Interactions between homocyst(e)ine and nitric oxide during acute submaximal exercise in adult males

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 be en demonstrated to represent an independent risk factor for cardiovascular disease. The exact mechanism through which H(e) exerts its effects on the a rteries is unknown but it is thought to involve nitric oxide (NO). The pres ent study was designed to assess the effects of acute submaximal exercise o n H(e) while levels of NO inhalation were manipulated using an air-filter m ask. The study was completed by seven male volunteers, aged 21.6 +/- 1.3 yr ((x) over bar +/- SD), (V)over dot O(2)max: 48.6 +/- 7.6 mL x kg(-1) x 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)ove r dot O(2)max. The two trials were completed in random order (with and with out mask). Data were collected before (PRE) and after (POST) the acute exer cise bouts. Plasma H(e) was directly measured by HPLC and NO by quantifying the enzymatic oxidation to nitrite (NO2-) & nitrate (NO3-). Mean H(e) conc entrations were 10.89 +/- 2.05 nmol/ mt (PRE) & 11.21 +/- 1.81 nmol/mL (POS T) 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 corr elation (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 sobmaximal exercise; (2) there is insufficient evidence to support the view that plasma H(e) le vels are being mediated by NO during either rest or exercise.