Gender influence on post-resistance exercise hypotension and hemodynamics.

Post-resistance exercise hypotension has been extensively described in men and women. However, gender influence on this response has not yet been clear. Gender might change post-exercise hemodynamics, since men and women respond differently during exercise. Thus, the purpose was to compare post-resistance exercise hypotension and its hemodynamic determinants in men and women. Normotensive subjects (22-male, 22-female) underwent 2 sessions: control (40 min of rest) and exercise (6 resistance exercises, 3 sets, 20 repetitions, at 40-50% of 1RM). Blood pressure, heart rate, and cardiac output were measured prior to and following interventions. Blood pressure decrease after exercise was similar between the genders. However, hemodynamic determinants responded differently in men and women. Systemic vascular resistance reduced in women (-4.6±1.9U, P<0.05), while cardiac output decreased in men (-0.6±0.2 L/min, P<0.05). This response was accompanied by a decrease in stroke volume in men (-21.6±5.1 ml, P<0.05) and a more pronounced increase in heart rate in men than in women (+11.3±1.3 vs. +6.5±1.7 bpm, P<0.05, respectively). In conclusion, post-resistance exercise hypotension was similar in men and women. However, its hemodynamic determinants differ between the genders, depending on cardiac output decrease in men and on systemic vascular resistance decrease in women.

Post-resistance exercise hypotension, hemodynamics, and heart rate variability: influence of exercise intensity.

UNLABELLED: The occurrence of post-exercise hypotension after resistance exercise is controversial, and its mechanisms are unknown. To evaluate the effect of different resistance exercise intensities on post-exercise blood pressure (BP), and hemodynamic and autonomic mechanisms, 17 normotensives underwent three experimental sessions: control (C-40 min of rest), low- (E40%-40% of 1 repetition maximum, RM), and high-intensity (E80%-80% of 1 RM) resistance exercises. Before and after interventions, BP, heart rate (HR), and cardiac output (CO) were measured. Autonomic regulation was evaluated by normalized low- (LF(R-R)nu) and high-frequency (HF(R-R)nu) components of the R-R variability. In comparison with pre-exercise, systolic BP decreased similarly in the E40% and E80% (-6 +/- 1 and -8 +/- 1 mmHg, P < 0.05). Diastolic BP decreased in the E40%, increased in the C, and did not change in the E80%. CO decreased similarly in all the sessions (-0.4 +/- 0.2 l/min, P < 0.05), while systemic vascular resistance (SVR) increased in the C, did not change in the E40%, and increased in the E80%. Stroke volume decreased, while HR increased after both exercises, and these changes were greater in the E80% (-11 +/- 2 vs. -17 +/- 2 ml/beat, and +17 +/- 2 vs. +21 +/- 2 bpm, P < 0.05). LF(R-R)nu increased, while ln HF(R-R)nu decreased in both exercise sessions. IN CONCLUSION: Low- and high-intensity resistance exercises cause systolic post-exercise hypotension; however, only low-intensity exercise decreases diastolic BP. BP fall is due to CO decrease that is not compensated by SVR increase. BP fall is accompanied by HR increase due to an increase in sympathetic modulation to the heart.

Postexercise hypotension and hemodynamics: the role of exercise intensity.

AIM: Although postexercise hypotension (PEH) has already been extensively demonstrated, the influence of exercise intensity on its magnitude and mechanisms is still controversial. METHODS: Twenty-three normotensive subjects were submitted to a control (45 minutes of rest) and 3 exercise sessions (cycle ergometer, 45 minutes at 30%, 50% and 75% of .VO(2peak)) to investigate the role of exercise intensity on PEH. Blood pressure (BP - auscultatory), heart rate (HR - ECG), and cardiac output (CO - CO2 rebreathing) were measured before and after the control and exercise sessions. RESULTS: Systolic BP decreased significantly after exercise at 50% and 75% of .VO(2peak). Diastolic BP increased significantly during the control session, did not change after exercise at 30% of .VO(2peak), and decreased significantly after exercise at 50% and 75% of .VO(2peak). This fall was greater and longer after more intense exercise. CO and systemic vascular resistance (SVR) responses were similar between sessions, CO increased whereas SVR decreased significantly. Stroke volume (SV) increased and heart rate (HR) decreased following control and exercise at 30% of .VO(2peak) whereas SV decreased and HR increased after exercise at 50% and 75% of .VO(2peak). CONCLUSION: PEH is greater and longer after more intense exercise. BP profile is followed by a decrease in SVR and an increase in CO, what was not influenced by previous exercise. The increase in CO is caused by an increase in SV after rest and low intensity exercise and by an increase in HR after moderate and more intense aerobic exercise.