Cardiorespiratory fitness modulates the acute flow-mediated dilation response following high-intensity but not moderate-intensity exercise in elderly men

Impaired endothelial function is observed with aging and in those with low cardiorespiratory fitness (V̇o_2peak). Improvements in endothelial function with exercise training are somewhat dependent on the intensity of exercise. While the acute stimulus for this improvement is not completely understood, it may, in part, be due to the flow-mediated dilation (FMD) response to acute exercise. We examined the hypothesis that exercise intensity alters the brachial (systemic) FMD response in elderly men and is modulated by V̇o_2peak. Forty-seven elderly men were stratified into lower (V̇o2peak = 24.3 ± 2.9 ml·kg−1·min−1; n = 27) and higher fit groups (V̇o_2peak = 35.4 ± 5.5 ml·kg−1·min−1; n = 20) after a test of cycling peak power output (PPO). In randomized order, participants undertook moderate-intensity continuous exercise (MICE; 40% PPO) or high-intensity interval cycling exercise (HIIE; 70% PPO) or no-exercise control. Brachial FMD was assessed at rest and 10 and 60 min after exercise. FMD increased after MICE in both groups {increase of 0.86% [95% confidence interval (CI), 0.17–1.56], P = 0.01} and normalized after 60 min. In the lower fit group, FMD was reduced after HIIE [reduction of 0.85% (95% CI, 0.12–1.58), P = 0.02] and remained decreased at 60 min. In the higher fit group, FMD was unchanged immediately after HIIE and increased after 60 min [increase of 1.52% (95% CI, 0.41–2.62), P < 0.01, which was correlated with V̇o_2peak, r = 0.41; P < 0.01]. In the no-exercise control, FMD was reduced in both groups after 60 min (P = 0.05). Exercise intensity alters the acute FMD response in elderly men and V̇o_2peak modulates the FMD response following HIIE but not MICE. The sustained decrease in FMD in the lower fit group following HIIE may represent a signal for vascular adaptation or endothelial fatigue.