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...

Sleep deprivation is common in Western societies and is associated with increased cardiovascular morbidity and mortality in epidemiological studies. However, the effects of partial sleep deprivation on the cardiovascular system are poorly understood. In the present study, we evaluated 13 healthy male volunteers (age: 31 ± 2 yr) monitoring sleep diary and wrist actigraphy during their daily routine for 12 nights. The subjects were randomized and crossover to 5 nights of control sleep (>7 h) or 5 nights of partial sleep deprivation (<5 h), interposed by 2 nights of unrestricted sleep. At the end of control and partial sleep deprivation periods, heart rate variability (HRV), blood pressure variability (BPV), serum norepinephrine, and venous endothelial function (dorsal hand vein technique) were measured at rest in a supine position. The subjects slept 8.0 ± 0.5 and 4.5 ± 0.3 h during control and partial sleep deprivation periods, respectively (P < 0.01). Compared with control, sleep deprivation caused significant increase in sympathetic activity as evidenced by increase in percent low-frequency (50 ± 15 vs. 59 ± 8) and a decrease in percent high-frequency (50 ± 10 vs. 41 ± 8) components of HRV, increase in low-frequency band of BPV, and increase in serum norepinephrine (119 ± 46 vs. 162 ± 58 ng/ml), as well as a reduction in maximum endothelial dependent venodilatation (100 ± 22 vs. 41 ± 20%; P < 0.05 for all comparisons). In conclusion, 5 nights of partial sleep deprivation is sufficient to cause significant increase in sympathetic activity and venous endothelial dysfunction. These results may help to explain the association between short sleep and increased cardiovascular risk in epidemiological studies.

Home-based IMT represents an important strategy to improve cardiac and peripheral autonomic controls, functional capacity, and quality of life in patients with CHF.