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Improvement in exercise hyperemia via ascorbic acid in older healthy adults: role for nitric oxide?
Author(s) -
Crecelius Anne R,
Voyles Wyatt F,
Dumke Breanna R,
Davis Julia A,
Kirby Brett S,
Dinenno Frank A
Publication year - 2009
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.23.1_supplement.777.1
Subject(s) - medicine , vasodilation , nitric oxide , ascorbic acid , brachial artery , saline , blood flow , cyclooxygenase , reactive hyperemia , nitric oxide synthase , forearm , endothelium , endocrinology , anesthesia , blood pressure , chemistry , surgery , biochemistry , food science , enzyme
Acute ascorbic acid (AA) administration increases muscle blood flow during dynamic exercise in older adults, and this is associated with improved endothelium‐dependent vasodilation. Here, we test the hypothesis that the increase in muscle blood flow during AA administration is independently mediated via the endothelium‐dependent vasodilators nitric oxide (NO) and prostaglandins (PGs). In 7 healthy older adults (64±3 yrs), we measured forearm blood flow (FBF; Doppler ultrasound) during rhythmic handgrip exercise at 10% maximum voluntary contraction. After 5 minutes of steady‐state exercise with saline, AA was infused via brachial artery catheter for 10 minutes during continued exercise, and this increased FBF ~23% from 126±20 to 154±22 ml/min (P<0.05). AA was infused for the remainder of the study. Next, subjects performed a 15 minute exercise bout where AA + saline was infused for 5 minutes, followed by 5 minutes of the NO synthase inhibitor L‐NMMA, and then 5 minutes of the cyclooxygenase inhibitor ketorolac. NOS inhibition reduced steady‐state FBF by ~19% (P <0.05) and FBF was no longer different than control exercise (118±16 ml/min). PG inhibition did not change FBF (Δ = 4±6%). Our preliminary data indicate that the increase in muscle blood flow during dynamic exercise during acute AA administration in older adults is mediated primarily via an endothelial NO‐dependent mechanism. Supported by AG‐027150