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1994 Publications

Venous Nitric Oxide Metabolites Decrease in Highly Trained Endurance Athletes During Maximal Exerciseby Gilbert W. Gleim, Guillermo A. Zeballos, Beth W. Glace, Gabor Kaley, Thomas H. HintzeLenox Hill Hospital, New York, NY and New York Medical College, Valhalla, NY - last modified 2013-02-09 00:00
Circulation, Vol. 90, No. 4, Part 2, October 1994


Exercise training in animals enhances (1) endothelium-mediated dilation of epicardial coronary arteries, (2) coronary vascular nitric oxide (NO) production, (3) endothelial cell NO synthase gene expression, and (4) endothelial synthesis of NO induced by acetylcholine in skeletal muscle arterioles.

We hypothesized that highly trained human subjects adapt similarly to chronic exercise and that NO metabolites of total nitrates/nitrites would be elevated during exercise. Therefore, 8 highly trained endurance athletes (3 women, 5 men, aged 31 +/- 3 years, VO2max = 71.2 +/- 3.9 ml O2/kg/min) had antecubital vein blood sampled pre and post maximal exercise and 5 of these athletes were also sampled following 10 minutes of exercise at 60 and 75% VO2max.

The NO metabolites, total nitrates/nitrites (uM), were measured by chemiluminescence. Resting lactate (mM) was .93 +/- .13, and increased to 8.15 +/- .47 (p < .001) at maximum while NO metabolites decreased from 28.2 +/- 5.0 to 7.1 +/- 2.5 (p < .001).

No significant change in NO metabolites occurred with submaximal exercise (48.0 +/- 10.0 and 43.0 +/- 7.3) despite modest elevations (p < .05) in lactate (2.16 +/- .50 and 2.22. +/- .25, respectively).

If the reduction in nitrate/nitrite is not a result of altered NO disposal, these data suggest that NO production is not acutely associated with the high flow rates of maximal exercise in humans.