Influence of Locomotor Muscle Metaboreceptor Stimulation on the Ventilatory Response to Exercise in Heart Failure

BACKGROUND: Whether locomotor muscle afferent neural activity contributes to exercise hyperpnea and symptoms of dyspnea in heart failure (HF) is controversial. We examined the influence of metaboreceptor stimulation on ventilation with and without maintaining end-exercise end-tidal CO(2) levels. METHODS AND RESULTS: Eleven patients with HF aged 51+/-5 years (ejection fraction, 32+/-3%; New York Heart Association class, 1.6+/-0.2) and 11 age- and gender-matched healthy control participants aged 43+/-3 years were studied. Participants underwent 3 steady-state cycling sessions at 60% of peak oxygen consumption for 4 minutes. The first exercise session was a baseline control trial. Bilateral thigh tourniquets were inflated to suprasystolic pressure at end exercise for 2 minutes during 2 of the trials (regional circulatory occlusion) with the addition of inspired CO(2) to maintain end-exercise partial pressure of end-tidal CO(2) during 1 trial (regional circulatory occlusion+CO(2)). Minute ventilation was measured continuously throughout each trial. At 2 minutes postexercise during the baseline control trial in patients with HF, minute ventilation was 54% of end exercise, whereas the control group averaged 41% (P=0.11). During regional circulatory occlusion in patients with HF, minute ventilation was 60% of end exercise; however, the control group averaged 35% (P<0.001). During regional circulatory occlusion+CO(2), the minute ventilation of patients with HF averaged 67% of end exercise, whereas the control group averaged 44% (P<0.001). CONCLUSIONS: These data suggest that increased afferent neural activity from the large locomotor muscles associated with metabolites generated during exercise contribute to the augmented ventilatory response to exercise in patients with HF.