During maximal upright exercise, blood flow to working skeletal muscle is frequently reduced in patients with nonedematous chronic heart failure. It has been speculated that this reduced muscle flow may be caused in part by an intrinsic impairment of skeletal muscle vasodilatory capacity. To test this hypothesis, forearm blood flow and resistance were comparead during forearm exercise and in response to transient forearm ischemia (10 min) in 22 patients with heart failure and in 1 1 normal subjects. During forearm exercise, both groups exhibited comparable forearm blood flows (ml/min/100 ml) (0.2 W: normal 5.9 ± 3.1, heart failure 6.5 ± 2.8; 0.4 W: normal 8.2 ± 5.5, heart failture 8.2 ± 3.6; 0.6 W: normal 11.5 ± 6.8, heart failure 11.8 + 4.8 [all p = NS]) and forearm vascular resistances (mm Hg/ml/min/100 ml) (0.2 W: normal 23.1 ± 12.4, heart failure 18.5 ± 7.8; 0.4 W: normal 16.9 ± 7.7, heart failure 14.7 ± 6.4; 0.6 W: normal 13.1 ± 7.7, heart failure 10.3 ± 4. 1 Lall p = NS]). Ten minutes of forearm ischemia, an intervention that produces maximal forearm vasodilation, also resulted in comparable forearm vascular resistances in both groups (normal 4.1 ± 2.4, heart failure 3.8 ± 1.3 mm Hg/ml/min/100 ml/ p = NS). These data suggest that skeletal muscle vasodilatory capacity is not intrinsically impaired in patients with nonedematous chronic heart failure.