Previous studies demonstrate that exercise training improves endothelial function and provides protection against numerous cardiovascular diseases. SIRT1, a NAD‐dependent deacetylase, has recently been shown to increase eNOS activity and alter endothelium dependent relaxation. The purpose of this study is to examine SIRT1 and eNOS expression in rat aortas during the course of an exercise training program. 8–9 month‐old, male, Wistar rats were divided into four groups Sedentary (SED, n= 11), 1 day (1DY, n=12), 2 week (2WK, n=10), 6 week (6WK, n=8). Animals ran on a motor‐driven treadmill at 15 m/min, 15% grade for 40 min (1D) or increased up to 1 h at the end of 2 weeks (2WK) and sustained for an additional 4 weeks (6WK). Aorta SIRT1, eNOS, and GAPDH expression were evaluated by Western blot. Although there was a trend towards exercise‐induced increase in SIRT1 and eNOS expression, the results of this study did not indicate any significant differences in SIRT1 and eNOS expression at the various time points. Although previous studies have shown that vascular reactivity is altered during the course of an exercise training program including altered responses to SIRT1 inhibition, these data suggest that neither changes in SIRT1 expression or eNOS expression appear to play a role. Therefore, other mechanisms are likely involved in the exercise‐induced changes in vascular reactivity and altered responses to SIRT1 inhibition.

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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