We previously reported that a single bout of dynamic exercise induces a sustained post-exercise vasodilatation independent of enhanced circulating NO bioavailability (New et al, 2008). Recent evidence however points to reactive oxygen species as important mediators of angiotensin ΙΙ (ANG ΙΙ) induced vascular dysfunction (Pena-Silver & Heistad, 2010). The present study therefore investigated the influence of exercise-induced increases in ANG II on circulating biomarkers of oxidative stress and concomitant post-exercise haemodynamics. 9 older males, MAP = 106 ± 5 mmHg (50 ± 10 yr), not on medication, were studied following 30-minutes of cycle exercise at 70% maximal oxygen consumption. Subjects were followed post-exercise for 2-hours. Left ventricular haemodynamics were assessed via echocardiography and systemic vascular resistance (SVR)/vascular conductance (SVC) determined by the quotient of MAP/Q and Q/MAP, respectively. Peripheral venous blood was sampled from an antecubital vein pre-, immediately post-, 1-hour post- (P1) and 2-hours post- (P2) exercise and metabolite concentrations corrected for plasma volume shifts. ANG ΙΙ concentrations were determined in venous plasma, following an extraction procedure, via a double-antibody radioimmunoassay. Indirect markers of oxidative stress were determined spectrophotometrically detecting lipid hydroperoxides (LOOH) whilst blood was also assayed for selective antioxidants by HPLC. Data were analysed with a repeated measures ANOVA and post-hoc Bonferroni-corrected paired samples T-tests. Exercise decreased SVR whilst concomitantly elevating ANG ΙΙ and LOOH concentration (Table 1) (P<0.05; Paired samples T-tests). The lowered systemic vascular resistance post-exercise transcended into a mean arterial pressure reduction of ~5mmHg (P<0.05; Paired samples T-tests). These results indicate that attenuated vascular resistance following exercise occurs despite increases in ANG ΙΙ and oxidative stress and that increased oxidative stress may follow elevated ANG ΙΙ in the exercising human. A profound vasodilatory mechanism capable of buffering powerful vasoconstriction exists mediating the exercise-induced hyperaemia.