Cutaneous vascular conductance (CVC) rises during heat stress in normal humans. Recently, we showed that this response is attenuated in chronic heart failure (CHF), even though the skin sympathetic nerve activity response to heat stress was not attenuated. Of note, heat stress evokes significant increases in muscle sympathetic nerve activity (MSNA) in healthy individuals. This effect may allow flow to be distributed to other tissues. The MSNA response to heat stress in CHF has not been reported. We postulated that in CHF the MSNA response to heat stress is attenuated. Passive whole body heating was applied with water-perfused suits on 9 male (60 ± 3 yrs) patients with stable class II-III CHF and 9 age-matched male healthy subjects. Whole body heating induced similar increases in skin temperature (~4 °C), internal temperature (~0.6 °C), similar reduction in blood pressure, and similar increase in heart rate. The elevation in forearm CVC in CHF patients was significantly lower than that in healthy control subjects (102 ± 29 vs. 312 ± 54 units, P < 0.001). While baseline MSNA in CHF was higher than in controls (P < 0.05); heat stress increased MSNA in the controls (33.2 ± 3.8 to 47.3 ± 4.4 bursts/min; 618 ± 74 to 934 ± 93 units/min, both P < 0.001, N = 9), but not in CHF (43.4 ± 5.7 to 49.6 ± 7.0 bursts/min; 996 ± 104 to 1039 ± 108 units/min, both P > 0.15, N = 6; two-factor ANOVA with repeated measure on one factor). Moreover, the MSNA change by heating in CHF was significantly lower than that in the controls (6.2 ± 2.6 to 14.1 ± 1.5 bursts/min; 43 ± 45 to 316 ± 34 units/min; both P < 0.01, unpaired t-test). The attenuated MSNA response to heating was not due to a ceiling effect as that static fatiguing handgrip in CHF in a control trial evoked significant increases in MSNA. These data show that the MSNA response to heat stress is attenuated in CHF patients. We postulate that the attenuated MSNA response contributes to an impaired re-distribution of blood low to the skin during heat stress in CHF.