ROLE OF NITRIC-OXIDE IN EXERCISE-INDUCED VASODILATION OF THE FOREARM

Background We wished to determine the role of NO in exercise-induced metabolic forearm vasodilation. Methods and Results 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 mu mol/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. Conclusions 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.