Abstract
Evidence indicates that chronic reduction in blood pressure (BP) due to physical exercise depends on the acute decrease in BP after a training bout, phenomenon referred as post-exercise hypotension (PEH). This study reviews research on PEH after acute aerobic, strength and concurrent exercise and its potential underlying mechanisms. The PEH has been observed following different exercise modalities in both normotensive and hypertensive subjects. However, the optimal dose of aerobic exercise [i.e. relationship between intensity, duration, mode and form of execution] and strength training [i.e. relationship between intensity, volume and muscle mass involved] to maximize its occurrence remains unclear. Questions also persist with regard to the physiological pathways of PEH, which seem to be different in strength and aerobic exercise. Central and local mechanisms associated to decreased cardiac output (CO) and peripheral vascular resistance (PVR) are frequently mentioned in the literature. Mechanisms underlying PEH after aerobic exercise seemto include both central [i.e. decreased activity sympathetic nerve] and peripheral factors[i.e. vasodilation sustained by nitric oxide releasing, prostaglandins and histamine receptors]. On the other hand, after strength or concurrent training, the PEH seems to bemostly related to a decrease in CO and systolic volume, in response to a decrease in myocardial perfusion during exercise due to compression of vessels by sequential muscle contraction.
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