Oral estrogen therapy may mitigate the effects of aerobic training on cardiorespiratory fitness in postmenopausal women: a double-blind, randomized clinical pilot study.

OBJECTIVE: The aim of this study was to evaluate the isolated and associated effects of oral estrogen therapy and aerobic training on cardiorespiratory fitness in postmenopausal women. METHODS: Forty-two hysterectomized healthy postmenopausal women were randomly divided (in a double-blind manner) into four groups: placebo-control (n = 9), estrogen therapy-control (n = 12), placebo-aerobic training (PLA-AT; n = 11), and estrogen therapy-aerobic training (ET-AT; n = 10). The estrogen therapy groups received estradiol valerate (1 mg/day) and the aerobic training groups trained on a cycle ergometer three times per week at moderate intensity. Before and 6 months after the interventions, all women underwent a maximal cardiopulmonary exercise test on a cycle ergometer. RESULTS: Regardless of hormone therapy, aerobic training increased oxygen uptake at anaerobic threshold (P = 0.001), oxygen uptake at respiratory compensation point (P = 0.043), and oxygen uptake at peak exercise (P = 0.020). The increases at respiratory compensation point and peak exercise were significantly greater in the groups receiving placebo than in the groups receiving estrogen (oxygen uptake at respiratory compensation point: PLA-AT +5.3 [2.8] vs ET-AT +3.0 [2.5] mL kg(-1) min(-1), P = 0.04; oxygen uptake at peak exercise: PLA-AT +5.8 [3.4] vs ET-AT +2.8 [1.4] mL kg(-1) min(-1), P = 0.02). CONCLUSIONS: Oral estrogen therapy may mitigate the cardiorespiratory fitness increase induced by aerobic training in hysterectomized healthy postmenopausal women.

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.

Aerobic training abolishes ambulatory blood pressure increase induced by estrogen therapy: a double blind randomized clinical trial.

Emerging data reveal that oral estrogen therapy can increase clinic blood pressure (BP) in post-menopausal women; however, it is important to establish its effects on ambulatory BP, which is a better predictor for target-organ damage. Besides estrogen therapy, aerobic training is widely recommended for post-menopausal women, and it can decrease ambulatory BP levels. This study was designed to evaluate the effect of aerobic training and estrogen therapy on the ambulatory BP of post-menopausal women. Forty seven healthy hysterectomized women were randomly divided (in a double-blind manner) into 4 groups: placebo-control (PLA-CO=12), estrogen therapy-control (ET-CO=14), placebo-aerobic training (PLA-AT=12), and estrogen therapy-aerobic training (ET-AT=09). The ET groups received estradiol valerate (1 mg/day) and the AT groups performed cycle ergometer, 3×/week at moderate intensity. Hormonal status (blood analysis), maximal cardiopulmonary exercise test (VO(2) peak) and ambulatory BP (24-h, daytime and nighttime) was evaluated before and 6 months after interventions. A significant increase in VO(2) peak was observed only in women who participated in aerobic training groups (+4.6±1.0 ml kg(-1) min(-1), P=0.00). Follicle-stimulating hormone was a significant decreased in the ET groups (-18.65±5.19 pg/ml, P=0.00), and it was accompanied by an increase in circulating estrogen (56.1±6.6 pg/ml). A significant increase was observed in the ET groups for daytime (P=0.01) and nighttime systolic BP (P=0.01), as well as nighttime diastolic BP (P=0.02). However, daytime diastolic BP was increased only in the ET-CO group (+3.4±1.2 mmHg, P=0.04), and did not change in any other groups. No significant effect was found in ambulatory heart rate. In conclusion, aerobic training abolished the increase of daytime ambulatory BP induced by estrogen therapy in hysterectomized, healthy, normotensive and postmenopausal women.

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.

Neurovascular and hemodynamic responses to hyperinsulinemia in healthy postmenopausal women.

Acute hyperinsulinemia produces sympathetic activation, vasodilation, and cardiovascular changes in healthy young men. Postmenopausal period is accompanied by sympathetic, vascular and cardiovascular changes. Nevertheless, the effects of acute insulin infusion were not known in postmenopausal women. To study this aspect, 26 postmenopausal healthy women were submitted to an euglycemic hyperinsulinemic clamp performed during 120 min. Heart rate (HR: ECG), blood pressure (BP: oscillometric method), forearm blood flow (FBF: plethysmography), plasma norepinephrine (NE), plasma epinephrine (EP), and cardiovascular autonomic modulation (spectral analysis of R-R interval and BP variabilities) were measured before and during the clamp. Glycemia was kept similar to baseline during the clamp (84.6+/-1.2mg/dl versus 87.1+/-1.6 mg/dl), while plasma insulin increased significantly to a level of 89.3+/-5.6 microU/ml. Insulin infusion significantly increased plasma NE (+45+/-17 pg/ml), EP (+20+/-9 pg/ml), and low to high frequency ratio of R-R interval variability (LH/HF: 1.2+/-0.4), but did not change low frequency component of BP variability. FBF (+0.7+/-0.2 ml min(-1)100ml(-1)) was also significantly enhanced by hyperinsulinemia. HR and systolic BP increased with insulin infusion (+4+/-1 bat/min and +6+/-2 mmHg, respectively, P<0.05), while diastolic BP did not change. In conclusion, in healthy postmenopausal women, acute hyperinsulinemia produces sympathetic activation, and vasodilation, which results in HR and systolic BP enhancements, with no change in diastolic BP. This pattern of response is similar to the one usually observed in healthy young men.