Ascorbic acid does not influence skeletal muscle contraction‐induced rapid vasodilation in older healthy humans

Abstract

Age‐related increases in oxidative stress impair endothelium‐dependent vasodilation in humans, which could possibly explain our recent observations of blunted contraction‐induced rapid vasodilation in older adults. Therefore, we tested the hypothesis that endothelial dysfunction impairs the rapid vasodilator responses to brief muscle contractions in aging humans. In 13 young (24±1 yrs) and 13 healthy older adults (62±2 yrs), we measured forearm blood flow (FBF; Doppler ultrasound) and calculated vascular conductance (FVC) responses to single, 1 sec dynamic contractions at 10, 20, and 40% maximum voluntary contraction (MVC) before and after intra‐arterial administration of ascorbic acid (AA). Prior to AA, peak vasodilator responses to all contraction intensities were impaired ~35–50% in older adults (P<0.05), as were the immediate (1st cardiac cycle post contraction) vasodilator responses at 20 and 40% MVC (~50%; P<0.05). AA did not influence vasodilator responses to sodium nitroprusside in either group, but significantly improved vasodilation to acetylcholine in older adults only (P<0.05). In contrast, AA did not influence contraction‐induced rapid vasodilation in either group (all NS). Together, our findings suggest that endothelial dysfunction is not the primary mechanism underlying impaired contraction‐induced rapid vasodilation with human aging.Supported by AG‐027150