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Telemetric Cardiovascular Monitoring in Exercise Trained Rats 31 Journal of Exercise Physiologyonline (JEPonline) Volume 13 Number 2 April 2010 Managing Editor Tommy Boone, PhD, MPH Editor-in-Chief Jon K. Linderman, PhD Review Board Todd Astorino, PhD Julien Baker, PhD Tommy Boone, PhD Eric Goulet, PhD Robert Gotshall, PhD Alexander Hutchison, PhD M. Knight-Maloney, PhD Len Kravitz, PhD James Laskin, PhD Derek Marks, PhD Cristine Mermier, PhD Chantal Vella, PhD Ben Zhou, PhD Official Research Journal of the American Society of Exercise Physiologists (ASEP) ISSN 1097-975 Systems Physiology – Cardiopulmonary Telemetric Monitoring of Cardiovascular Parameters after Exercise Training in Normotensive Rats LENICE BECKER1, JOSÉ SILVA1, ROBSON SANTOS1, MARIA CAMPAGNOLE-SANTOS1 1Department of Physiology and Biophysics, ICB, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil ABSTRACT Becker LK, Silva JR, Santos RAS, Campagnole-Santos MJ. Telemetric Monitoring Of Cardiovascular Parameters After Exercise Training In Normotensive Rats. JEPonline 2010;13(2):31-41. In the present study we have evaluated, through telemetric recordings, the circadian alterations in mean arterial pressure (MAP) and heart rate (HR) and the variability of MAP and HR induced by exercise training (ET) in normotensive rats. Sprague-Dawley (SD) rats were submitted to 20 sessions of swimming, 1 h duration, 5 days a week for 4 weeks. MAP and HR were continuously recorded every 10 min for 24 h by a telemetric implant. In order to evaluate the effect of an entire week of exercise training, data collected on the 3 last days of each week were used for the analyses. ET did not change the circadian rhythm or acrophase of the MAP and HR or the resting values of MAP during the day or during the night. As expected, ET induced a fall in baseline HR while resting bradycardia was only significant during the night period (wakefulness). The resting bradycardia started at the 2nd week of training. Trained animals did not present alteration in the HR variability. However, there was a significant increase in MAP variability during the day (sleep period) of trained rats in comparison to the night values or to the sedentary period. In addition, the motor activity was significantly smaller after ET during the night in comparison to SE. The data suggest that ET differentially interferes with the mechanism of control of arterial pressure during the day (sleep) and night (wakefulness) periods. Key words: Telemetry, Exercise Training, Blood Pressure, Heart Rate, Blood Pressure Variability. Telemetric Cardiovascular Monitoring in Exercise Trained Rats 32 INTRODUCTION The cardiovascular parameters such as blood pressure (BP), heart rate (HR), stroke volume and cardiac output change rhythmically according to the 24h cycle, being higher in the active phase in relation to the resting phase (4,16). The internal body clock, which is responsible for generating 24h rhythms, is located in the hypothalamic suprachiasmatic nucleus (SCN) that receives light information from the retina and several others peripheral stimuli (sleep/ awake, hormones, body temperature). It has been shown that the rhythm of BP and HR may be controlled by an endogenous circadian oscillating system (34) in which the SCN plays an important role in rats (24). It is not completely understood how the circadian information from the SCN is modulated/ processed to regulate the 24h rhythm of BP and HR. The neuronal activity originating in the SCN translates in circadian rhythms by inducing the release of hormones from hyphothalamus and modifying the autonomic outflow through hypothalamic or brain stem efferent pathways (8,16). Thus, it is well accepted that the autonomic nervous system, which also follows a circadian pattern, is importantly involved in mediating the circadian variation of BP (8). Exercise is recognized to affect circadian rhythmicity in a variety of ways. However, how exercise or arousal provides a feedback to the biological clock is not well understood. Studies have observed that exercise can affect circadian rhythm of different biological functions and it has been proposed that exercise may alter the functioning of the circadian system in order to facilitate the emergence of circadian rhythms in previously arrhythmic animals (4,15). Exercise training (ET) has been associated to improvement of cardiovascular function and reduction of cardiovascular risk factors and mortality (1,31) Exercise training performed at moderate intensity produces resting bradycardia and a significant reduction in mean arterial pressure (MAP) in hypertensive patients and animals (1,14,30). Studies by Krieger, Negrão and colleagues have shown that in hypertensive animals (SHR), ET improves baroreflex function, reduces resting HR and reduces the sympathetic drive to the heart (28,29,32). However, in normotensive animals, results are controversial. Studies showed no change or attenuation of the baroreflex bradycardia or a decrease in the overall sensitivity of the baroreflex control of HR (7,21). On the other hand, after ET normotensive rats present an increased gain of the aortic baroreceptor function (3), suggesting that the attenuation in baroreflex may take place in other sites of the reflex arch. Accordingly, it was shown that normotensive rats submitted to ET present in addition to a reduction in sympathetic tone, a decreased vagal tone, a decreased bradicardic response to efferent vagal nerve stimulation and a decrease in the pacemaker rate (20). Thus, decrease in the sensitivity of pacemaker cells may overcome the increased gain of the aortic baroreceptor function. Studies in humans, using spectral analysis of 24h ECG, have shown that the resting bradycardia is more proeminent during the day (wakefulness) (5,27). In addition, there are an increase in HR variability (5,17) accompanied by a decrease in the ratio LF/HF of the power spectrum, which is an index of sympathetic activity (22,27), or an increase in HF component, which reflects parasympathetic tone (12), mostly in the night period (sleep). The contribution and the understanding of the mechanisms triggered by ET on circadian rhythm of BP may help to improve our knowledge on the mechanisms involved in the control of BP. However, very few studies have addressed this issue. Thus, the purpose of the present study was to investigate the circadian rhythm of BP and HR in trained rats through telemetric monitoring, which allows a more efficient assessment of cardiovascular parameters without the stress produced by the investigator manipulation of the animals. Telemetric Cardiovascular Monitoring in Exercise Trained Rats 33 METHODS Animals Male Sprague-Dawley rats (300-350 g) were obtained from the animal facilities of the Hypertension laboratory ICB, UFMG. Before the experiments were started, the animals underwent a 12-day acclimatization period in an isolated telemetry room. The rats were housed in separated cages under controlled conditions of temperature (25°C) and a 12:12-h light/dark cycle (light: 6:00 AM to 6:00 PM; dark: 6:00 AM to 6:00 PM). Radiotelemetry Monitoring of Blood Pressure (BP), Heart Rate (HR) and Motor Activity (MA) A telemetry system (Data Sciences International, MN) was used for measuring systolic, diastolic, and MAP, HR and locomotor activity. Arterial pressure was monitored by a radiofrequency transducer model TA11-PA C40, a receiver, a matrix, and a personal computer with the software (Dataquest A.R.T., Gold 2.0) to store and analyze the data. Under tribromoethanol anesthesia 2.5% (1 ml/100 g body weight), the catheter-transducer was implanted into the abdominal aorta just above the bifurcation of the iliac arteries, and the sensor was fixed to the abdominal wall. The animals were returned to their individual cages for 7-10 days for the reestablishment of 24-hours oscillations of BP and HR. Exercise Training (ET) ET was performed by 20 sessions of 1 hour swimming daily (Monday through Friday, between 1 to 2 pm), 5 days a week. At the first day the rats swam for 20 minutes, at the second day for 40 minutes, and from the third day for 1 hour. Swimming was performed in individual pools at a water temperature of 30oC, controlled by a thermostat. The blood pressure receiver was positioned beside of the pools to record the cardiovascular parameters during the training session. Data Analysis The MAP and HR were calculated simultaneously from the pulsatile arterial pressure values with software Dataquest ART. Data were sampled for 10s, every 10min, during 24h. The parameters collected in the three days before the first week of training were considered resting values (sedentary). To evaluate time course of blood pressure changes induced by exercise training, the three last days of each training week were used (Friday, Saturday, and Sunday), because in these days the data collected show the effect of the entire week of training. MAP and HR of night period (wakefulness) were the data collected from 6:00 PM to 5:55 AM (72 values) and the MAP and HR for the day period (sleep) were the data collected from 6:00 AM to 5:55 PM (72 values), except Friday when day values refers to 6:00 AM to 01:00 PM ( 42 values). Data from 01:00PM to 05:55PM on Friday were not used to eliminate the alterations caused by the exercise session and to assure that the values were back to baseline. For statistical analysis, all values collected in these periods (1 value at each 10 min) for each rat were computed. Comparisons between day and night values within the same rat were assessed by paired Student’s t-test (Prism 4.0, Graphpad Software). Comparisons between the control period and the training period were analyzed by repeated measures one-way ANOVA, followed by the Newman-Keuls test. The degree of oscillation moment to moment, MAP and HR variability, was evaluated by the averaged standard deviation (SD) of the MAP and HR values collected during the day or night in each rat. The acrophase of the MAP and HR, which corresponds to the time of the 24h of the highest value (peak of the circadian rhythm) expressed in hours, were obtained by rhythmic analysis (DQFIT software; 35,36) of the data collected in each of the last 3 days of each period (sedentary and 4th week of training). Individual acrophases, derived from the DQ-FIT analysis, were averaged and compared using circular statistics software (Software Oriana, version 1.06, Kovoch Computing Services, 1994). Telemetric Cardiovascular Monitoring in Exercise Trained Rats 34 The comparisons between the circular mean of the acrophases were performed using the Watson f-test (33). Data are presented as mean ± SE and p< 0.05 was considered statistically significant. RESULTS MA Counts/ min HR beats/ min BP mmHg MA counts/ min HR beats/ min Figure 1 shows the typical recording of arterial pressure, HR and motor activity of one rat, during sedentary period and trained period. A Sedentary Training Weeks As expected, resting values of 500 15/02 06:00:00 MAP, HR and 400 motor activity were 300 smaller during the 200 day (sleep) in 100 comparison to the 30 values during the 20 night 10 (wakefulness) 0 period, illustrating the circadian oscillatory pattern 200 of the 160 cardiovascular 120 parameters, which 80 was kept during 40 the weeks of 0 24.0 4.0 8.0 12.0 16.0 20.0 28.0 32.0 36.0 days training. In SAP DAP MAP addition, in Figure 1C between TRAINED SEDENTARY B C arrows, it can be seen the MAP, HR 22/03 06:00:00 500 22/02 06:00:00 and MA changes 300 during a session of 100 exercise. 30 20 10 MAP mmHg Figure 2 shows that after 4 weeks 200 of ET there was no change in 120 circadian rhythm 40 6 12 18 24 30 36 42 48 54 60 66 72 0 0 6 12 18 24 30 36 42 48 54 60 66 72 of MAP, HR or hours hours MA. Accordingly, Figure 1. A- Heart rate (HR, beats/ min- top panel), motor activity (MA, counts/ min- middle the acrophase of panel) and blood pressure (BP mmHg, bottom panel) data collected by telemetry system in all parameters the sedentary (green bar) and training weeks (red bar) of one animal. Systolic (SAP, black line), mean (MAP, red line) and diastolic (DAP, blue line) arterial pressure are also shown. In evaluated were detail are HR, MA and MAP values collected in three consecutives days of the sedentary not changed after period (B) and in the 4th week of training (C). Yellow bars on top represent day and the blue ET: acrophase of bars, night periods. Arrows in C set the limits of the duration of one exercise session (1h) and HR (sedentary its recovery (2h). period: 10:4201:04 PM vs trained period: 11:4800:22 PM); acrophase of the MAP (sedentary period: 0 Telemetric Cardiovascular Monitoring in Exercise Trained Rats 35 09:110:34 PM vs trained period 09:2902:21 PM), and acrophase of the motor activity (sedentary: 11:4104:07 PM vs trained: 11:5102:46 PM). More interestingly, as shown in Fig 4A, exercise did not significantly alter HR variability, during the night (5.2±1.0 beats/ min vs 6.0±1.1beats/ min, sedentary period) or day period (8.8±1.1 beats/ min vs 5.6±2.2 beats/ min, sedentary period). However, after ET there was a significant increase in the MAP variability during the day (sleep period; 4.31.04 mmHg; Fig. 4B) in comparison to sedentary period (2.1±0.4mmHg) p<0.05. During the night (wakefulness period) the MAP variability was not changed (1.10.2 mmHg vs 1.7±0.5 mmHg, sedentary period; Fig. 4B). HR, bpm Day 400 350 * Night *† 300 250 200 B MA counts/ min In addition, ET induced a significant fall in MA from the first week of training (Figure 2B and Table 1 p<0.05). ET did not alter MAP values during the day or night (Fig 2C, Table 1). The smaller HR value during the night with no change in day HR, resulted in a small difference between the day and night HR values (34±4 beats/ min vs 43±2 beats/ min in the sedentary period; Fig 3A). No change was observed in the day and night difference of MAP (Fig. 3B). A C Sedentary Trained 3 * 2 *† 1 0 Sedentary Trained 110 * MAP, mmHg ET induced a significant decrease in HR, however, only during the night period (wakefulness; Table 1 and Fig. 2 A p<0.05). The HR resting values during the day were not significantly different from the sedentary period, except for the third week of training p<0.05 (Table 1). In contrast, resting HR values during the night period were significantly smaller from the second week of training in comparison to the sedentary period (Table 1). * 100 90 During the training session, as expected, swimming 80 Sedentary Trained induced an increase in MAP (130 ± 4 mmHg vs 99 ± st 2 mmHg, resting values; in the 1 week of training) Figure 2. Heart rate (HR, beats/ min; A), motor accompanied by an increase in HR (406±5 activity (MA, counts/ min; B) and mean arterial beats/min vs 300±2 beats/min, resting values; in the pressure (MAP, mmHg; C) during the period of day night (wakefulness) in sedentary or 1st week of training). The pressor and tachycardic (sleep) and trained (4th week) rats (n=5). *p< 0.05 in comparison response to exercise did not change over the 4 to day (paired Student t test); +p<0.01 in comparison weeks of training (data not shown). After 2 hours of to respective sedentary (repeated measures one-way the end of the exercise session, both BP and HR ANOVA followed by Newman-Keuls). were back to baseline values (data not shown). The time of recovery of the cardiovascular parameters did not alter in the 4 weeks of training (data not shown). Telemetric Cardiovascular Monitoring in Exercise Trained Rats 36 DISCUSSION Telemetric Monitoring Advantages The present study evaluated for the first time the cardiovascular parameters during 24h in rats submitted to Table 1. Mean arterial pressure (MAP, mmHg), heart rate (HR, beats/ min) exercise and motor activity (MA, counts/ min) values during the day and night in each training. The BP week of training. recording by Sedentary Training weeks telemetry allowed an 1 2 3 4 evaluation of the Day 99 0.6 99 0.5 100 0.6 98 0.5 101 0.7 cardiovascular MAP parameters Night 1050.4* 1030.2* 1060.3* 1030.5* 104 0.3* without the stress produced Day 3023.3 300 1.8 2962.0 2881.2* 297 2.0 by investigator HR manipulation of Night 3462.4* 341 2.2* 334 2.1*† 329 2.4*† 332 2.4*† the animals. Day 0.7 0.09 1.0 0.07 0.6 0.05 0.8 0.08 0.7 0.1 The rats were MA submitted to 1h Night 2.5 0.11*† 1.9 0.07*† 1.7 0.08*† 1.7 0.07*† 1.5 0.06*† swimming, 5 days a week, Values are mean SD. *; p< 0.05 compared to day, †; p< 0.05 compared to sedentary, n=5. during 4 weeks without extra-workload, such as, the addition of tail weights. This protocol of swimming training is considered to induce low exercise intensity (11). It has been shown that sedentary rats are able to keep a stable lactate blood entry/ removal ratio in workload up to 6% of the body weight (11). Therefore ET carried out below 6% of the body weight can be considered sub-threshold. mmHg beats/min Exercise Training Effects on Circadian BP and HR It is well accepted, both in humans and animals, that low intensity exercise produces beneficial effects in reference to the HR Difference MAP Difference cardiovascular system, (night - day) (night - day) especially in lowering MAP 50 15 and HR of hypertensive * subjects (30,1). The results 10 obtained in the present work 30 showing that the ET did not 5 change resting values of the 10 MAP or HR or the circadian rhythm of MAP and HR in 0 0 normotensive rats, is in Sedentary Trained Sedentary Trained agreement with data obtained Figure 3. Difference between day and night values of heart rate (HR, beats/ in normotensive individuals min; A) and mean arterial pressure (MAP, mmHg; B) during the sedentary (14,6). The fall in BP that is period and after 4 weeks of ET (n=5). *p< 0.05 in comparison to sedentary observed in hypertensive rats (paired Student t test). is believed to be related to the higher prevailing sympathetic tone of these animals. Telemetric Cardiovascular Monitoring in Exercise Trained Rats 37 mmHg beats/min From the second week of training, it was observed a significant decrease in resting HR during the night, and the bradycardia was maintained until the end of the training period. A significant reduction in HR during the day was only observed after the third week of training. Resting bradycardia is observed in several studies after a low intensity exercise by treadmill and swimming (10,13, 14,26,28,32), which serves as a marker for exercise training adaptation (13,2). In addition, our study shows that the effect of exercise in producing resting bradycardia was more effective during the wakefulness MAP variability HR variability A B Day 15 6 period (night) of † Night the rat. This 5 result is in 4 10 agreement with previous studies 3 in men (5, 25, 2 5 27,29). It is not 1 clear which are the mechanisms 0 0 Sedentary Sedentary Trained Trained involved in the HR reduction Figure 4. Heart rate (HR, beats/ min; A) and mean arterial pressure (MAP, mmHg; B) variability th after ET. In during the day (sleep) and night (wakefulness) period in sedentary and trained (4 week) rats (n=5). †; p< 0.05 in comparison to respective sedentary period (repeated measures one-way normotensive ANOVA followed by Newman–Keuls). rats it was shown a decrease in both the sympathetic and parasympathetic components of the HR control after exercise training (20). In addition, the alterations in autonomic control were accompanied by a decrease in the intrinsic HR, which suggest alteration in the sinus node cells (20). Other studies however, suggest that resting bradycardia induced by exercise may result from an increase in vagal tone (31). In hypertensive rats, ET induces a fall in sympathetic activity to a similar level found in the normotensive rats, however, without changes in vagal tone (10). Our data suggested that ET induces alteration preferentially in the sympathetic system, since during the wakefulness period this system predominates in the control of the HR. During the sleep period, the autonomic control of arterial pressure is mainly regulated by the parasympathetic system, since the decrease in sympathetic activity is higher, especially during the REM phase (18). Our data suggest that the fall in HR can also be related to the decrease in motor activity during the night (awake period) that was shown by the animals after ET. The decrease in motor activity after ET can be attributed to an increase in the release of endorphins and/or another opioid peptides, which are well known to be released after ET and are involved, among others, with the activity behavior of the animal (9). In parallel to the HR changes, ET produced no consistent changes in resting MAP values, which is in agreement with studies (3,21) that showed that low or moderate exercise intensities does not change the resting MAP of normotensive rats. However, MAP variability was significantly higher, after 4 weeks of exercise training, only during the sleep period (day). The increase in MAP variability suggests a decrease in baroreflex sensitivity during the day (sleep period). Negrão et al.(21) have shown that ET performed on a motor treadmill for 13 weeks in normotensive rats induce a significant lower renal sympathetic nerve activity (RSNA) accompanied by an impairment of baroreflex control of RSNA (in response to MAP fall) and baroreflex control of HR (bradycardia). Reduced sensitivity of the baroreflex control of HR was observed after exercise training in both humans (19,23) and animals (7,20). Our study adds new data showing that the possible impairment of baroreflex sensitivity induced by ET is only attained to the day period, where sympathetic influence to the control of BP is Telemetric Cardiovascular Monitoring in Exercise Trained Rats 38 lower. Thus, this result is in keeping with the hypothesis that the main effect of the ET in normotensive rats is on the modulation of the sympathetic tonus. CONCLUSION This is the first study to show the cardiovascular effects induced by ET using a continuous (24 hours) BP monitoring by telemetry. Our data, showing an increased MAP variability during the day and a decreased baseline HR (resting bradycardia) during the night, reinforces the hypothesis that ET induces an important alteration in autonomic balance towards a significant decrease in sympathetic tonus to the cardiovascular system, which is a key modulator of physiological functions during wakefulness. 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