Abstract

Acute endurance exercise impairs endothelial dependent dilation whereas chronic endurance exercise improves endothelial dependent dilation which may be related to changes in redox status. The purpose of this study is to determine whether vitamin E supplementation alters endothelium dependent vasorelaxation in response to acute and chronic endurance exercise. 8–9 month‐old, male, Wistar rats were divided into six groups (n=10–12/group): sedentary (S), 1 day (1C), 1 day + vitamin E (1DE), 2 week (2WK), 2 week + vitamin E (2WKE), 6 week (6C), and 6 week + vitamin E (6WKE). Rats ran on a motor‐driven treadmill at 15 m/min, 15% grade for 40 min (1D) increasing up to 1 h by 2 weeks (2WK) and sustained for an additional 4 weeks (6WK). Aortic dose response curves to phenylephrine (PE, 10−7–10−4 M), sodium nitroprusside (SNP, 10−8–10−5 M), and acetylcholine (ACh, 10,−7–3×10−5 M) were constructed. Acute (1 day) endurance exercise significantly impaired Ach‐induced vasorelaxation in aortas which was attenuated by vitamin E supplementation. Chronic exercise (2WK and 6WK) with or without vitamin E supplementation resulted in no significant changes in vascular function. eNOS expression was significantly increased in all exercise groups regardless of supplementation. These data suggest acute exercise impairs endothelium dependent relaxation through oxidative stress which can be attenuated by vitamin E supplementation.

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