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Indexed/Abstracted in: Chemical Abstracts, CINAHL, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,111
Online ISSN 1827-1928
Forjaz C. L. M., Cardoso C. G. Jr, Rezk C. C., Santaella D. F., Tinucci T.
School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil
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 V.O2peak) 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 V.O2peak. Diastolic BP increased significantly during the control session, did not change after exercise at 30% of V.O2peak, and decreased significantly after exercise at 50% and 75% of V.O2peak. 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 V.O2peak whereas SV decreased and HR increased after exercise at 50% and 75% of V.O2peak.
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.