Impact of sympathetic nervous system activity on post-exercise flow-mediated dilatation 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% HR(max). Prior to exercise, individuals ingested either a placebo or an α1-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, P = 0.03). In contrast, FMD increased (37%) immediately following exercise in the prazosin condition (t-test, P = 0.004, interaction effect P = 0.01). Post-exercise FMD remained different between conditions after correction for baseline diameters preceding cuff deflation and also post-deflation SR. No differences in FMD or other variables were evident 60 min following recovery. Our results indicate that sympathetic vasoconstriction competes with endothelium-dependent dilator activity to determine post-exercise arterial function. These findings have implications for understanding the chronic impacts of interventions, such as exercise training, which affect both sympathetic activity and arterial shear stress.

© 2015 The Authors. The Journal of Physiology © 2015 The Physiological Society.

Figures

Figure 1. Mean arterial pressure (MAP), heart rate (HR), stroke volume (SV), cardiac output (CO) and total peripheral resistance index (TPRi) across 30 min of cycle exercise at 75% HRmax

Grey squares denote ‘Placebo’ condition and black squares denote ‘prazosin’ condition. Error bars represent SEM. Statistical significance was assumed at P ≤ 0.05; #statistical significance between conditions. (NB: subjects were exercised at a target HR of 75%HRmax, resulting in mean workloads of 161 ± 16 W in the placebo condition and 140 ± 20 W in the prazosin condition.)

Figure 2. Mean, antegrade and retrograde shear rate (SR) comparisons across 30 min of cycle exercise at 75% HRmax under ‘Placebo’ (grey squares) and ‘prazosin’ (black squares)

Error bars represent SEM. Statistical significance was assumed at P ≤ 0.05; #statistical significance between conditions. (NB: subjects were exercised at a target HR of 75%HRmax, resulting in mean workloads of 161 ± 16 W in the placebo condition and 140 ± 20 W in the prazosin condition.)

Figure 3. Blood flow, conductance, brachial artery velocity and arterial diameter across 30 min of cycle exercise at 75% HRmax under ‘Placebo’ (grey squares) and ‘prazosin’ (black squares)

Error bars represent SEM. Statistical significance was assumed at P ≤ 0.05; #statistical significance between conditions. (NB: subjects were exercised at a target HR of 75%HRmax, resulting in mean workloads of 161 ± 16 W in the placebo condition and 140 ± 20 W in the prazosin condition.)

Figure 4. Brachial artery flow‐mediated dilatation (FMD) prior to, immediately post and 60 min following 30 min cycle exercise at 75%HRmax

A, placebo condition (grey bars); B, prazosin condition (black bars). Error bars represent SEM. Statistical significance was assumed at P ≤ 0.05; *statistical significance from ‘Pre’ value. (NB: subjects were exercised at a target HR of 75%HRmax, resulting in mean workloads of 161 ± 16 W in the placebo condition and 140 ± 20 W in the prazosin condition.)