Hemodynamic and vascular response to resistance exercise with L-arginine

L-arginine, the precursor to nitric oxide (NO), has been shown to improve endothelial function in patients with endothelial dysfunction. Resistance exercise has been shown to increase arterial stiffness acutely with no definitive cause. It is possible that a reduction in NO bioavailability is responsible for this. The purpose of this study was to examine the effect of acute L-arginine supplementation and resistance exercise on arterial function.

Eighteen (N = 18) young men (24.2 +/- 0.7 yr) volunteered for this study. In a crossover design, subjects underwent body composition testing, 1-repetition maximum testing for the bench press and the biceps curls and performed two acute bouts of resistance exercise in which they consumed either placebo or 7 g L-arginine before each resistance exercise bout. Anthropometric measures, augmentation index (AIx), arterial stiffness, and forearm blood flow (FBF) were assessed before and after each treatment condition.

There were significant (P < 0.05) time effects after the resistance exercise; there was a reduction in brachial stiffness (P = 0.0001), an increase in central aortic stiffness (P = 0.004), an increase in AIx (P = 0.023), an increase in FBF (P = 0.000), and an increase in arm circumference (P = 0.0001) after exercise.

The increase in central arterial stiffness and wave reflection was not attenuated by acute supplementation with L-arginine; furthermore, blood flow was not augmented with supplementation. On the basis of these data, l-arginine does not appear to change the hemodynamic and vascular responses to resistance exercise.