Acute and Chronic Effects of Exercise on Baroreflexes in Spontaneously Hypertensive Rats
Abstract We studied the effects of acute and chronic exercise on the arterial baroreflex and chemosensitive cardiopulmonary baroreflex (CCB) in spontaneously hypertensive rats (SHR). Arterial baroreflex and CCB were evaluated in normotensive rats (NR, n=11) and SHR (n=5) at rest and after 30 minutes of an acute bout of exercise (45 minutes at 50% of Vo2max). In addition, these baroreflexes were evaluated in sedentary (n=5) and exercise-trained (n=9) SHR. Exercise training was performed on a motor treadmill, 5 days/week, during 60 minutes, at 50% of Vo2max. Baroreflex bradycardia and tachycardia, analyzed by baroreflex sensitivity index (Δ heart rate/Δ mean arterial pressure), were significantly lower in SHR than in NR (0.7±0.1 versus 2.0±0.1 and 1.8±0.2 versus 3.4±0.1 beats per minute [bpm]/mm Hg, respectively). During the recovery period from acute exercise, baroreflex bradycardia was significantly higher than at rest only in SHR (1.7±0.1 versus 0.7±0.1 bpm/mm Hg). Hypotension and bradycardia induced by CCB stimulation (5-hydroxytryptamine, IV) were similar between SHR and NR, and an acute exercise bout did not change these responses. Exercise training markedly improved baroreflex bradycardia and tachycardia in SHR (1.9±0.1 versus 0.7±0.1 and 2.9±0.1 versus 1.8±0.2 bpm/mm Hg, respectively). Exercise-trained rats had greater bradycardiac (118±26 versus 14±2 and 209±30 versus 19±5 bpm to 1 and 2 μg/kg 5-HT, respectively) and hypotensive (30±6 versus 15±3 and 45±7 versus 17±2 mm Hg to 1 and 2 μg/kg 5-hydroxytryptamine, respectively) responses to CCB stimulation. In conclusion, an acute bout of exercise increases baroreflex bradycardia in SHR, and exercise training attenuates hypertension concomitant with improved arterial baroreflex and CCB sensitivity in SHR.
Acute and chronic antihypertensive effects of exercise have been observed in both animals1 2 3 and humans.4 5 6 7 However, the reduction in arterial pressure after a single bout of exercise seems to be transitory.4 8 9 In contrast, exercise training performed at a range of 40% to 70% of maximal oxygen uptake has a long-term effect on arterial pressure in hypertensives,3 10 11 12 which raises the recommendation for exercise training as a nonpharmacological treatment for hypertension.
Arterial and cardiopulmonary baroreflexes contribute importantly to the reflex control of circulation.13 14 Stimulation of the ventricular mechanosensitive receptors provokes bradycardia and vasodilatory response.15 Similar responses have been proposed to the chemosensitive receptors.15 In established hypertension, arterial baroreflex control is depressed,16 17 and the functioning of cardiopulmonary baroreflex seems also to be altered.16 Therefore, both arterial and cardiopulmonary baroreflex dysfunction may contribute to the worsening of blood pressure regulation in hypertension.
Previous studies have demonstrated that chronic exercise can modify baroreflex sensitivity in both animals and humans. Negrão et al18 19 reported that exercise training decreased baroreflex bradycardia and baroreflex control of sympathetic renal nerve activity in rats. Both investigations, however, were restricted to the study of arterial baroreflex control in NR. In addition, the attenuation in arterial baroreflex bradycardia was associated with a significant alteration in intrinsic HR, which might mask a true effect of exercise on baroreflex bradycardia. Furthermore, we have learned from other studies performed in our laboratory18 20 that the neurovegetative changes provoked by chronic exercise in SHR can be distinct from those observed in NR. Although in NR chronic exercise provokes bradycardia by reducing intrinsic HR without changing sympathetic tone, in SHR, bradycardia is achieved by restoration of normal sympathetic tone. Therefore, it is possible that the effect of chronic exercise on arterial baroreflex and CCB in SHR is quite different from that reported in NR. Pagani et al21 and Somers et al22 found an increased arterial baroreflex sensitivity after exercise training in hypertensive subjects. In these studies, baroreflex sensitivity was evaluated only to increases in arterial pressure. Baroreflex sensitivity, in fact, can be different for bradycardia and tachycardia.23
In the present study, we hypothesized that acute exercise would increase the sensitivity of the arterial baroreflex and CCB in SHR. Moreover, chronic exercise would improve arterial baroreflex and CCB sensitivity and attenuate hypertension in SHR.
Eleven male Wistar NR (Medical School, University of São Paulo) and 19 male SHR (Paulista Medical School, Brazil), 100 to 150 g body weight (3 to 4 per cage), were fed standard laboratory chow and water ad libitum in a temperature-controlled room (22°C) with a dark-light cycle of 12/12 hours. The rats were assigned to four groups: NR (n=11) and SHR (n=5) (protocol 1); hypertensive S (n=5) and hypertensive T (n=9) rats (protocol 2).
Maximal Oxygen Uptake
Maximal oxygen uptake (Vo2max) was measured by means of expired gas analysis during a maximal progressive exercise test, performed on a motor treadmill with 5 m/min increments every 4 minutes and no grade. Samples of expired gases were collected in a 20-mL syringe during the last 30 seconds of every workload, as previously described by one of us.20 Oxygen and carbon dioxide concentrations were analyzed with Scholander microtechnique (Godart-Statham).
Measurement of Arterial Blood Pressure
Two cannulas were implanted, under ether anesthesia, into the carotid artery (PE-50) and jugular vein (PE-50) and emerged through the back of the rat. Arterial pressure was monitored in conscious rats by connecting the carotid artery cannula (inserted 1 day before, under ether anesthesia) to a strain-gauge transducer (Statham P23 Db). For direct arterial pressure measurements on a beat-to-beat basis, the transducer signal was fed to both an amplifier (GPA-4 model 2, Stemtech, Inc) and a 16-channel analog-to-digital converter (Stemtech, Inc), which was interfaced to a computer (Gateway 2000, 4DX2-66V) and sampled at 100 Hz. HR was taken from arterial blood pressure pulses.
Arterial Baroreflex and CCB
Arterial baroreflex control of HR was evaluated by at least three pressure responses (from 3 to 30 mm Hg) to phenylephrine (0.25 to 4 μg/kg IV; Sigma Chemical Company) and sodium nitroprusside (0.1 to 4 μg/kg IV; Sigma) injections. Three different procedures were performed: (1) calculation of the ratio of the mean of all values of HR responses to the mean of all MAP changes (HR:MAP); (2) calculation of the ratio of HR responses to MAP changes in response to increasing doses of phenylephrine and sodium nitroprusside, evaluated in different ranges of MAP changes (0 to 10, 11 to 20, and 21 to 30 mm Hg); and (3) regression analysis as previously described.18
CCB sensitivity was evaluated by bradycardia and hypotension (Bezold-Jarisch reflex) induced by increasing doses of serotonin (5-HT; 1, 2, and 4 μg/kg IV; Sigma).
Protocol 1: Acute Exercise
One week before the experiment, the rats were submitted to a short period of exercise (10 minutes) on a treadmill, at 50% of Vo2max (10 m/min), to enable them to become accustomed to the experimental procedures. Twenty-four hours before the experiment, NR and SHR groups had arterial and venous cannulas implanted for assessment of arterial pressure and drug injections, respectively. One day later, arterial pressure was monitored at rest (30 minutes) and during the recovery period (60 minutes). Arterial baroreflex and CCB sensitivity in both NR (n=11) and SHR (n=5) were evaluated at rest and after 30 minutes of exercise. The interval between phenylephrine, sodium nitroprusside, and serotonin injections was determined by the time required for the HR and MAP to return to baseline level.
Protocol 2: Chronic Exercise
After Vo2max determination, the T SHR were submitted to a 12-week exercise training on a motor treadmill, 5 days/week, gradually progressing toward 50% of Vo2max (15 to 20 m/min) for 60 minutes. The age-matched S SHR were handled daily to let them become accustomed to the experimental procedures. Twenty-four hours after the last training session, S ( n=5) and T (n=9) SHR had an arterial and venous cannula implanted for assessment of arterial pressure and drug injections, respectively. One day later, arterial pressure was monitored for 30 minutes in quiet, conscious unrestrained rats on a beat-to-beat basis (AT/Codas). HR was taken from arterial blood pressure pulses. Subsequently, both arterial baroreflex and CCB sensitivity were evaluated in S and T SHR groups, as described before.
After acute exercise, baroreflex sensitivity, calculated by the ratio of the mean of all values of HR responses to the mean of all MAP changes and the ratio of HR responses to MAP changes in response to increasing doses of phenylephrine and sodium nitroprusside, was tested by profile analysis. Baroreflex sensitivity, assessed by regression analysis (slope and γ-intercept), was tested by Student’s t test. CCB sensitivity in both NR and SHR was compared at rest and during the recovery period by profile analysis. Baroreflex sensitivity by all three procedures and CCB sensitivity between S and T SHR groups were compared by unpaired Student’s t test. P<.05 was considered as statistically significant. Data are presented as mean±SE.
Baseline levels of MAP were significantly greater in SHR than in NR (182±6 versus 115±6 mm Hg), but HR levels were similar between these two groups (360±21 versus 349±22 bpm in SHR and NR, respectively). At 5 minutes of recovery, MAP and HR levels were significantly greater in SHR (183±3 versus 113±6 mm Hg and 430±19 versus 359±12 bpm, respectively). During the recovery period, SHR showed a significant fall in MAP compared with their respective baseline levels (25 minutes, −11±4; 35 minutes, −11±5; and 45 minutes, −10±5 mm Hg). In NR, MAP was not changed during the recovery period.
The sensitivity index of bradycardia and tachycardia, when all values of HR:MAP were used, was significantly lower in SHR compared with NR (Fig 1⇓).
During the recovery period, baroreflex bradycardia and tachycardia, studied by all three procedures (see “Methods”), were not changed in NR. In SHR, the sensitivity index of baroreflex bradycardia, when all values of HR:MAP were used, showed a significant increase (Fig 1A⇑). However, this increase was not the same along the entire range of MAP increases, because baroreflex bradycardia was significantly improved in MAP increases of 8 and 15 mm Hg (0.69±0.11 versus 1.91±0.33 and 0.72±0.1 versus 1.76±0.15 bpm/mm Hg) but not changed in the range of 25 to 30 mm Hg (0.76±0.18 versus 1.28±0.32 bpm/mm Hg). Further assessment, by regression analysis, showed that there was no significant difference between recovery and resting levels in the slope (0.89±0.19 versus 0.79±0.36) and that there was a tendency toward significance in the γ-intercept (1.90±2.39 versus 8.65±4.99, P<.06). In SHR, baroreflex tachycardia, when analyzed by all three procedures studied, was not changed in the recovery period (Fig 1B⇑).
Hypotension produced by 1 and 2 μg/kg 5-HT was similar between SHR and NR (Table⇓). Hypotension produced by 4 μg/kg 5-HT was significantly greater in SHR (Table⇓). Bradycardiac responses to CCB stimulation were similar between SHR and NR. At the recovery period, bradycardiac responses in both NR and SHR were similar to those observed at resting state (Table⇓).
Body weight was not significantly different between T and S rats (309±8 versus 317±36 g, respectively). Two days after the last training session and 1 day after cannula insertion, arterial pressure and HR were monitored for 30 minutes in quiet, conscious unrestrained rats. Exercise training at 50% of Vo2max reduced significantly systolic pressure, diastolic pressure, and MAP (212±10 versus 167±3, 157±4 versus 121±4, and 182±6 versus 144±4 mm Hg, respectively), as well as HR (375±15 versus 347±7 bpm) in SHR.
In SHR, exercise training significantly increased baroreflex bradycardia, when all of the values of HR:MAP were used (Fig 2A⇓). In addition, baroreflex bradycardia was significantly greater during MAP increases of 8 and 15 mm Hg (0.59±0.11 versus 2.7±0.15 and 0.72±0.1 versus 1.96±0.23 bpm/mm Hg, respectively). The regression analysis showed no significant change in slope (0.89±0.18 versus 0.93±0.24) and a significant increase in γ-intercept (1.9±2.4 versus 17.9±5.33). Similarly, the baroreflex tachycardia, when all values of HR:MAP were used, was significantly greater in T rats (Fig 2B⇓). Baroreflex tachycardia during MAP decreases of 7, 16, and 25 mm Hg (2.00±0.72 versus 3.07±0.22, 1.92±0.26 versus 3.05±0.24, and 1.54±0.34 versus 2.93±0.20 bpm/mm Hg, respectively) was significantly increased in T rats. The regression analysis showed that T rats had significant increase in slope (1.59±0.25 versus 2.66±0.30) but no significant change in γ-intercept compared with S rats (0.80±4.69 versus 4.46±4.99).
Hypotension induced by increasing doses of 5-HT was significantly greater in T rats (Fig 3A⇓). Likewise, exercise training significantly increased bradycardiac responses to 5-HT, except for the highest dose (4 μg/kg).
The main findings of the present study are: (1) acute exercise increases baroreflex bradycardia in SHR, (2) exercise training significantly attenuates high blood pressure in SHR, (3) exercise training increases baroreflex control of HR in SHR, and (4) exercise training increases the response to serotoninergic activation of chemosensitive cardiopulmonary afferents in SHR.
Acute Effect of Exercise
Postexercise hypotension has been reported by many investigators.1 2 4 5 24 However, this acute effect of exercise is mainly observed in hypertensive subjects.1 2 4 5 In the present study, we found postexercise hypotension and increased baroreflex bradycardia in SHR.
Established arterial hypertension is associated with depression of baroreflex control of HR.16 17 The present study confirms these findings. We observed a 66% decrease in bradycardia and a 47% decrease in tachycardia in SHR compared with NR. More interesting, however, was the fact that an acute bout of dynamic low-intensity exercise restored baroreflex bradycardia by 45% in SHR. The mechanisms involved in this partial recovery of baroreflex bradycardia in SHR are not clarified, but some potential mechanisms can be suggested. First, the maintained tachycardia and hypertension during exercise could increase baroreflex sensitivity postexercise. Chapleau et al,25 studying isolated carotid sinus in anesthetized dogs, observed that increases in HR (frequency) and pulse pressure (amplitude) sensitized the baroreceptors. Second, exercise increases the magnitude and frequency of the shear stress acting on the endothelial cells, releasing some endothelial factors, which can enhance the baroreceptor sensitivity at exercise offset.26 Third, acute exercise may change the autonomic regulatory mechanisms during the postexercise period in SHR. Chen et al27 reported a decrease in cardiac sympathetic tone after a bout of moderate-intensity dynamic exercise in SHR, which was concomitant with a postexercise hypotension. Depressed sympathetic tone may result from desensitization of β1-adrenergic receptors after exercise,28 which may explain the unchanged postexercise baroreflex tachycardia. Fourth, the decreased blood pressure levels during the recovery period can explain the augmented baroreflex bradycardia. Moreira et al29 reported a restoration of baroreflex bradycardia after reversal of hypertension. The tendency toward significant alteration in the operating point of the baroreflex (γ-intercept, P<.06) in the present study may facilitate the baroreflex control to increases in blood pressure at the recovery period of exercise in SHR.
There is no conclusive evidence of altered CCB sensitivity in hypertension.16 Some investigators14 have reported attenuated CCB sensitivity in severe hypertension, and others16 reported unchanged CCB sensitivity in borderline and mild hypertension. In the present study, we found no difference between SHR and NR in hypotension and bradycardiac responses to 5-HT injections at rest and during recovery. Bennett et al30 reported an increased CCB sensitivity to lower body negative pressure after an acute bout of exercise in humans. However, this response was only observed in high levels of lower body negative pressure (20 mm Hg or more), which does not exclude arterial baroreflex control in those responses. The serotonin infusion caused a CCB stimulation, which in turn produced a marked hypotension and bradycardia. One could argue that this hypotension could elicit baroreflex activation, which would mask the CCB response. Nevertheless, this seems not to be the case because the bradycardiac response during CCB stimulation precedes the tachycardia baroreflex response. In the present study, we took into consideration only the first response, ie, the bradycardiac response.
Chronic Effect of Exercise
In the present study, we observed that hypertension was attenuated and arterial baroreflex and CCB sensitivity of HR were significantly increased in T SHR. Baroreflex bradycardia and tachycardia were restored by 54% and 33%, respectively, in SHR.
Previous studies6 21 22 have in fact shown that low- to moderate-intensity exercise training is an efficient nonpharmacological treatment of hypertension. However, the mechanisms involved in the attenuation of hypertension are not fully understood. Some investigators3 6 have reported that exercise training causes a reduction in cardiac output in humans and animals, whereas others31 32 have observed a decrease in total peripheral resistance in humans. Véras-Silva et al33 demonstrated that arterial pressure reduction, observed after exercise training (55% of Vo2max) in SHR, was related to a decreased HR and cardiac output. Although the increased arterial baroreflex and CCB sensitivity could also provoke a decrease in cardiac output and, in consequence, attenuation of hypertension, the present study provides no evidence of cause-effect relationship between these physiological changes.
An increased baroreflex bradycardia after exercise training has been found in borderline hypertensive humans.21 22 In the present study, we observed that exercise training in SHR improved baroreflex sensitivity for bradycardiac and tachycardiac responses. Although T NR were not studied in this experiment, we have previously demonstrated that exercise training affects baroreflex bradycardia and tachycardia in the opposite direction in NR.19 23 This difference could be explained partially by alterations in afferent and efferent reflex pathways. The long-term baroreceptor dysfunction in hypertension is commonly associated with structural changes in large arteries, as well as a reduced distensibility of blood vessel wall, where baroreceptors are located.34 These changes could explain the decreased baroreflex sensitivity in the presence of hypertension. Conversely, it has been suggested that exercise training produces an increase in brachial compliance in normotensive subjects.35 Therefore, the increased baroreflex sensitivity in SHR after low-intensity exercise training could be in part explained by the increased compliance of blood vessels. Another possibility is the hypothesis of endothelial factors acting on the smooth muscle cell tone increasing arterial compliance or directly modifying the activity of baroreceptor endings. However, we cannot exclude the possibility of an increased baroreflex central gain or a more sensitive efferent pathway.
Cardiopulmonary baroreflex sensitivity seems not to be modified by exercise training in normotensives.36 37 However, the present results show that exercise training increases CCB but provide no information about mechanosensitive cardiopulmonary baroreflex. The increased CCB sensitivity in T SHR may be partially explained by a structural alteration of the heart, including an increase in capillary density and a reduction in intercapillary distance.38 In addition, myocardial structural changes after exercise training could lead to an increased ventricular compliance and hence improved CCB sensitivity. However, we cannot exclude changes in the central integration level or in efferent level.39 A previous study from our laboratory demonstrated that low-intensity exercise training significantly decreased intrinsic HR in NR18 and sympathetic tone to the heart in SHR.20
In conclusion, an acute bout of exercise increases baroreflex bradycardia in SHR, and exercise training attenuates hypertension concomitant with improved arterial baroreflex and CCB sensitivity in SHR.
Selected Abbreviations and Acronyms
|bpm||=||beats per minute|
|CCB||=||chemosensitive cardiopulmonary baroreflex|
|MAP||=||mean arterial pressure|
|SHR||=||spontaneously hypertensive rat(s)|
This study was supported by Financiadora de Estudos e Projetos (FINEP/No. 66.93.0023.00), Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP/No. 95/9909-1 and No. 97/00657-5), and Fundação E.J. Zerbini. We also thank Katt Coelho Mattos for technical contributions, Luciana M.P. Kalil for suggestions in this study, and Júlia Tizue Fukushima for performing the statistical analysis throughout this study.
- Received March 17, 1997.
- Revision received April 17, 1997.
- Accepted May 9, 1997.
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