Acute ascorbic acid administration improves exercise hyperemia during rhythmic but not single contractions in aging humans
Simpson, Carrie Beth
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Age-related increases in oxidative stress are known to impair endothelium dependent vasodilation in older healthy humans. As a result, many researchers have speculated that endothelial dysfunction contributes to impaired muscle blood flow and vascular control during exercise. Further, elevations in oxidative stress and subsequent endothelial dysfunction could possibly explain our recent observations of impaired contraction-induced rapid vasodilation in older adults. Therefore, we directly tested the hypothesis that acute ascorbic acid administration would augment (1) rapid vasodilation in response to single muscle contractions as well as (2) the hyperemic response to sustained rhythmic contractions in older healthy humans, and that this would be due to improved endothelium-dependent vasodilation. In 14 young (22±1 yrs) and 14 healthy older men and women (65±2 yrs), we measured forearm blood flow (FBF; Doppler ultrasound) and calculated vascular conductance (FVC) responses to single, 1 second dynamic contractions at 10, 20, and 40% maximum voluntary contraction (MVC) before and after intra-arterial administration of ascorbic acid (AA). We also measured these variables during rhythmic handgrip exercise at 10% maximum voluntary contraction. After 5 minutes of steady-state exercise with saline, ascorbic acid (AA) was infused via brachial artery catheter for 10 minutes during continued exercise. For single contractions, 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). In contrast to our hypothesis, AA did not influence contraction-induced rapid vasodilation in either group (all NS). Regarding rhythmic handgrip exercise, FBF (~28%) and FVC (~31%) were lower in older vs young adults (P=0.06 and P<0.05) prior to AA. In young adults, AA administration did not significantly influence FBF and FVC, whereas FBF and FVC increased 30±4% in older adults at end exercise (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). We conclude that endothelial dysfunction is not the primary mechanism underlying impaired contraction-induced rapid vasodilation with human aging; however acute AA administration increases muscle blood flow during dynamic exercise in older adults, which is likely due to an improvement in endothelium dependent vasodilation.