Maintained exercise pressor response in heart failure

The impact of forearm blood flow limitation on muscle reflex (metaboreflex) activation during exercise was examined in 10 heart failure (HF) (NYHA class III and IV) and 9 control (Ctl) subjects. Rhythmic handgrip contractions (25% maximal voluntary contraction, 30 contractions/min) were performed over 5 min under conditions of ambient pressure or with + 50 mmHg positive pressure about the exercising forearm. Mean arterial blood pressure (MAP) and venous effluent hemoglobin (Hb) O₂ saturation, lactate and H⁺ concentrations ([La] and [H⁺], respectively) were measured at baseline and during exercise. For ambient contractions, the increase (Δ) in MAP by end exercise (ΔMAP; i.e., the exercise pressor response) was the same in both groups (10.1 ± 1.2 vs. 7.33 ± 1.3 mmHg, HF vs. Ctl, respectively) despite larger Δ[La] and Δ[H⁺] for the HF group (P < 0.05). With ischemic exercise, the ΔMAP for HF (21.7 ± 2.7 mmHg) exceeded that of Ctl subjects (12.2 ± 2.8 mmHg) (P < 0.0001). Also, for HF, Δ[La] (2.94 ± 0.4 mmol) and Δ[H⁺] (24.8 ± 2.7 nmol) in the ischemic trial were greater than in Ctl (1.63 ± 0.4 mmol and 15.3 ± 2.8 nmol; [La] and [H⁺], respectively) (P < 0.02). Hb O₂ saturation was reduced in Ctl from -43% in the ambient trial to ~27% with ischemia (P < 0.0001). O₂ extraction was maximized under ambient exercise conditions for HF but not for Ctl. Despite progressive increases in blood perfusion pressure over the course of ischemic exercise, no improvement in Hb O₂ saturation or muscle metabolism was observed in either group. These data suggest that muscle reflex activation of the pressor response is intact in HF subjects but the resulting improvement in perfusion pressure does not appear to enhance muscle oxidative metabolism or muscle blood flow, possibly because of associated increases in sympathetic vasoconstriction of active skeletal muscle.