Nitric oxide in the regulation of vasomotor tone in human skeletal muscle.

The role of nitric oxide (NO) as a regulator of vasomotor tone has been investigated in resting and exercising human skeletal muscle. At rest, NO synthase (NOS) inhibition by intra-arterial infusion of NG-monomethyl-L-arginine decreased femoral artery blood flow (FABF, ultrasound Doppler) from 0.39 +/- 0.08 to 0.18 +/- 0.03 l/min (P < 0. 01), i.e., by approximately 52%, and increased leg O2 extraction from 62.1 +/- 9.8 to 100.9 +/- 4.5 ml/l (P < 0.004); thus leg O2 uptake (VO2, 22 +/- 4 ml/min, approximately 0.75 ml. min-1. 100 g-1) was unaltered [not significant (P = NS)]. Mean arterial pressure (MAP) increased by 8 +/- 2 mmHg (P < 0.01). Heart rate (HR, 53 +/- 3 beats/min) was unaltered (P = NS). The NOS inhibition had, however, no effect on the initial rate of rise or the magnitude of FABF (4.8 +/- 0.4 l/min, approximately 163 ml. min-1. 100 g-1), MAP (117 +/- 3 mmHg), HR (98 +/- 5 beats/min), or leg VO2 (704 +/- 55 ml/min, approximately 24 ml. min-1. 100 g-1, P = NS) during submaximal, one-legged, dynamic knee-extensor exercise. Similarly, FABF (7.6 +/- 1.0 l/min, approximately 258 ml. min-1. 100 g-1), MAP (140 +/- 8 mmHg), and leg VO2 (1,173 +/- 139 ml/min, approximately 40 ml. min-1. 100 g-1) were unaffected at termination of peak effort (P = NS). Peak HR (137 +/- 3 beats/min) was, however, lowered by 10% (P < 0.01). During recovery, NOS inhibition reduced FABF by approximately 34% (P < 0.04), which was compensated for by an increase in the leg O2 extraction by approximately 41% (P < 0.04); thus leg VO2 was unaltered (P = NS). In conclusion, these findings indicate that NO is not essential for the initiation or maintenance of active hyperemia in human skeletal muscle but support a role for NO during rest, including recovery from exercise. Moreover, changes in blood flow during rest and recovery caused by NOS inhibition are accompanied by reciprocal changes in O2 extraction, and thus VO2 is maintained.