The purpose of this study was to determine whether the autonomic nervous sy
stem is involved in skeletal muscle vasodilation at the onset of exercise.
Mongrel dogs (n = 7) were instrumented with flow probes on both external il
iac arteries. Before treadmill exercise at 3 miles/h, 0% grade, hexamethoni
um (10 mg/kg) and atropine (0.2 mg/kg) or saline was infused intravenously.
Ganglionic blockade increased resting heart rate from 87 +/- 5 to 145 +/-
8 beats/min (P < 0.01) and reduced mean arterial pressure from 100 +/- 4 to
88 +/- 5 mmHg (P < 0.01). During steady-state exercise, heart rate was una
ffected by ganglionic blockade (from 145 +/- 8 to 152 +/- 5 beats/min), whe
reas mean arterial pressure was reduced (from 115 +/- 4 to 72 +/- 4 mmHg; P
< 0.01). Immediate and rapid increases in iliac blood flow and conductance
occurred with initiation of exercise with or without ganglionic blockade.
Statistical analyses of hindlimb conductance at 5-s intervals over the firs
t 30 s of exercise revealed a statistically significant difference between
the control and ganglionic blockade conditions at 20, 25, and 30 s (P < 0.0
1) but not at 5, 10, and 15 s of exercise. Hindlimb conductance at 1 min of
exercise was 9.21 +/- 0.68 and 11.82 +/- 1.32 ml.min(-1).mmHg(-1) for the
control and ganglionic blockade conditions, respectively. Because ganglioni
c blockade did not affect the initial rise in iliac conductance, we conclud
ed that the autonomic nervous system is not essential for the rapid vasodil
ation in active skeletal muscle at the onset of exercise in dogs. Autonomic
control of skeletal muscle blood flow during exercise is manifested throug
h vasoconstriction and not vasodilation.