The detrimental effects of hyperoxia on haemodynamics have been shown to persist for some time following return to normoxia (Waring 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 & 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) were 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). Hyperoxic exercise blunted post-exercise haemodynamics by significantly attenuating the reductions (from normoxic baseline) in SVR (21 ± 20.7 vs. 38 ± 19.3 %, 11 ± 8.2 vs. 19 ± 5.5 % and 11 ± 8.9 vs. 15 ± 9.6%, P<0.05 vs. normoxic exercise at post, P1 and P2 respectively) and MAP (3 ± 4 [elevation] vs. 0.5 ± 5 mmHg, 3 ± 3 vs. 6 ± 4 mmHg, 3 ± 3 vs. 4 ± 3 mmHg, P<0.05 vs. normoxic exercise at post, P1 and P2 respectively) (Paired samples T-tests). Indices of NO metabolism, total plasma NO and LOOH failed to differ between conditions (P>0.05, Paired samples T-tests; Table 1). 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.