Experimental studies investigating the effects of exercise on plasma total homocyst(e)ine (H[e]) levels in humans are almost non-existent. H(e) has been demonstrated to represent an independent risk factor for cardiovascular disease. The exact mechanism through which H(e) exerts its effects on the arteries is unknown but it is thought to involve nitric oxide (NO). The present study was designed to assess the effects of acute submaximal exercise on H(e) while levels of NO inhalation were manipulated using an air-filter mask. The study was completed by seven male volunteers, aged 21.6 ± 1.3 yr (X¯ ± SD), V˙O2max: 48.6 ± 7.6 mL × kg−1 × min−1. During two separate occasions the subjects performed a 1-hour bout of submaximal exercise on a stationary cycle ergometer at 60 % of their V˙O2max. The two trials were completed in random order (with and without mask). Data were collected before (PRE) and after (POST) the acute exercise bouts. Plasma H(e) was directly measured by HPLC and NO by quantifying the enzymatic oxidation to nitrite (NO2−) & nitrate (NO3−). Mean H(e) concentrations were 10.89 ± 2.05 nmol/mL (PRE) & 11.21 ± 1.81 nmol/mL (POST) and were not significantly altered by submaximal exercise. When wearing a mask, the correlation of the PRE/POST H(e) differences with the PRE/POST differences in NO3− were 0.77 (P = 0.07). No correlation was found between either H(e) and NO2− or between NO2− and NO3−. However, a significant correlation (r = − 0.86, P = 0.03) was also observed between H(e) and NO2− but only for the post-exercise values when wearing a mask. The results suggest that: (1) plasma H(e) levels are not affected by acute submaximal exercise; (2) there is insufficient evidence to support the view that plasma H(e) levels are being mediated by NO during either rest or exercise.
01 Presented in part at the 46th Annual Meeting of the American College of Sports Medicine, Seattle, WA, June 2 to 5, 1999 (Session C-32).
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