Effects of estrogen therapy and aerobic training on sympathetic activity and hemodynamics in healthy postmenopausal women: a double-blind randomized trial.

OBJECTIVE: The aim of this study was to evaluate the isolated and associated effects of aerobic training and estrogen therapy on sympathetic nerve activity and hemodynamics in healthy postmenopausal women. METHODS: Forty-five postmenopausal women (mean [SD] age, 51 [3] y) were randomly divided into four groups: sedentary-placebo (SED-PLA; n = 11), sedentary-estrogen therapy (SED-ET; n = 14), aerobic training-placebo (AT-PLA; n = 12), and aerobic training-estrogen therapy (AT-ET; n = 8). The ET groups received oral estradiol valerate (1 mg/d), whereas the PLA groups received placebo. The AT groups performed aerobic exercise three times a week on a cycle ergometer for 50 minutes, whereas the SED groups remained sedentary. All participants were evaluated before and after 6 months. Muscle sympathetic nerve activity (MSNA; microneurography), forearm blood flow (plethysmography), blood pressure (oscillometry), and heart rate (HR) were measured at rest for 10 minutes. Data were analyzed by three-way analysis of variance. RESULTS: Estrogen administration itself did not change any of the studied parameters. AT improved forearm blood flow (AT-PLA, 2.02 [0.85] vs 2.92 [1.65] mL min(-1) 100 mL(-1), P = 0.03; AT-ET, 1.68 [1.11] vs 2.27 [0.76] mL min(-1) 100 mL(-1), P = 0.03), reduced MSNA in the AT-PLA group (39 [6] vs 34 [5] bursts/min(-1), P = 0.01), and decreased HR in the AT-ET group (65 [8] vs 62 [7] beats/min, P = 0.01). CONCLUSIONS: AT reduces sympathetic nerve activity and improves muscle blood flow in healthy hysterectomized postmenopausal women. Moreover, AT decreases HR when combined with ET. However, ET abolishes the reducing effect of AT on MSNA.

Sympathetic nerve activity is decreased during device-guided slow breathing.

It is known that slow breathing (<10 breaths min(-1)) reduces blood pressure (BP), but the mechanisms involved in this phenomenon are not completely clear. The aim of this study was to evaluate the acute responses of the muscle sympathetic nerve activity, BP and heart rate (HR), using device-guided slow breathing (breathe with interactive music (BIM)) or calm music. In all, 27 treated mild hypertensives were enrolled. Muscle sympathetic nerve activity, BP and HR were measured for 5 min before the use of the device (n=14) or while subjects listened to calm music (n=13), it was measured again for 15 min while in use and finally, 5 min after the interventions. BIM device reduced respiratory rate from 16+/-3 beats per minute (b.p.m) to 5.5+/-1.8 b.p.m (P<0.05), calm music did not affect this variable. Both interventions reduced systolic (-6 and -4 mm Hg for both) and diastolic BPs (-4 mm Hg and -3 mm Hg, respectively) and did not affect the HR (-1 and -2 b.p.m respectively). Only the BIM device reduced the sympathetic nerve activity of the sample (-8 bursts min(-1)). In conclusion, both device-guided slow breathing and listening to calm music have decreased BP but only the device-guided slow breathing was able to reduce the peripheral sympathetic nerve activity.

Low-dose estrogen therapy does not change postexercise hypotension, sympathetic nerve activity reduction, and vasodilation in healthy postmenopausal women.

The aim of this study was to determine whether estrogen therapy enhances postexercise muscle sympathetic nerve activity (MSNA) decrease and vasodilation, resulting in a greater postexercise hypotension. Eighteen postmenopausal women received oral estrogen therapy (ET; n=9, 1 mg/day) or placebo (n=9) for 6 mo. They then participated in one 45-min exercise session (cycle ergometer at 50% of oxygen uptake peak) and one 45-min control session (seated rest) in random order. Blood pressure (BP, oscillometry), heart rate (HR), MSNA (microneurography), forearm blood flow (FBF, plethysmography), and forearm vascular resistance (FVR) were measured 60 min later. FVR was calculated. Data were analyzed using a two-way ANOVA. Although postexercise physiological responses were unaltered, HR was significantly lower in the ET group than in the placebo group (59+/-2 vs. 71+/-2 beats/min, P<0.01). In both groups, exercise produced significant decreases in systolic BP (145+/-3 vs. 154+/-3 mmHg, P=0.01), diastolic BP (71+/-3 vs. 75+/-2 mmHg, P=0.04), mean BP (89+/-2 vs. 93+/-2 mmHg, P=0.02), MSNA (29+/-2 vs. 35+/-1 bursts/min, P<0.01), and FVR (33+/-4 vs. 55+/-10 units, P=0.01), whereas it increased FBF (2.7+/-0.4 vs. 1.6+/-0.2 ml x min(-1) x 100 ml(-1), P=0.02) and did not change HR (64+/-2 vs. 65+/-2 beats/min, P=0.3). Although ET did not change postexercise BP, HR, MSNA, FBF, or FVR responses, it reduced absolute HR values at baseline and after exercise.