Role of nitric oxide in exercise-induced vasodilation of the forearm.

We wished to determine the role of NO in exercise-induced metabolic forearm vasodilation. Young healthy volunteers (n = 11) underwent static handgrip exercise (4 to 5 kg, 3 minutes). Forearm blood flow (FBF) measured by strain plethysmography increased from 4.1 +/- 0.7 mL.min-1.100 mL-1 at rest to 9.8 +/- 1.2 mL.min-1.100 mL-1 immediately after exercise and gradually decreased thereafter. Exercise was repeated after intrabrachial artery infusion of NG-monomethyl-L-arginine (L-NMMA) at 4.0 mumol/min for 5 minutes. L-NMMA did not alter blood pressure and heart rate. L-NMMA decreased FBF at rest to 2.9 +/- 0.4 mL.min-1.100 mL-1 (P < .01), peak FBF immediately after exercise to 7.2 +/- 0.7 mL.min-1.100 mL-1 (P < .01), and FBF during the mid to late phase of metabolic vasodilation (P < .01). Calculated oxygen consumption during peak exercise was comparable before and after L-NMMA. Intra-arterially infused L-arginine (10 mg/min, 5 minutes) reversed the inhibitory effect of L-NMMA. To determine the effect of the decrease in resting FBF on exercise-induced hyperemia, we normalized FBF after exercise by resting FBF. The percent increases in FBF after exercise from resting FBF were similar before and after L-NMMA. Furthermore, we examined the effect of intra-arterially infused angiotensin II on FBF at rest and after exercise (n = 7). Angiotensin II decreased FBF at rest from 3.1 +/- 0.3 to 1.8 +/- 0.3 mL.min-1.100 mL-1 (P < .01), peak FBF after exercise from 8.1 +/- 0.5 to 5.6 +/- 0.5 mL.min-1.100 mL-1 (P < .01), and FBF during the mid to late phase of metabolic vasodilation. The effects of L-NMMA and angiotensin II on FBF at rest and exercise were similar. Our results suggest that L-NMMA decreased FBF after exercise largely by decreasing resting FBF. These results suggest that NO may not play a significant role in exercise-induced metabolic arteriolar vasodilation in the forearm of healthy humans.