Background We wished to determine the role of NO in exercise-induced m
etabolic forearm vasodilation. Methods and Results Young healthy volun
teers (n=11) underwent static handgrip exercise (4 to 5 kg, 3 minutes)
. Forearm blood flow (FBF) measured by strain plethysmography increase
d 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 thereaf
ter. Exercise was repeated after intrabrachial artery infusion of NG-m
onomethyl-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 r
est to 2.9+/-0.4 mL.min(-1).100 mL(-1) (P<.01), peak FBF immediately a
fter exercise to 7.2+/-0.7 mL.min(-1).100 mL(-1) (P<.01), and FBF duri
ng the mid to late phase of metabolic vasodilation (P<.01). Calculated
oxygen consumption during peak exercise was comparable before and aft
er L-NMMA. Intra-arterially infused L-arginine (10 mg/min, 5 minutes)
reversed the inhibitory effect of L-NMMA. To determine the effect of t
he decrease in resting FBF on exercise-induced hyperemia, we normalize
d FBF after exercise by resting FBF. The percent increases in FBF afte
r exercise from resting FBF were similar before and after L-NMMA. Furt
hermore, we examined the effect of intra-arterially infused angiotensi
n 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 m
L(-1) (P<.01), and FBF during the mid to late phase of metabolic vasod
ilation. The effects of L-NMMA and angiotensin II on FBF at rest and e
xercise were similar. Conclusions Our results suggest that L-NMMA decr
eased FBF after exercise largely by decreasing resting FBF. These resu
lts suggest that NO may not play a significant role in exercise-induce
d metabolic arteriolar vasodilation in the forearm of healthy humans.