Effects of hyperoxic exercise on post-exercise haemodynamis and redox regulation of circulating NO bioavailability in Man.

The detrimental effects of hyperoxia on haemodynamics have been shown to persist for some time following return to normoxia (Warring et al, 2003; Thomson et al, 2006). The present study sought to determine the role of a redox-mediated regulation of circulating Nitric Oxide (NO) bioavailability as a mediator of the underlying augmented vasoconstriction following hyperoxic exposure. To examine this hypothesis, 9 pre-hypertensive males, mean arterial pressure (MAP) = 106 (mean) ± 5 (SD) mmHg (50 ± 10 yr), not on medication, were studied following 30-minutes of cycle exercise at 70% normoxic maximal oxygen consumption in hyperoxia (50% O2) and normoxia (21% O2). Echocardiography determined cardiac output (Q) and systemic vascular resistance (SVR) was computed by the quotient of MAP and Q. Venous blood was sampled from an antecubital vein pre-, immediately post-, 1-hour post- (P1) and 2-hours post- (P2) exercise and corrected for plasma volume shifts. Plasma nitrate (NO-3) and nitrite (NO-2) was determined fluorometrically, whilst S-Nitrosothiol (RSNO) concentrations were assayed by the Saville reaction Indirect markers of oxidative stress were determined spectrophotometrically detecting lipid hydroperoxides (LOOH). In conclusion, our results indicate that hyperoxic exercise has a deleterious effect on post-exercise haemodynamics and do not support a role for a redox-mediated regulation of circulating NO bioavailability as being a principle governor of the attenuated vasodilatation following hyperoxic exercise. This suggests that the vasoconstriction is resultant from a metabolic pathway independent of NO.