Four studies investigatied the phenomenon of post exercise hypotension in the human condition of pre (borderline)-hypertension.

Study one investigated the effects of an acute bout of 30-minutes upright cycling on postexercise haemodynamics and compared the results to a non-exercise control condition. Findings revealed that acute exercise is capable of sustained reductions in arterial pressure and vascular resistance beyond the usual labile fluctuations and that the octapeptide ANP may exert a modulatory influence over the post-exercise response.

Increases in O2 tension beyond the physiological range induces complex effects on the circulatory system with a dominant vasoconstriction following hyperoxia. The purpose of study 2 was to assess the effects of hypoxic (16% O2) and hyperoxic (50% O2) exercise on subsequent haemodynamic control when compared with normoxia. Results indicated that acute modest hyperoxia reflexively induces measurable physiological derangement partly explained by decreased circulating concentrations of ANP.

Study three determined the role of free-radical mediated oxidative stress and redox regulation of circulating NO. metabolism as a primary modulator of vascular tone following exercise in pre-hypertensive humans. The results demonstrate that augmented oxidative stress exerts a deleterious effect on post-exercise haemodynamics and implicates a potential redox regulation pathway of NO. as being a mechanism by which free radical-induced oxidative stress blunts the degree of PEH in the recovery period.

Study four investigated the potential role of a redox-mediated regulation of circulating NO. bioavailability as a modulator of the augmented vasoconstriction following hyperoxic exercise. The data demonstrated an effective endogenous antioxidant response and argues against a redox regulation pathway of NO. metabolism as a primary mediator of blunted vasodilatation in this scenario. This elucidates a more complex regulationof arterial tone, resulting from a metabolic pathway independent of NO. in older subjects with pre-hypertension.

This work demonstrates that (1) aerobic exercise exerts a hypotensive effect in humans with pre-hypertension, (2) ANP plays a part in the vasodilatation following exercise, (3) Free-radical mediated oxidative stress & subsequent modulation of NO. metabolism exerts a deleterious influence on post-exercise haemodynamics (4) Acute hyperoxic exercise induces a sustained vasoconstriction that is mediated via circulating ANP concentration but not by redox regulation of NO. metabolism.


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