Dietary arginine supplementation speeds pulmonary VO2 kinetics during cycle exercise

To test the hypothesis that L-arginine (the substrate for nitric oxide synthase [NOS]) administration slows the VO2 kinetics at the onset of moderate-intensity exercise in humans.

Seven physically active males were randomly assigned to receive either placebo (lactose) or L-arginine hydrochloride capsules (7.2 g x d(-1)) for 14 d in a double-blind crossover design, with a 7-d washout period between the two conditions. On day 11 and day 14 of each condition, the subjects completed two consecutive 6-min bouts of cycle exercise at 80% of the ventilatory threshold with a 12-min rest interval. VO2 was measured on a breath-by-breath basis, and VO2 kinetics were determined with a single exponential model from the averaged data derived from four repetitions. Capillary and venous blood samples were taken to determine plasma [La] and serum [arginine], respectively.

There were no differences in circulating lactate either before or during exercise. However, serum [arginine] was higher (P < 0.05) in the arginine condition at rest (119.0 +/- 12.6 vs 103.6 +/- 15.7 micromol x L(-1) in the control condition) and after exercise (113.3 +/- 26.0 vs 103.8 +/- 12.6 micromol x L(-1) in the control condition). With regard to the pulmonary VO2 kinetics, no significant difference was observed in the time at which the phase II response emerged or in the phase II amplitude between the two conditions. However, contrary to our hypothesis, the time constant was significantly reduced after arginine administration (i.e., 13.9 +/- 3.1 vs 15.8 +/- 2.6 s in the control condition, P < or = 0.014).

Exogenous L-arginine administration speeds the phase II pulmonary VO2 response by 12% at the onset of moderate-intensity exercise in humans.