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Ascorbic acid increases muscle blood flow during dynamic exercise in older healthy humans
Author(s) -
Kirby Brett S,
Voyles Wyatt F,
Simpson Carrie B,
Carlson Rick E,
Schrage William G,
Dinenno Frank A
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1235.8
Subject(s) - medicine , vasodilation , brachial artery , ascorbic acid , sodium nitroprusside , endocrinology , endothelium , endothelial dysfunction , cardiology , blood flow , blood pressure , nitric oxide , chemistry , food science
Age‐related increases in oxidative stress impair endothelium‐dependent vasodilation in humans, leading many to speculate that endothelial dysfunction contributes to impaired muscle blood flow and vascular control during exercise in older adults. We directly tested this hypothesis in 13 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) 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. Prior to AA, FBF (∼28%) and FVC (∼31%) were lower in older vs young adults (P<0.05). 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). This increase in FBF and FVC during exercise in older adults was associated with improvements in vasodilator responses to acetylcholine (ACH; endothelium‐dependent) but not sodium nitroprusside (SNP; endothelium independent). AA had no effect on ACH or SNP responses in the young. We conclude that acute AA administration increases muscle blood flow during dynamic exercise in older adults, and this is likely due to an improvement in endothelium‐dependent vasodilation. Supported by AG‐027150