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Item does not contain fulltext, KEY POINTS: Previous studies indicate a transient reduction in arterial function following large muscle group exercise, but the mechanisms involved are unknown. Sympathetic nervous system activation may contribute to such reductions through direct effects in the artery wall, or because of decreases in arterial shear stress. Administration of prazosin (an alpha1 -adrenoreceptor blocker) abolished the transient reduction in vascular function observed under placebo conditions following exercise. This effect could not be explained by drug-induced changes in arterial shear stress. These results suggest that sympathetic vasoconstriction directly competes with endothelium-dependent dilator activity to influence post-exercise vascular function. These findings have implications for understanding the stimuli responsible for exercise-induced adaptations in arterial function and health in humans. ABSTRACT: Transient reduction in vascular function following systemic large muscle group exercise has previously been reported in humans. The mechanisms responsible are currently unknown. We hypothesised that sympathetic nervous system activation, induced by cycle ergometer exercise, would contribute to post-exercise reductions in flow-mediated dilatation (FMD). Ten healthy male subjects (28 +/- 5 years) undertook two 30 min sessions of cycle exercise at 75% HRmax . Prior to exercise, individuals ingested either a placebo or an alpha1 -adrenoreceptor blocker (prazosin; 0.05 mg kg(-1) ). Central haemodynamics, brachial artery shear rate (SR) and blood flow profiles were assessed throughout each exercise bout and in response to brachial artery FMD, measured prior to, immediately after and 60 min after exercise. Cycle exercise increased both mean and antegrade SR (P < 0.001) with retrograde SR also elevated under both conditions (P < 0.001). Pre-exercise FMD was similar on both occasions, and was significantly reduced (27%) immediately following exercise in the placebo condition (t-test

Item does not contain fulltext, KEY POINTS: Previous studies indicate a transient reduction in arterial function following large muscle group exercise, but the mechanisms involved are unknown. Sympathetic nervous system activation may contribute to such reductions through direct effects in the artery wall, or because of decreases in arterial shear stress. Administration of prazosin (an alpha1 -adrenoreceptor blocker) abolished the transient reduction in vascular function observed under placebo conditions following exercise. This effect could not be explained by drug-induced changes in arterial shear stress. These results suggest that sympathetic vasoconstriction directly competes with endothelium-dependent dilator activity to influence post-exercise vascular function. These findings have implications for understanding the stimuli responsible for exercise-induced adaptations in arterial function and health in humans. ABSTRACT: Transient reduction in vascular function following systemic large muscle group exercise has previously been reported in humans. The mechanisms responsible are currently unknown. We hypothesised that sympathetic nervous system activation, induced by cycle ergometer exercise, would contribute to post-exercise reductions in flow-mediated dilatation (FMD). Ten healthy male subjects (28 +/- 5 years) undertook two 30 min sessions of cycle exercise at 75% HRmax . Prior to exercise, individuals ingested either a placebo or an alpha1 -adrenoreceptor blocker (prazosin; 0.05 mg kg(-1) ). Central haemodynamics, brachial artery shear rate (SR) and blood flow profiles were assessed throughout each exercise bout and in response to brachial artery FMD, measured prior to, immediately after and 60 min after exercise. Cycle exercise increased both mean and antegrade SR (P < 0.001) with retrograde SR also elevated under both conditions (P < 0.001). Pre-exercise FMD was similar on both occasions, and was significantly reduced (27%) immediately following exercise in the placebo condition (t-test

Item does not contain fulltext, KEY POINTS: Previous studies indicate a transient reduction in arterial function following large muscle group exercise, but the mechanisms involved are unknown. Sympathetic nervous system activation may contribute to such reductions through direct effects in the artery wall, or because of decreases in arterial shear stress. Administration of prazosin (an alpha1 -adrenoreceptor blocker) abolished the transient reduction in vascular function observed under placebo conditions following exercise. This effect could not be explained by drug-induced changes in arterial shear stress. These results suggest that sympathetic vasoconstriction directly competes with endothelium-dependent dilator activity to influence post-exercise vascular function. These findings have implications for understanding the stimuli responsible for exercise-induced adaptations in arterial function and health in humans. ABSTRACT: Transient reduction in vascular function following systemic large muscle group exercise has previously been reported in humans. The mechanisms responsible are currently unknown. We hypothesised that sympathetic nervous system activation, induced by cycle ergometer exercise, would contribute to post-exercise reductions in flow-mediated dilatation (FMD). Ten healthy male subjects (28 +/- 5 years) undertook two 30 min sessions of cycle exercise at 75% HRmax . Prior to exercise, individuals ingested either a placebo or an alpha1 -adrenoreceptor blocker (prazosin; 0.05 mg kg(-1) ). Central haemodynamics, brachial artery shear rate (SR) and blood flow profiles were assessed throughout each exercise bout and in response to brachial artery FMD, measured prior to, immediately after and 60 min after exercise. Cycle exercise increased both mean and antegrade SR (P < 0.001) with retrograde SR also elevated under both conditions (P < 0.001). Pre-exercise FMD was similar on both occasions, and was significantly reduced (27%) immediately following exercise in the placebo condition (t-test