Sympathetic vasoconstriction during exercise in ambulatory patients with left ventricular failure

Abstract

In patients with heart failure, exercise is thought to increase sympathetic vasoconstrictor tone. To investigate the extent of this sympathetic activation, we studied the effect of maximal exercise on nonexercising vascular beds in 35 patients with left ventricular failure (ejection fraction, 21 ± 8%; peak exercise oxygen uptake (V̇2), 12.3 ± 3.5 ml/min/kg). In 28 patients, cardiac output and leg blood flow were measured during maximal upright bicycle exercise. Total flow to nonexercising tissue was then calculated as cardiac output-(2xleg flow). In seven patients and six normal subjects, forearm blood flow was measured during supine bicycle exercise before and after α-adrenergic blockade with intravenous phentolamine. Maximal upright exercise increased the vascular resistance of nonexercising tissue from 34 ± 16 units at upright rest to 45 ± 25 units (p < 0.02) but did not affect total flow to nonexercising tissue (rest, 2.9 ± 1.0; maximal exercise, 2.8 ± 1.4 l/min; p = NS). Supine exercise had no significant effect on forearm blood flow or vascular resistance in the normal subjects. In the patients with heart failure, supine exercise increased forearm vascular resistance from 45 ± 17 to 58 ± 25 mm Hg/ml/min/100 ml (p < 0.02), again with no change in tissue flow (rest, 2.4 ± 0.1; maximal exercise, 2.4 ± 0.9 ml/min/100 ml; p = NS). The increase in forearm vascular resistance was associated with only a modest increase in plasma norepinephrine levels (rest, 258 ± 129; maximal exercise, 635 ± 188 pg/ml) and was unaffected by prior administration of phentolamine. These findings suggest that exercise does not produce a major increase in sympathetic vasoconstrictor tone in ambulatory patients with left ventricular failure.