Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.494060
Title: Exercise, arterial pressure control and systemic 0₂ tension : implications for post exercise hypotension in hypertension
Author: New, Karl James
ISNI:       0000 0001 3442 9057
Awarding Body: University of Glamorgan
Current Institution: University of South Wales
Date of Award: 2008
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Abstract:
This thesis presents four studies investigating 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 post-exercise haemodynamics and compared the results to a non-exercise control condition. This research reveals 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. 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. The findings indicate 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 indicate 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. The first study 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 demonstrate 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 regulation of arterial tone, resulting from a metabolic pathway independent of NO* in older subjects with pre-hypertension.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.494060  DOI: Not available
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