Abstract des Autors

We evaluated whether a reduction in cardiac output during dynamic exercise results in vasoconstriction of active skeletal muscle vasculature. Nine subjects performed four 8-min bouts of cycling exercise at 40-84% VO2max. Exercise was repeated after cardioselective (beta 1) adrenergic blockade. Leg blood flow and cardiac output were determined. Femoral arterial and venous pressures were monitored for measurement of heart rate, mean arterial pressure, and calculation of systemic and leg vascular conductance. Leg norepinephrine spillover was used as an index of regional sympathetic activity. During control, the highest heart rate and cardiac output were 171 +/- 3 beats/min and 18.9 +/- 0.9 l/min, respectively. Beta 1-blockade reduced these values to 147 +/- 6 beats/min and 15.3 +/- 0.9 l/min, respectively. At the highest work rate in the control condition, leg blood flow and vascular conductance were 5.4 +/- 0.3 l/min and 5.2 +/- 0.3 cl/min/mmHg, respectively, and were reduced during beta 1-blockade to 4.8 +/- 0.4 l/min and 4.6 +/- 0.4 cl/min/mmHg. During the same exercise condition leg norepinephrine spillover increased from a control value of 2.64 +/- 1.16 to 5.62 +/- 2.13 nM/min with beta 1-blockade. At least one-third of the increase in mean arterial pressure during exercise with beta 1-blockade could be accounted for by leg vasoconstriction. We concluded that neurogenic vasoconstriction of active skeletal muscle can offset metabolic vasodilation during intense dynamic exercise when cardiac output is compromised. Verf.-Referat