Abstract-The protection from coronary events that young women have is sharply reduced at menopause. Oxidative stress and baroreflex sensitivity impairment of the circulation have been demonstrated to increase cardiovascular risk. On the other hand, exercise training has been indicated as a nonpharmacological treatment for many diseases. The aim of the present study was to test the hypothesis that exercise training can improve baroreflex sensitivity associated with reduction in oxidative stress in ovariectomized rats, an experimental model of menopause. Exercise training was performed on a treadmill for 8 weeks. Arterial pressure and baroreflex sensitivity, which were evaluated by tachycardic and bradycardic responses to changes in arterial pressure, were monitored. Oxidative stress was evaluated by chemiluminescence and superoxide dismutase and catalase antioxidant enzyme activities. Exercise training reduced resting mean arterial pressure (112Ϯ2 vs 122Ϯ3 mm Hg in the sedentary group) and heart rate (325Ϯ4 vs 356Ϯ12 bpm in the sedentary group) and also improved baroreflex sensitivity (tachycardic response, 63% and bradycardic response, 58%). Myocardium (25%) and gastrocnemius muscle (48%) chemiluminescence were reduced, and myocardial superoxide dismutase (44%) and gastrocnemius catalase (97%) activities were enhanced in trained rats in comparison with sedentary rats. Myocardium chemiluminescence was positively correlated with systolic arterial pressure (rϭ0.6) and inversely correlated with baroreflex sensitivity (tachycardic response, rϭϪ0.8 and bradycardic response, rϭϪ0.7). These results indicate that exercise training in ovariectomized rats improves resting hemodynamic status and reflex control of the circulation, probably associated with oxidative stress reduction, suggesting a homeostatic role for exercise training in reducing cardiovascular risk in postmenopausal women. Key Words: exercise Ⅲ baroreflex Ⅲ oxidative stress Ⅲ rat Ⅲ estrogen Ⅲ menopause M enopause has been associated with impairment of aerobic fitness, muscle strength, and bone mineral density, as well as an increase in body weight, type 2 diabetes, osteoporotic fractures, and cardiovascular disease (CVD). 1 Many CVD states are associated with baroreflex impairment, the most important short-term regulator of arterial blood pressure. Moreover, the baroreflex has been recognized as a marker of autonomic control and as a predictor of CV mortality. 2 Estrogen deprivation induces endothelial dysfunction and autonomic impairment and increases oxidative stress in fertile young women 3 and postmenopausal women, 4,5 thus increasing the CV risk. Oxidative stress has been implicated in the pathophysiology of a large number of diseases, and it plays a possible mechanistic role in baroreflex dysfunction, because antioxidant substances seem to improve baroreflex sensitivity (BRS) in different species. 6 -9 However, the role of oxidative stress on CV autonomic dysfunction during estrogen deprivation is not well understood.Since the Women's Health Initiative...

Abstract-Diabetes and menopause markedly increase the risk of cardiovascular disease in women. The objective of the present study was to investigate the effects of exercise training on cardiovascular autonomic dysfunction and on total mortality in diabetic female rats undergoing ovarian hormone deprivation. Female Wistar rats were divided into ovariectomized groups: sedentary and trained controls and sedentary and trained diabetic rats (streptozotocin, 50 mg/kg IV). Trained groups were submitted to an exercise training protocol on a treadmill (8 weeks). The baroreflex sensitivity was evaluated by heart rate responses to arterial pressure changes. Heart rate variability was determined using the SD of the basal heart rate. Vagal and sympathetic tonus were evaluated by pharmacological blockade. Diabetes impaired baroreflex sensitivity (Ϸ55%), vagal tonus (Ϸ68%), and heart rate variability (Ϸ38%). Exercise training improved baroreflex sensitivity and heart rate variability in control and diabetic groups in relation to their sedentary groups. Trained control rats presented increased vagal tonus compared with that of sedentary ones. The sympathetic tonus was reduced in the trained diabetic group as compared with that of other studied groups. Significant correlations were obtained between heart rate variability and vagal tonus with baroreflex sensitivity. Mortality, assessed during the training period, was reduced in trained diabetic (25%) rats compared with mortality in sedentary diabetic rats (60%). Together, these findings suggest that decreases in baroreflex sensitivity and heart rate variability may be related to increased mortality in female diabetic subjects and that improved autonomic regulation induced by exercise training may contribute to decreased mortality in this population.

Several investigators have demonstrated that diabetes is associated with autonomic and myocardial dysfunction. Exercise training is an efficient non-pharmacological treatment for cardiac and metabolic diseases. The aim of the present study was to investigate the effects of exercise training on hemodynamic and autonomic diabetic dysfunction. After 1 week of diabetes induction (streptozotocin, 50 mg/kg, iv), male Wistar rats (222 ± 5 g, N = 18) were submitted to exercise training for 10 weeks on a treadmill. Arterial pressure signals were obtained and processed with a data acquisition system. Autonomic function and intrinsic heart rate were studied by injecting methylatropine and propranolol. Left ventricular function was assessed in hearts perfused in vitro by the Langendorff technique. Diabetes (D) bradycardia and hypotension (D: 279 ± 9 bpm and 91 ± 4 mmHg vs 315 ± 11 bpm and 111 ± 4 mmHg in controls, C) were attenuated by training (TD: 305 ± 7 bpm and 100 ± 4 mmHg). Vagal tonus was decreased in the diabetic groups and sympathetic tonus was similar in all animals. Intrinsic heart rate was lower in D (284 ± 11 bpm) compared to C and TD (390 ± 8 and 342 ± 14 bpm, respectively). Peak systolic pressure developed at different pressures was similar for all groups, but +dP/dt max was decreased and -dP/dt max was increased in D. In conclusion, exercise training reversed hypotension and bradycardia and improved myocardial function in diabetic rats. These changes represent an adaptive response to the demands of training, supporting a positive role of physical activity in the management of diabetes.

. Exercise training changes autonomic cardiovascular balance in mice. J Appl Physiol 96: 2174-2178, 2004. First published January 16, 2004 10.1152/ japplphysiol.00870.2003.-Experiments were performed to investigate the influence of exercise training on cardiovascular function in mice. Heart rate, arterial pressure, baroreflex sensitivity, and autonomic control of heart rate were measured in conscious, unrestrained male C57/6J sedentary ( n ϭ 8) and trained mice (n ϭ 8). The exercise training protocol used a treadmill (1 h/day; 5 days/wk for 4 wk). Baroreflex sensitivity was evaluated by the tachycardic and bradycardic responses induced by sodium nitroprusside and phenylephrine, respectively. Autonomic control of heart rate and intrinsic heart rate were determined by use of methylatropine and propranolol. Resting bradycardia was observed in trained mice compared with sedentary animals [485 Ϯ 9 vs. 612 Ϯ 5 beats/min (bpm)], whereas mean arterial pressure was not different between the groups (106 Ϯ 2 vs. 108 Ϯ 3 mmHg). Baroreflex-mediated tachycardia was significantly enhanced in the trained group (6.97 Ϯ 0.97 vs. 1.6 Ϯ 0.21 bpm/ mmHg, trained vs. sedentary), whereas baroreflex-mediated bradycardia was not altered by training. The tachycardia induced by methylatropine was significantly increased in trained animals (139 Ϯ 12 vs. 40 Ϯ 9 bpm, trained vs. sedentary), whereas the propranolol effect was significantly reduced in the trained group (49 Ϯ 11 vs. 97 Ϯ 11 bpm, trained vs. sedentary). Intrinsic heart rate was similar between groups. In conclusion, dynamic exercise training in mice induced a resting bradycardia and an improvement in baroreflex-mediated tachycardia. These changes are likely related to an increased vagal and decreased sympathetic tone, similar to the exercise response observed in humans. bradycardia; autonomic nervous system; baroreflex; blood pressure RESTING BRADYCARDIA, INDUCED by exercise training, has been well documented in humans and animals; however, the mechanisms underlying the effect are not well understood. Studies in humans suggest that increased vagal activity is responsible for the decrease in heart rate (HR) (31, 32). In contrast, in young trained rats the resting bradycardia was more likely due to alterations in cardiac pacemaker function, a regulator of intrinsic heart rate (IHR), rather than to increased vagal activity (24). Moreover, the improvement in baroreflex control of HR observed in trained animals (3, 10, 11) and humans (1, 26) may also play a role in the basal HR changes.Exercise training induces cardiovascular and metabolic changes that are dependent on exercise intensity and duration as well as physiological condition (1, 8-10, 26, 30). Studies in mice demonstrate that treadmill exercise resulted in linear increases in HR, maximum oxygen consumption (V O 2 max ), and respiratory exchange ratio, similar to that seen in larger species (11). A test of ␤-adrenergic stimulation suggested that sympathetic tone was not altered, whereas vagal input was reduced. Swimming (4-w...

Background: The aim of the present study was to investigate the relationship between speed during maximum exercise test (ET) and oxygen consumption (VO 2 ) in control and STZ-diabetic rats, in order to provide a useful method to determine exercise capacity and prescription in researches involving STZ-diabetic rats.