the present study showed LV twist and circumferential strain to respond similarly to exercise in trained and untrained males. However, the trained group was shown to have a significantly lower LV untwisting rate in response to exercise which may reflect a more efficient diastolic function. Key words Left ventricular, twist, untwisting rate, exercise. Introduction LV twist and untwisting rate have been identified in playing a significant role with respect to resting systolic and diastolic myocardial deformation, influencing both LV ejection and early diastolic filling, respectively (44, 11, 38). Specifically, early modeling studies suggest that LV twist acts to reduce fiber stress during ventricular contraction by equalizing the distribution of stress across the myocardial wall (4, 10), thus maximizing the efficiency of systolic ejection (44). In addition, LV twist also acts as a mechanism whereby the deformation of the subendocardial and subepicardial fiber matrix during ejection results in stored potential energy that is utilized during diastolic recoil (5, 44, 46). During the subsequent untwisting of the apex and base, the stored potential energy is released which assists in generating a negative intraventricular pressure gradient, initiating the passive suction of blood from the atrium to the ventricle and thus contributing to early diastolic filling (11, 18). Taken Cooke et al. LV twist mechanics during exercise. together, LV twist and the subsequent untwisting rate have been identified as important markers of LV function within both healthy and diseased population groups (41, 9, 18), whereby LV twist mechanics have shown to be reduced within various disease states (50, 8, 14). In addition to the previous evidence concerning diseased populations, recent research has also observed LV mechanical parameters, including LV twist, untwisting rate and strain (longitudinal, radial, and circumferential), to be significantly reduced within highly trained individuals in comparison to untrained individuals at rest (57, 37, 47). Yet, taking into consideration the adaptive characteristics associated with the athlete’s heart, e.g. increased LV mass, chamber size and thickness of the ventricular wall (29, 6), such reductions in LV twist mechanics are suggested to reflect a physiological adaptation to exercise training (57). However, it is important to highlight that there is evidence that contradicts these findings, whereby several longitudinal studies have shown LV twist mechanics to remain unchanged (56) and even increase (54, 1) in response to exercise training. Such findings have therefore led researchers to suggest that the behavior of LV twist mechanics at rest may be dependent upon the training status of an individual (54, 56). Although the alterations in resting LV twist mechanics are suggested to reflect a physiological adaptation to exercise training, there is also evidence to suggest that not all cardiac adaptations associated with exercise training are entirely beneficial. (39, 24). Therefore, in order to further understand the relationship between adaptive myocardial mechanics and heart function, it is crucial to measure LV twist mechanics under the stress of exercise. Research had previously observed LV twist, untwisting rate and strain to progressively increase with exercise intensity within both trained (47) and untrained cohorts (36, 17, 48, 51). 3 However, as to whether the biomechanical behavior of the LV responds differently during exercise in trained and untrained individuals is yet to be fully elucidated. Stöhr and colleagues (47) had recently shown LV twist mechanics to be significantly lower during submaximal exercise in individuals with higher levels of aerobic fitness in comparison to individuals with moderate levels of aerobic fitness. Yet, it is important to note that these findings were established in a heterogeneous population, and that LV twist mechanics were examined in response to a single bout of exercise only. Therefore, to determine whether the observed alterations in myocardial mechanics at rest bear any functional significance during exercise, we aimed to examine the differences in LV twist mechanics at rest and in response to progressive submaximal exercise in trained and untrained individuals. Conducting this study would help to provide a greater insight into identifying and understanding differences in biomechanical behavior of the LV between individuals with contrasting levels of aerobic fitness. Furthermore, knowledge acquired from this study could support future research in further understanding the differences in LV mechanics between the heart of an athlete and a pathological heart, thereby potentially contributing to the treatment of various pathological states. It was hypothesized that LV mechanical parameters would be significantly lower at rest and throughout progressive submaximal exercise in trained individuals in comparison to untrained individuals. Methodology Ethical approval and study population Cooke et al. LV twist mechanics during exercise. Upon attaining ethical approval from the Cardiff Metropolitan University School of Sport Research Ethics sub-committee, 13 healthy untrained males (Age: 20 ± 1 years ± SD; Height: 178.1 ± 6.5 cm ± SD; Body mass: 79.0 ± 11.3 kg ± SD) and 11 healthy trained runners (Age: 26 ± 6, years ± SD; Height: 181.3 ± 4.8 cm ± SD; Body mass: 74.1 ± 6.5 kg ± SD) voluntarily enrolled to participate in this research study. All participants provided both written and verbal informed consent, and completed a health questionnaire sheet prior to testing. Participants were excluded if: 1) any structural or functional myocardial abnormalities were suspected using echocardiography, 2) were known or suspected to have any underlying medical conditions e.g. systematic diseases, high blood pressure, and 3) were currently smoking during the past 6 months. An a priori sample size calculation suggested that a sample of n = 13 per group was required in order to identify significant differences using an α value of 0.05. This study conformed to the standards established by the most recent amendment of the Declaration of Helsinki. Untrained males were recruited using an eligibility criteria stating that individuals must be male, aged 18 – 35 years, and undertake no more than 2 hours of structured exercise per week. Trained runners were recruited using an eligibility criteria stating that individuals must be male, aged 18 – 35 years, and compete in either an endurance discipline performing no less than 40km running per week, or as a 400m sprinter with a personal best of sub 50 seconds. Research design This study utilized a cross sectional research design in order to investigate the differences in LV twist mechanics between trained and untrained individuals at rest and during progressive submaximal exercise. Participants were requested to attend the physiology laboratory, located at Cardiff Metropolitan University, Cyncoed campus, on two separate occasions: 1) to attain 4 measurements of PPO and VO2peak, and 2) to undergo a cardiovascular assessment during submaximal exercise in order to assess LV twist, untwisting rate and circumferential strain. The purpose of the first visit was to assess PPO and VO2peak and calculate submaximal exercise intensities relative to each participant in preparation for visit 2. Experimental procedure Visit 1: Initial height and body mass measurements were taken using an electronic weighing scale and stadiometer, and were recorded to the nearest millimeter and 100g respectively. A standardized incremental exercise test was then performed in order to determine both VO2peak and PPO. Exercise was performed on a supine cycle ergometer, on which participants were placed in the left lateral position at a 45-degree angle (Angio 2003, LODE, Groningen, Netherlands). The exercise protocol consisted of an initial 3minute exercise period at an intensity of 40 Watts at a cadence between 60 – 65 revolutions per minute (RPM). The exercise intensity then increased in 40 Watt increments every 3 minutes thereafter until the point of maximal volitional fatigue. Breath-by-breath VO2 was measured throughout the exercise protocol using a fitted gas mask attached to a computer gas analysis system (OxyconPro, JAEGER at Viasys Healthcare, Warwick, UK). HR was recorded throughout the exercise protocol using a wireless HR monitor (Polar T31, POLAR ELECTRO, Kempele, Finland). VO2peak was recorded as the greatest 5 second average value obtained during the exercise protocol, and both PPO and maximal HR (HRmax) were recorded at the point of task failure. For the purpose of blood lactate analysis, capillary blood samples (20μL) were extracted from the right index finger into a capillary tube containing an anti-hemolyzing solution at rest, during the remaining 30 seconds of each 3-minute interval, and at 3-minute post exercise cessation. All blood lactate Cooke et al. LV twist mechanics during exercise. samples were calculated using an offline lactate analysis system (Biosen, C-Line Sport, EKF DIAGNOSTICS, Magdeburg, Germany). Visit 2: Upon arrival, participants were briefed with regards to the intended procedure of visit 2. Both height and body mass were measured and recorded to the nearest millimeter and 100g respectively. Participants were then positioned upon a supine ergometer (Angio 2003, LODE, Groningen, Netherlands) and prepared for the attachment of test equipment. A finger cuff was placed around the right middle finger and an arm cuff around the right upper arm in order to provide an estimation of the brachial blood pressure waveform as part of a non-invasive beat-to-beat arterial blood pressure monitoring system (FinometerPRO, FINAPRES, Arnhem, Netherlands). The brachial blood pressure waveform was recorded in real time throughout the protocol for the purpose of off-line analysis using a data capture system (PowerLab; ADINSTRUMENTS, Chalgrove, UK). Electrocardiogram leads inherent to the ultrasound system (Vivid E9, GE Vingmed Ultrasound, Horten, Norway) were attached to provide a continuous measurement of HR. A nose clip and a separate mouthpiece comprising of a two-way respiratory valve attached to a respiratory turbine were fitted. The respiratory turbine was connected to a computer gas analysis system (OxyconPro, JAEGER at Viasys Healthcare, Warwick, UK) in order to record continuous breathby-breath ventilatory data. Once test equipment was attached, participants were placed in the left lateral position at a 45-degree angle and a blood capillary sample (20μL) was drawn from the right ear lobe for the purpose of blood lactate analysis. Echocardiographic images were then recorded by an experienced sonographer using a 2D and 4D probe (M5S-D and 4V-D, GE VINGMED ULTRASOUND, Horten, Norway) as part of a commercially accessible ultrasound 5 system (Vivid E9, GE VINGMED ULTRASOUND, Horten, Norway). Images were recorded for three to five consecutive cardiac cycles during brief periods of endexpiratory breath holds that participants were made familiar with, prior to the recording of data. Echocardiographic images were recorded from the following anatomical windows; parasternal short-axis at the base and apex, parasternal long-axis, and apical triplane images. To ensure the reproducibility of echocardiographic images throughout each exercise interval, the transducer location on the chest at rest was marked with a marker pen and used as a reference point to reproduce the same image during the three exercise stages. This allowed for easier identification of a similar apical imaging window, enabling the sonographer to amend and obtain visually comparable cross-sectional views. As outlined in previous publications (47), parasternal short-axis images at both the base and apex were obtained at a rate of 80 frames per second. Both the frame rate as well as the image depth remained consistent throughout within-subject acquisition. Recorded images were attained in agreement with existing guiding principles (26), and as summarized by similar methodologies undertaken by the same research group (48, 47). Following the collection of baseline data, the participant’s feet were strapped to the supine cycle ergometer and the ergometer adjusted according to the participant’s height. Each participant then performed an exercise protocol identical to the one during the first visit up to the point of completion of the initial warm up period. Participants then proceeded to complete three consecutive 5-minute exercise bouts performed at 30%, 40% and 50% of each participant’s PPO at a cadence of 60 – 65 RPM. Echocardiographic images were recorded during the last 3 minutes of each 5-minute exercise bout. For the purpose of blood lactate analysis, capillary blood samples were extracted from the right ear Cooke et al. LV twist mechanics during exercise. lobe at the last 30 seconds of each 5-minute increment, and at 3-minute post exercise cessation. Data analysis Conventional echocardiography: Recorded echocardiographic images were saved within the ultrasound machine and then exported to commercially accessible data analysis software for the purpose of offline echocardiography analysis (EchoPAC Version 112 revision 1.0, GE VINGMED ULTRASOUND, Horten, Norway). LV parasternal long axis images were analyzed for the purpose of attaining dimensional measurements including LV posterior wall thickness (LVPW), LV internal diameter (LVID) and intraventricular septum (IVS) at both diastole and systole. As defined by previous research (58), sphericity index was quantified by dividing the maximal LV length over the maximal LV diameter at end-diastole. As previously described (26) the area length method was used to calculate LV mass. Manual tracing of the apical triplane images at both the enddiastolic and end-systolic phase was performed in order to obtain EDV, ESV and SV. CO values were quantified through the calculation of HR multiplied by SV. All dimensional measurements, SV and CO were indexed to body surface area (BSA) using the Du Bois and Du Bois formula (20, 53) (see equation section). The final values reported for each variable represent the average value taken from three cardiac cycles. Speckle tracking echocardiography: Parasternal short-axis images at both the base and apex were obtained for the purpose of quantifying LV twist mechanics and circumferential strain. The endocardial border of both the apical and basal parasternal short-axis images were traced post-hoc, and a region of interest formed to incorporate the whole contractile myocardium whilst eliminating any valves and trabeculations. The data analysis software (EchoPAC Version 112 revision 6 1.0, GE VINGMED ULTRASOUND, Horten, Norway) produced raw speckle tracking data, in which cubic spline interpolation was applied using custom software (2D Strain Analysis Tool, Version 1.0beta14, Stuggart, Germany) in order to intercalate raw data to 600 points during both systole and diastole. As described in previous research (36, 45, 47), frame by frame values of twist and untwisting rate were acquired by subtracting the apical rotation data from the basal rotation data. LV twist and untwisting rate were reported as the peak systolic and early diastolic values respectively. The relative change in LV twist and untwisting rate were expressed as the percentage change from baseline to each exercise intensity and calculated using a simple formula (see equation section). All LV mechanical parameters documented were established through interpolated results and constitute the mean of all the myocardial segments. Statistical analyses Normal distribution was assessed for all data sets using the Sharpio-Wilk test. Differences in baseline characteristics between the trained and untrained group were determined using an unpaired t-test, provided that the data were identified as normally distributed. In the event that the data were non-parametric, the MannWhitney U test was applied. To determine the influence of exercise and training status, along with the interaction between the two factors, a two-way repeated measures ANOVA was utilized followed by a Bonferroni post-hoc test when significant main effects were detected. Unless otherwise stated, all data are reported as means ± SD. All statistical analyses were carried out using GraphPad prism 6 (version 6.00 for Windows; GRAPHPAD SOFTWARE, San Diego, California, USA). Results Baseline data and cardiac measurements Cooke et al. LV twist mechanics during exercise. All data is reported as trained vs. untrained. Age (26 ± 6 vs. 21 ± 1 years; P < 0.05), VO2peak (46.2 ± 6.1 vs. 36.4 ± 6.4; ml.kg1 .min-1 P < 0.001), PPO (251 ± 20 vs. 193 ± 33; Watts P < 0.001), and the point at which lactate threshold occurred (13.6 ± 2.1 vs. 10.2 ± 2.0; Min P < 0.05) were significantly higher in the trained group. In addition, the trained group also demonstrated a significantly greater LV mass (180.20 ± 28.31 vs. 141.20 ± 18.10; g P < 0.001), and EDV (147 ± 20 vs. 130 ± 19; ml P < 0.05), yet, a significantly lower IVS index (0.5 ± 0.01 vs. 0.6 ± 0.08; cm.m2 P < 0.001). In contrast, height, body mass, BSA, systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial blood pressure (MAP) were not significantly different between the two groups (P > 0.05). Similarly, no significant differences were observed in any remaining parameters associated with LV wall thickness, cardiac dimensions or LV mechanics (P > 0.05). All baseline data are presented in Table 1. Response to submaximal exercise Cardiovascular parameters including HR, SBP, DBP, MAP, ESV and CO significantly increased in response to exercise, and were shown to increase to the same extent in both groups. In addition, the absolute and relative change in LV twist (Figure 1 and 3, respectively), absolute LV untwisting rate (Figure 2), and both apical and basal circumferential strain also increased to a similar degree in response to exercise in both cohorts. In contrast, exercise significantly increased VO2, SV, SV index, sphericity index and the relative change in LV untwisting rate, but not to the same extent in both groups. Post-hoc analysis revealed the trained group to have a significantly higher VO2 at 30% (P < 0.05), 40% (P < 0.01), and 50% (P < 0.001) exercise intensity. Similarly, the trained group were shown to have a greater SV (108 ± 10 vs. 94 ± 11 ml; P < 0.01) and SV index (56 ± 6 vs. 48 ± 8 ml.m2; P < 0.05) at 50% exercise intensity, whereas, the relative change in LV untwisting rate was 7 significantly lower in the trained group (246 ± 107 vs. 332 ± 110 %; P < 0.05) at 50% exercise intensity (Figure 4). EDV was significantly higher in the trained group during exercise, but did not significantly change from resting values. All exercise data are presented in Table 2. Discussion Main findings It has previously been suggested that exercise training induces significant alterations in resting LV twist mechanics. However, it is unknown as to whether LV twist mechanics respond differently during exercise in trained and untrained individuals. The primary aim of the current study was to examine the differences in LV twist mechanics in trained and untrained individuals in response to exercise. To the best of the author’s knowledge, this is the first study to investigate the effect of training status/aerobic fitness on LV twist mechanics in response to progressive submaximal exercise. There were two novel findings from this investigation: 1) no significant differences were identified in LV twist or circumferential strain at rest or during exercise between the trained and untrained individuals, and 2) although the differences in absolute values of LV untwisting rate were non-significant, the relative change in LV untwisting rate was significantly lower during exercise in trained individuals. Thus the present data suggests that LV twist and circumferential strain are similar at rest and change in a similar manner from rest to moderate exercise. However, the lower LV untwisting rate in trained individuals may reflect a more efficient diastolic function under conditions of exercise stress. Baseline data It is evident that there is a clear division in training status between the trained and untrained cohorts as manifested by the distinct differences in VO2peak, PPO and lactate threshold. However, an interesting Cooke et al. LV twist mechanics during exercise. observation was the similar values in resting HR and peripheral blood pressure between the two cohorts. In particular, the relatively low resting HR in the untrained group was unexpected, and disputes previous evidence (21, 13, 19); though this may be reflective of the untrained group representing a young and healthy population, not a sedentary population. In contrast, taking into consideration the chosen study cohorts, it was expected that the trained group had a greater LV mass in addition to a concomitant increase in EDV. It is widely acknowledged that dynamic exercise training induces morphological adaptations to the heart including an increase in LV mass, chamber size and wall thickness, caused by volume overload associated with the sustained elevation in CO during endurance training (40, 30, 55). However, a notable finding showed both trained and untrained individuals to have a similar LV wall thickness. It is understood that the increase in LV mass and chamber size associated with eccentric hypertrophy is accompanied by a proportional increase in LV wall thickness (40, 23). Yet, there is evidence to suggest that exercise training can augment LV mass and chamber size without any significant changes in LV wall thickness (56). Specifically, it was proposed that individuals experience a phasic response to exercise induced cardiac remodeling, whereby acute exercise training is associated with an increase in LV mass and EDV, whereas, adaptations in LV wall thickness occur in response to chronic exercise training (56). Although the individuals recruited in the trained cohort are considered to be experienced athletes, it could be suggested that there is potential for further cardiac remodeling. In addition to the non-significant differences in LV wall thickness, resting LV mechanical parameters were also similar in both cohorts. These findings dispute the proposed hypothesis suggesting that LV twist mechanics are significantly reduced in trained individuals at rest and 8 contradicts the majority of previous evidence showing either a reduction (57, 37, 47) or an increase (54, 1) in parameters of LV twist mechanics as a result of exercise training. Yet, there is existing evidence that complements the findings of the present study (56), and may help explain why no significant differences were evident between the trained and untrained cohorts. Specifically, the longitudinal study by Weiner and colleagues (56) suggested that short term exercise training is associated with an increase in LV twist mechanics, whereas, long term exercise training is accompanied by a regression in LV twist mechanics back to baseline values. It was therefore concluded that the duration of training is a major determinant of the degree of LV twist mechanics (56). Thus, the similar values in LV twist mechanics in the present study may in part, be explained by the fact that the individuals recruited in the trained cohort have been exercise training for an extensive period of time. Conversely, whilst the data presented by Weiner and colleagues (56) may complement the outcomes of the current study, it must be considered that the findings were established in young rowers. There is strong evidence to suggest that different modalities of exercise impose differential hemodynamic loads upon the right and left ventricle, thus producing diverging patterns of exercise induced cardiac remodeling (33, 32, 35, 27). Similarly, LV twist mechanics have also been shown to differ in response to a variety of different exercise modalities (15, 42). To the best of the author’s knowledge, this is the first study to examine LV twist mechanics involving trained runners. There is, therefore, a distinct possibility that our findings apply specifically to the running population and that differences in findings between studies may in part be explained by the differences in the studied population groups. Cooke et al. LV twist mechanics during exercise. Cardiovascular responses and LV twist mechanics during exercise It is understood that LV twist mechanics play an integral role in augmenting cardiac function during exercise (18). Previous evidence suggests that in response to physiological stimuli LV twist is increased, resulting in a greater amount of stored potential energy in compressed titin (5). Consequently, titin expands with greater force during diastolic recoil, which in turn, augments LV untwisting rate and facilitates a more rapid diastolic filling in order to maintain CO (36, 18). As anticipated, the majority of LV functional parameters including LV twist mechanics increased in response to exercise in both groups. This is primarily a result of the body’s need to increase LV output in order to meet the increased oxygen demands of the exercising skeletal muscles (22, 43, 49). However, a notable observation was the non-significant differences in CO between the two groups despite a differential response in SV. Although a similar HR response throughout the exercise protocol was evident, the trained cohort presented a significantly greater EDV and SV. Clearly the magnitude of difference in EDV and SV between the trained and untrained groups was insufficient in producing any significant differences in either the absolute or relative values of CO. Similarly, with respect to the response in LV twist mechanics to exercise, LV twist and circumferential strain were also identified as non-significant. These findings, in part, disprove our stated hypothesis that LV twist mechanics would be significantly lower in trained individuals during exercise, and further disagrees with recent evidence showing LV twist to be significant lower in trained individuals in response to submaximal exercise (47). However, these findings may advance the proposed theory that parameters of LV twist mechanics may be dependent upon the duration of exercise training (56), suggesting that the training status of an 9 individual may provide a good indication as to the degree of LV twist during low to moderate exercise intensities. Yet, further research is warranted in order to strengthen this theory. Conversely, although such findings may advance the theory proposed by Weiner and colleagues (56), it is also important to interpret the findings with respect to LV twist in the context of several functional parameters. Numerous studies have implicated various physiological factors including preload, afterload, HR and myocardial contractility to have a significant influence upon the degree of LV twist during exercise. Specifically, a directly proportional relationship was suggested to exist between EDV and LV twist, whereas the relationship between ESV and LV twist was proposed to be inversely related (28, 16). Similarly, an increase in HR as well as myocardial contractility has been shown to directly correlate with LV twist (31, 12). Therefore, taking into consideration that LV twist has been suggested to be volume- and HRdependent, the non-significant differences in LV twist during exercise in the present study, may in part, be explained by the nonsignificant differences in HR and ESV; along with the minor changes in EDV from rest to exercise. In addition, considering that both the trained and untrained cohort demonstrated a similar amount of blood being delivered to the periphery as manifested by the non-significant differences in CO, it is logical that LV twist was similar during exercise. In contrast, although the absolute values of LV twist mechanics were non-significant between the two groups, the relative change in LV untwisting rate was significantly lower in the trained group in response to exercise. This finding, in part, agrees with the stated hypothesis that LV twist mechanics would be significantly lower in trained individuals in response to progressive submaximal exercise; and may suggest that trained individuals have a more efficient diastolic function when the Cooke et al. LV twist mechanics during exercise. cardiovascular system is stressed. Specifically, data in the present study showed the trained cohort to have a greater EDV and a lower untwisting rate in response to exercise, whereas, the untrained cohort were shown to have a lower EDV and a greater LV untwisting rate. This suggests therefore, that trained individuals are able to draw a larger amount of blood to the LV for a lower LV untwisting rate during exercise, which may be reflective of a more efficient diastolic suction and relaxation. This would fall in agreement with previous evidence that also proposes that exercise training enhances parameters of diastolic function including LV suction, relaxation and filling within trained (40) and diseased populations (2, 3, 7). However, although the lower untwisting rate in trained individuals could be regarded as a highly novel finding, it is not exactly clear as to how this has occurred. Thus, further discussion is warranted with respect to the potential mechanisms behind this finding. Potential mechanisms for a lower LV untwisting rate Taking into consideration that LV twist mechanics have been shown to play a crucial role in overall LV performance within several disease states, the small number of studies investigating the adaptive response in LV twist mechanics to exercise training is somewhat surprising. Consequently, the underlying mechanisms behind the adaptive response in LV twist mechanics to physiological stimuli are poorly understood. Despite this, there is existing evidence that may, in part, help explain the findings in the current study. It is known that the strength of restoring forces play an important role in the magnitude of LV untwisting rate (36, 38). Specifically, deformation of the subendocardial and subepicardial fiber matrix during systole results in the generation of restoring forces known as potential energy (38). During systole, potential energy is stored in myocyte 10 components known as titin (5, 38). It is during diastolic recoil that titin expands and releases the stored potential energy which assists LV untwisting (36). It is suggested that an increased amount of stored potential energy allows the compressed titin to expand with greater force during diastolic recoil, thereby generating a greater amount of LV untwisting (36, 38). Thus, one potential mechanism could be that the trained and untrained group are storing a different amount of potential energy or have differential restorative properties despite similar values in LV twist. This in turn may be a causative factor for the observed differences in LV untwisting rate. Yet, further research is needed to strengthen this theory. In addition, another potential mechanism with respect to the differential response in LV untwisting rate may be related to the observed differences in the shape of the LV between the trained and untrained cohort. It has previously been suggested that the more spherical the LV cavity the lesser amount of LV twist occurs in conjunction with a more evenly distributed myofiber stress in diseased populations (58, 34). However, a limitation of the study by Van Dalen and colleagues (58) is that the influence that the shape of the LV has upon diastolic function, and in particular LV untwisting rate, was not investigated. Data in the present study shows that the trained cohort possess a more spherical LV cavity during exercise, whereas, the untrained cohort demonstrate a more elongated LV cavity. It is therefore possible that the differences in the shape of the LV cavity may help explain why a lower LV untwisting rate was observed within the trained cohort. However, the suggestion that a more spherical LV cavity may result in a lower LV untwisting is speculative at this point in time, and requires the direct study between LV cavity shape and diastolic untwisting rate. Finally, it has also previously been suggested that the rate of myocardial relaxation is a strong determinant of peak Cooke et al. LV twist mechanics during exercise. LV untwisting rate (38). Specifically, an increase in LV untwisting rate was shown to have been associated with a faster myocardial relaxation rate (38). In the present study, trained individuals demonstrate a lower LV untwisting rate, which was suggested to reflect alterations in diastolic function. It could therefore be suggested that the observed differences in LV untwisting rate in the present study may be as a result of the trained group having a more prolonged myocardial relaxation rate compared to the untrained individuals. Although a delayed myocardial relaxation rate is a key feature in various disease states (52, 25), a prolonged myocardial relaxation rate in trained individuals may reflect a physiological adaptation to exercise training. However, further research into the adaptive potential of LV mechanics in relation to heart function is needed to support this speculation. Study limitations and future research It is acknowledged that failing to recruit the required sample size precludes us from drawing conclusions that may be extrapolated to the entire running population as a whole. Furthermore, it is important to note that due to recruitment issues, the trained cohort in the present study consisted of endurance runners specializing in long distance disciplines as well as sprinters competing in events such as the 400m. As previously indicated, there is evidence to suggest that different training modalities elicits diverging patterns of exercise induced cardiac remodeling (33, 35). Thus, incorporating various exercise modalities in the trained cohort not only reduces the generalizability of the data, but may well have had a significant impact upon the findings. Another important limitation to consider is the low ecological validity of the study. In an ideal scenario, trained runners would perform an exercise protocol that is indicative of their discipline. However, taking into consideration current measuring techniques, LV twist mechanics could only 11 be obtained in the supine position. In relation to this, hemodynamics are known to alter in accordance with the posture in which one exercises (i.e. supine vs. upright cycling). Thus, it is also important to note that supine cycling exercise may be associated with a differential response in LV twist mechanics compared to different modalities of exercise testing. Finally, to the best of the author’s knowledge, normative values for LV twist and untwisting rate at rest and during exercise are yet to be established. This makes it difficult to compare findings to previous studies and prevents the use of LV twist mechanics in the present study as a marker of cardiac performance. It is clear that the number of studies investigating LV twist mechanics in response to exercise is extremely limited. This is somewhat surprising considering that LV twist mechanics have been shown to play an integral role in the pathophysiology of many disease states. It is still unclear whether alterations in LV twist mechanics represent a physiological or pathological adaptation to exercise. Further investigation into the response of LV twist mechanics to exercise is needed and will expand our understanding into the functional differences between the heart of an athlete and a pathological heart. In addition, such research may enhance our knowledge with respect to the pathophysiology of various disease states, and potentially contribute towards possible treatment strategies. Conclusion In summary, the novel data of this study suggests that in trained and untrained individuals LV twist and circumferential strain are similar at rest and respond in a similar manner to the stress of exercise. However, the trained cohort were shown to have a significantly lower LV untwisting rate in response to exercise, which may reflect a more efficient diastolic function related to LV suction and relaxation when Cooke et al. LV twist mechanics during exercise. the cardiovascular system is challenged. Further research investigating the adaptive potential of LV twist mechanics in response to physiological stimuli is needed, and may help expand our knowledge and further develop our understanding of the differences between the heart of an athlete and a diseased heart. Appendix Links to Journal of Applied Physiology “Author instructions” Appendix A. Formatting requirements http://www.theaps.org/mm/Publications/Info-ForAuthors/Formatting Appendix B. Manuscript composition http://www.theaps.org/mm/Publications/Info-ForAuthors/Composition Appendix C. Preparing Figures http://www.theaps.org/mm/Publications/Info-ForAuthors/Preparing-Figures Author contributions S.C. is responsible for the research and experimental design, collection and analysis of data, interpretation of results, and manuscript composition. The author approves the final form of the manuscript and is fully accountable for the work. Acknowledgements The author would like to take this opportunity to thank all participants and coaches for their efforts and commitment to this project. Grants 12 The author has no conflict of interest to report. References 1. Aksakal E, Kurt M, Oztürk ME, Tanboğa IH, Kaya A, Nacar T, Sevimli S, Gürlertop Y. The effect of incremental endurance exercise training on left ventricular mechanics: a prospective observational deformation imaging study. Anadolu Kardiyol Derg 13: C432 – C438, 2013. 2. Alves AJ, Ribeiro F, Goldhammer E, Rivlin Y, Rosenschein U, Viana JL, Duarte JA, Sagiv M, Oliveira J. Exercise training improves diastolic function in heart failure patients. Med Sci Sports Exerc 44: C776 – C785, 2012. 3. Amundsen BH, Rognmo O, HatlenRebhan G, Slørdahl SA. Highintensity aerobic exercise improves diastolic function in coronary artery disease. Scand Cardiovasc J 42: C110 – C117, 2008. 4. Arts T, Reneman RS, Veenstra PC. A model of the mechanics of the left ventricle. Ann Biomed Eng 7: C299 – C318, 1979. 5. Ashikaga H, Criscione JC, Omens JH, Covell JW, Ingels NB. Transmural left ventricular mechanics underlying torsional recoil during relaxation. Am J Physiol Heart Circ Physiol 286: C640 – C647, 2004. 6. Baggish AL, Wood MJ. Athlete's heart and cardiovascular care of the athlete: scientific and clinical update. Circulation 123: C2723 – C2735, 2011. None Disclosures 7. Belardinelli R, Georgiou D, Cianci C, Berman N, Ginzton L, Purcaro A. Exercise training improves left ventricular diastolic filling in patients Cooke et al. LV twist mechanics during exercise. with dilated cardiomyopathy. Circulation 91: C2775 – C2784, 1995. 8. Bertini M, Delgado V, Nucifora G, Ajmone Marsan N, Ng AC, Shanks M, Antoni ML, van de Veire NR, van Bommel RJ, Rapezzi C, Schalij MJ, Bax JJ. Left ventricular rotational mechanics in patients with coronary artery disease: differences in subendocardial and subepicardial layers. Heart 96: C1737 – C1743, 2010. 9. Bertini M, Bax JJ, Delgado V, Marsan NA, Narula J, Ng AC, Nucifora G, Sengupta PP, Schalij MJ, Shanks M, van Bommel RJ. Role of left ventricular twist mechanics in the assessment of cardiac dyssynchrony in heart failure. JACC Cardiovasc Imaging 2: C1425 – C1435, 2009. 10. Beyar R, Sideman S. Left ventricular mechanics related to the local distribution of oxygen demand throughout the wall. Circ Res 58: C664 – C677, 1986. 11. Burns AT, La Gerche A, Macisaac AI, Prior D. Left ventricular untwisting is an important determinant of early diastolic function. JACC Cardiovasc Imaging 2: C709 – C716, 2009. 12. Cameli M, Ballo P, Righini FM, Caputo M, Lisi M, Mondillo S. Physiologic determinants of left ventricular systolic torsion assessed by speckle tracking echocardiography in healthy subjects. Echocardiography 28: C641 – 648, 2011. 13. Carter JB, Banister EW, Blaber AP. Effect of endurance exercise on autonomic control of heart rate. Sports Med 33: C33 – C46, 2003. 14. Chang SA, Kim DH, Kim JC, Kim HC, Kim HK, Kim YJ, Oh BH, Park YB, Sohn DW. Left ventricular twist mechanics in patients with apical hypertrophic cardiomyopathy: 13 assessment with 2D speckle tracking echocardiography. Heart 96: C49 – C55, 2010. 15. De Luca A, Stefani L, Pedrizzetti G, Pedri S, Galanti G. The effect of exercise training on left ventricular function in young elite athletes. Cardiovasc Ultrasound 9: 2011. 16. Dong SJ, Hee SP, Huang WM, Buffer SA, Weiss JL, Shapiro EP. Independent effects of preload, afterload, and contractility on left ventricular torsion. Am J Physiol 277: C1053 – C1060, 1999. 17. Doucende G, Dauzat M, Nottin S, Obert P, Rupp T, Schuster I, Startun A. Kinetics of left ventricular strains and torsion during incremental exercise in healthy subjects: the key role of torsional mechanics for systolicdiastolic coupling. Circ Cardivasc Imaging 3: C586 – C594, 2010. 18. Drury C, Bredin S, Phillips A, Warburton D. Left ventricular twisting mechanics and exercise in healthy individuals: a systematic review. Open Access J Sports Med 20: C89 – C106, 2012. 19. D'Souza A, Bucchi A, Johnsen AB, Logantha SJ, Monfredi O, Yanni J, Prehar S, Hart G, Cartwright E, Wisloff U, Dobryznski H, DiFrancesco D, Morris GM, Boyett MR. Exercise training reduces resting heart rate via downregulation of the funny channel HCN4. Nat Commun 5: 2014. 20. Du Bois D, Du Bois E. A formula to estimate the approximate surface area if height and weight be known. Arch Intern Med 17: C863 – 871, 1916. 21. Fagard R. Athlete's heart. Heart 89: C1455 – C1461, 2003. 22. Hossack, KF. Cardiovascular responses to dynamic exercise. Cardiol Clin 5: C147 – C156, 1987. Cooke et al. LV twist mechanics during exercise. 23. Kehat I, Molkentin JD. Molecular pathways underlying cardiac remodeling during pathophysiological stimulation. Circulation 122: C2727 – C2735, 2010. 24. La Gerche A, Can intense endurance exercise cause myocardial damage and fibrosis? Curr Sports Med Rep 12: C63 – C69, 2013. 25. Lalande S, Johnson BD. Diastolic Dsyfunction: A link between hypertension and heart failure. Drugs today 44: C503 – C513, 2008. 26. Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L, Flachskampf FA, Foster E, Goldstein SA, Kuznetsova T, Lancellotti P, Muraru D, Picard MH, Rietzschel ER, Rudski L, Spencer KT, Tsang W, Voigt JU. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American society of echocardiography and the European association of cardiovascular imaging. J Am Soc Echocardiogr 28: C1 – C39, 2015. 27. Lewis EJH, McKillop A, Banks L. The Morganroth hypothesis revisited: endurance exercise elicits eccentric hypertrophy of the heart. J Physiol 590: C2833 – C2834, 2012. 28. MacGowan GA, Burkhoff D, Rogers WJ, Salvador D, Azhari H, Hees PS, Zweier JL, Halperin HR, Siu CO, Lima JA, Weiss JL, Shapiro EP. Effects of afterload on regional left ventricular torsion. Cardiovasc Res 31: C917 – C925, 1996. 29. Maron BJ, Pelliccia A. The heart of trained athletes: cardiac remodeling and the risks of sports, including sudden death. Circulation 114: C1633 – C1644, 2006. 30. Mihl C, Dassen WRM, Kuipers H. Cardiac remodelling: concentric versus eccentric hypertrophy in strength and 14 endurance athletes. Neth Heart J 16: C129 – C133, 2008. 31. Moon MR, Ingels NB, Daughters GT, Stinson EB, Hansen DE, Miller DC. Alterations in left ventricular twist mechanics with inotropic stimulation and volume loading in human subjects. Circulation 89: C142 – C150, 1994. 32. Morganroth J, Maron BJ. The athlete's heart syndrome: a new perspective. Ann N Y Acad Sci 301: C931 – C941, 1977. 33. Morganroth J, Maron BJ, Henry WL, Epstein SE. Comparative left ventricular dimensions in trained athletes. Ann Intern Med 82: C521 – C524, 1975. 34. Nakatani S. Left ventricular rotation and twist: why should we learn? J Cardiovasc Ultrasound 19: C1 – C6, 2011. 35. Naylor LH, George K, O'Driscoll G, Green DJ. The athlete's heart: a contemporary appraisal of the Morganroth hypothesis. Sports Med 38: C69 – C90, 2008. 36. Notomi Y, Deserranno D, Garcia MJ, Greenberg NL, MartinMiklovic MG, Oryszak SJ, Shiota T, Thomas JD. Enhanced ventricular untwisting during exercise: a mechanistic manifestation of elastic recoil described by doppler tissue imaging. Circulation 113: C2524 – C2533, 2006. 37. Nottin S, Doucende G, Dauzat M, Obert P, Schuster-Beck I. Alteration in left ventricular normal and shear strains evaluated by 2D-strain echocardiography in the athlete’s heart. J Physiol 586: C4721 – 4733, 2008. 38. Opdahl A, Remme EW, Helle-Valle T, Edvardsen T, Smiseth OA. Myocardial relaxation, restoring forces, and early-diastolic load are independent determinants of left Cooke et al. LV twist mechanics during exercise. ventricular untwisting rate. Circulation 126. C1441 – 1451, 2012. 39. Patil HR, O'Keefe JH, Lavie CJ, Magalski A, Vogel RA, McCullough PA. Cardiovascular damage resulting from chronic excessive endurance exercise. Mo Med 109: C312 – C321, 2012. 40. Pluim BM, Zwinderman AH, van der Laarse A, van der Wall EE. The athlete's heart. A meta-analysis of cardiac structure and function. Circulation 101: C336 – C344, 2000. 41. Rüssel IK, Bronzwaer JG, Götte MJ, Knaapen P, Paulus WJ, van Rossum AC. Left ventricular torsion: an expanding role in the analysis of myocardial dysfunction. JACC Cardiovasc Imaging 2: C648 – C655, 2009. 42. Santoro A, Alvino F, Antonelli G, Caputo M, Padeletti M, Lisi M, Mondillo S. Endurance and strength athlete's heart: analysis of myocardial deformation by speckle tracking echocardiography. J Cardiovasc Ultrasound 22: C196 – C204, 2014. 43. Schairer JR, Stein PD, Keteyian S, Fedel F, Ehrman J, Alam M, Henry JW, Shaw T. Left ventricular response to submaximal exercise in endurancetrained athletes and sedentary adults. Am J Cardiol 70: C930 – C933, 1992. 44. Sengupta PP, Chandrasekaran K, Khandheria BK, Tajik AJ. Twist mechanics of the left ventricle: principles and application. JACC Cardiovasc Imaging 1: C366 – C376, 2008. 45. Sengupta PP, Khandheria BK, Korinek J, Wang J, Jahangir A, Seward JB, Belohlavek M. Apex-tobase dispersion in regional timing of left ventricular shortening and lengthening. J Am Coll Cardiol 47: C163 – C172, 2006. 15 46. Song JK. How does the left ventricle work? ventricular rotation as a new index of cardiac performance. Korean Circ J 39: C347 – C351, 2009. 47. Stöhr EJ, Bull T, Cockcroft J, Houston R, McDonnell B, Shave R, Stone K, Thompson J. Left ventricular mechanics in humans with high aerobic fitness: adaptation independent of structural remodelling, arterial haemodynamics and heart rate. J Physiol 590: C2107 – C2119, 2012. 48. Stöhr EJ, González-Alonso J, Shave R. Left ventricular mechanical limitations to stroke volume in healthy humans during incremental exercise. Am J Physiol Heart Circ Physiol 301: C478 – C487, 2011. 49. Stratton JR, Levy WC, Cerqueira MD, Schwartz RS, Abrass IB. Cardiovascular responses to exercise. Effects of aging and exercise training in healthy men. Circulation 89: C1648 – 1655, 1994. 50. Takeuchi M, Kokumai M, Lang RM, Nakai H, Nishikage T, Otani S. The assessment of left ventricular twist in anterior wall myocardial infarction using two-dimensional speckle tracking imaging. J Am Soc Echocardiogr 20, C36 – C44, 2007. 51. Unnithan VB, Barker P, Garrard M, Lindley MR, Roche DM, Rowland T. Cardiac strain during upright cycle ergometry in adolescent males. Echocardiography 32: C638 – C643, 2015. 52. Vlahović A, Popović AD. Evaluation of left ventricular diastolic function using Doppler echocardiography. Med Pregl 52: C13 – C18, 1999. 53. Wang Y, Moss J, Thisted R. Predictors of body surface area. J Clin Anesth 4: C4 – C10, 1992. 54. Weiner RB, Hutter AM, Wang F, Kim J, Weyman AE, Wood MJ, Cooke et al. LV twist mechanics during exercise. Picard MH, Baggish AL. The impact of endurance exercise training on left ventricular torsion. JACC Cardivasc Imaging 3: C1001 – C1009, 2010. 55. Weiner RB, Baggish AL. Exerciseinduced cardiac remodeling. Prog Cardiovasc Dis 54: C380 – C386, 2012. 56. Weiner RB, DeLuca JR, Wang F, Lin J, Wasfy MM, Berkstresser B, Stöhr E, Shave R, Lewis GD, Hutter AM, Picard MH, Baggish AL. Exercise-induced left ventricular remodeling among competitive athletes: a phasic phenomenon. Circ Cardiovasc Imaging 8: 2015. 57. Zócalo Y, Armentano RL, Bia D, Giacche E, Guevara E, Pessana F, Peidro R. A reduction in the magnitude and velocity of left ventricular torsion may be associated with increased left ventricular efficiency: evaluation by speckletracking echocardiography. Rev Esp Cardiol 61: C705 – C713, 2008. 58. Van Dalen BM, Kauer F, Vletter WB, Soliman O, van der Zwaan HB, Ten Cate FJ, Geleijnse ML. Influence of cardiac shape on left ventricular twist. J Appl Physiol 108: C146 – C151, 2010. 16 Cooke et al. LV twist mechanics during exercise. 17 LV Figure captions untwisting rate was shown to significantly increase from rest to moderate Figure 1. Peak LV twist at rest and during intensity exercise in both groups, though exercise in the trained and untrained group. the relative change in LV untwisting rate LV twist is shown to significantly increase from rest to 50% exercise intensity was in response to exercise in both groups, significantly lower in the trained group (P though the observed differences between < 0.05). Data presented as mean ± SD. trained and untrained individuals were nonsignificant (P > 0.05). Data are presented as mean ± SD. Figure 2. Peak LV untwisting rate at rest and during exercise in the trained and untrained group. LV untwisting rate is shown to significantly increase in response to exercise in both groups, though the differences between the trained and untrained individuals were non-significant (P > 0.05). Data are presented as mean ± SD. Figure 3. The relative change in LV twist from rest to 30%, 40% and 50% exercise intensity in the trained and untrained group. The percentage change in LV twist was shown to significantly increase from rest to moderate intensity exercise, though the differences between trained and untrained individuals were found to be non- significant (P < 0.05). Data presented as mean ± SD. Figure 4. The relative change in LV untwisting rate from rest to 30%, 40% and 50% exercise intensity in the trained and untrained group. The percentage change in Cooke et al. LV twist mechanics during exercise. 18 Figures L V T w is t 40 T r a in e d T w is t (d e g .) 35 U n tr a in e d 30 25 20 15 10 5 % 5 0 % 0 4 0 3 R E S T % 0 E x e r c i s e w o r k lo a d Figure 1. Peak LV twist at rest and during exercise in the trained and untrained group. LV twist is shown to significantly increase in response to exercise in both groups, though the observed differences between trained and untrained individuals were non-significant (P > 0.05). Data are presented as mean ± SD. Cooke et al. LV twist mechanics during exercise. 19 L V U n t w is t in g R a t e U n tw is tin g r a te (d e g /s ) -4 0 0 T r a in e d -3 5 0 U n tr a in e d -3 0 0 -2 5 0 -2 0 0 -1 5 0 -1 0 0 -5 0 5 0 % % 0 4 0 3 R E S T % 0 E x e r c i s e w o r k lo a d Figure 2. Peak LV untwisting rate at rest and during exercise in the trained and untrained group. LV untwisting rate is shown to significantly increase in response to exercise in both groups, though the differences between the trained and untrained individuals were nonsignificant (P > 0.05). Data are presented as mean ± SD. Cooke et al. LV twist mechanics during exercise. 20 T w is t % c h a n g e 400 T r a in e d 350 T w is t ( % ) U n tr a in e d 300 250 200 150 100 50 % 5 0 % 0 4 0 3 R E S T % 0 E x e r c i s e w o r k lo a d Figure 3. The relative change in LV twist from rest to 30%, 40% and 50% exercise intensity in the trained and untrained group. The percentage change in LV twist was shown to significantly increase from rest to moderate intensity exercise, though the differences between trained and untrained individuals were found to be non-significant (P < 0.05). Data presented as mean ± SD. Cooke et al. LV twist mechanics during exercise. 21 Figure 4. The relative change in LV untwisting rate from rest to 30%, 40% and 50% exercise intensity in the trained and untrained group. The percentage change in LV untwisting rate was shown to significantly increase from rest to moderate intensity exercise in both groups, though the relative change in LV untwisting rate from rest to 50% exercise intensity was significantly lower in the trained group (P < 0.05). Data presented as mean ± SD. Cooke et al. LV twist mechanics during exercise. 22 Tables Table 1. Baseline characteristics of the untrained and trained groups. Untrained group (n = 13) Trained group (n = 11) P value Age (years) 21 ± 1 26 ± 6 < 0.05 Height (cm) 178.1 ± 6.5 181.3 ± 4.8 > 0.05 Body mass (kg) 79.0 ± 11.3 74.1 ± 6.5 > 0.05 1.97 ± 0.12 1.94 ± 0.09 > 0.05 36.4 ± 6.4 46.2 ± 6.1 < 0.001 PPO (Watts) 193 ± 33 251 ± 20 < 0.001 Lactate threshold (min) 10.2 ± 2.0 13.6 ± 2.1 < 0.05 53 ± 5 51 ± 6 > 0.05 SBP (mmHg) 124 ± 12 130 ± 15 > 0.05 DBP (mmHg) 73 ± 6 79 ± 17 > 0.05 MAP (mmHg) 91 ± 10 99 ± 16 > 0.05 EDV (ml) 130 ± 19 147 ± 20 < 0.05 ESV (ml) 54 ± 15 65 ± 13 > 0.05 74 ± 10 82 ± 14 > 0.05 38 ± 6 42 ± 8 > 0.05 CO (L.min-1) 4.2 ± 0.5 4.2 ± 0.9 > 0.05 CO index (L.min-1.m2) 2.1 ± 0.3 2.1 ± 0.4 > 0.05 141.20 ± 18.10 180.20 ± 28.31 < 0.001 5.0 ± 0.3 5. 2 ± 0.2 > 0.05 2.6 ± 0.2 2.7 ± 2.4 > 0.05 3.5 ± 0.3 3.7 ± 0.3 > 0.05 1.8 ± 0.2 1.9 ± 0.2 > 0.05 LVPWd (cm) 1.00 ± 0.2 1.1 ± 0.2 > 0.05 LVPWd index (cm.m2) 0.5 ± 0.1 0.6 ± 0.1 > 0.05 LVPWs (cm) 1.6 ± 0.2 1.7 ± 0.3 > 0.05 0.8 ± 0.1 0.9 ± 0.1 > 0.05 1.1 ± 0.2 1.2 ± 0.3 > 0.05 0.6 ± 0.08 0.5 ± 0.01 < 0.001 1.5 ± 0.1 1.6 ± 0.2 > 0.05 0.8 ± 0.1 0.8 ± 0.2 > 0.05 1.81 ± 0.19 1.71 ± 0.08 > 0.05 BSA (m2) VO2peak(ml. kg--1.min-1) HR (bpm) SV (ml) SV index (ml.m2) LV mass (g) LVIDd (cm) LVIDd index (cm.m2) LVIDs (cm) LVIDs index (cm.m2) LVPWs index (cm.m2) IVSd (cm) IVSd index (cm.m2) IVSs (cm) IVSs index (cm.m2) Sphericity Index All data presented as mean ± SD. d = diastole s= systole Cooke et al. LV twist mechanics during exercise. 23 Table 2. Systematic cardiovascular responses and peak left ventricular twist mechanics at rest and during submaximal exercise intensities in trained and untrained individuals. Untrained group (n = 13) Trained group (n = 11) Main effects Rest 30% 40% 50% Rest 30% 40% 50% 4.5 ± 1.2 16.0 ± 2.4 19.1 ± 2.8 21.6 ± 3.2 5.70 ± 1.3 19.3 ± 2.7* 23.5 ± 3.3** 27.8 ± 4.0*** # † ~ - 58.0 ± 10 77.3 ± 13 97 ± 16 - 75 ± 6*** 100.3 ± 8*** 125 ± 10*** # † ~ 0.77 ± 0.22 1.37 ± 0.43 1.75 ± 0.81 2.42 ± 1.06 1.06 ± 0.54 1.37 ± 0.51 1.69 ± 0.75 2.11 ± 1.07 † 53 ± 5 79 ± 18 83 ± 20 93 ± 24 51 ± 6 77 ± 10 88 ± 12 91 ± 13 † SBP (mmHg) 124 ± 12 165 ± 16 168 ± 17 171 ± 17 131 ± 15 168 ± 21 173 ± 21 175 ± 22 † DBP (mmHg) 74 ± 6 91 ± 12 90 ± 11 90 ± 11 79 ± 17 96 ± 22 96 ± 20 93 ± 18 † MAP (mmHg) 91 ± 10 118 ± 14 118 ± 13 120 ± 13 99 ± 16 123 ± 23 125 ± 21 124 ± 19 † EDV (ml) 130 ± 19* 133 ± 9 140 ± 17 139 ± 17 147 ± 20 154 ± 23 151 ± 19 157 ± 24 ~ ESV (ml) 54 ± 15 49 ± 10 50 ± 15 44 ± 15 65 ± 13 66 ± 20 55 ± 13 49 ± 19 † SV (ml) 74 ± 10 84 ± 6 90 ± 8 94 ± 11 82 ± 14 88 ± 9 96 ± 10 108 ± 10** †~ SV index (ml.m2) 38 ± 6 43 ± 5 46 ± 6 48 ± 8 42 ± 8 45 ± 6 50 ± 7 56 ± 6* †~ CO (L.min-1) 4.2 ± 0.5 8.2 ± 0.9 10 ± 1.0 11.6 ± 1.4 4.2 ± 0.9 7.8 ± 1.3 10.2 ± 2.0 12.6 ± 2.4 † CO index (L.min-1.m2) 2.1 ± 0.3 4.2 ± 0.6 5.1 ± 0.7 5.9 ± 1.0 2.1 ± 0.4 4.0 ± 0.7 5.3 ± 0.9 6.5 ± 1.2 † Sphericity index 1.81 ± 0.19 1.54 ± 0.06 1.60 ± 0.14 1.61 ± 0.15 1.71 ± 0.08 1.51 ± 0.15 1.47 ± 0.17 1.49 ± 0.14 # † ~ LV twist (°) 13.9 ± 3.9 20.2 ± 4.2 22.1 ± 5.9 25.9 ± 5.9 12.4 ± 7.2 18.5 ± 6.4 19.8 ± 8.3 21.2 ± 5.9 † - 156 ± 61 174 ± 90 198 ± 65 - 158 ± 82 166 ± 90 187 ± 114 † -91 ± 18 -203 ± 61 -242 ± 73 -292.2 ± 65 -114 ± 34 -183 ± 45 -227 ± 66 -265 ± 76 † - 226 ± 168 271 ± 90 332 ± 110 - 168 ± 50 212 ± 107 246 ± 107* †~ Basal circ strain (°) -15.4 ± 2.8 -18.1 ± 3.8 -19.1 ± 4.4 -19.3 ± 3.3 -16.3 ± 2.9 -18.2 ± 2.9 -19.2 ± 3.0 -17.6 ± 3.9 † Apical circ strain (°) -19.9 ± 2.8 -26.6 ± 1.6 -29.8 ± 3.6 -31.1 ± 3.7 -22.4 ± 3.4 -27.9 ± 2.8 -30.4 ± 2.2 -32.8 ± 4.4 † VO2 (ml. kg-1.min-1) PO (Watts) Lactate (mmol.L) HR (bpm) LV twist (% Δ) LV untwisting rate (°.sec-1) LV untwisting rate (% Δ) All data presented as mean ± SD. * = P < 0.05 ** = P < 0.01 *** = P < 0.001 # = Significant interaction main effects † = Significant exercise effect ~ = Significant group effect Cooke et al. LV twist mechanics during exercise. Equations Du Bois and Du Bois formula BSA = (Weight 0.425 x Height 0.725) x 0.007184 LV twist and untwisting rate percentage change formula Percentage change = 100/ baseline value x exercise intensity value 24