Leg blood flow, metabolism and exercise capacity in chronic stable heart failure.

OBJECTIVES: To assess the metabolic state of skeletal muscle during exercise in patients with chronic heart failure (CHF) and relate this to exercise capacity. BACKGROUND: During exercise in CHF, there is little relation between exercise capacity and central haemodynamic function. Skeletal muscle and limb blood flow are abnormal in CHF. We investigated the relationship between leg blood flow, metabolism and exercise capacity and ventilation in 10 patients (average age 63.3 +/- 6.0 years; 3 female) with stable CHF. METHODS: Patients undertook maximal exercise testing. Peak oxygen consumption (VO2) and the slope of the relationship between ventilation and carbon dioxide production (VE/CO2 slope) were derived. During a supine cycle exercise test, cardiac output (CO) by Doppler echocardiography, femoral blood flow (FBF) by thermodilution, pulse and blood pressure were recorded, and radial arterial and femoral venous blood samples taken for catecholamine, lactate and potassium estimation every 3 min. RESULTS: The average peak VO2 was 19.7 (+/- 5.2; range 11.3-29.0) ml/kg/min. The proportion of CO to the right leg increased from 0.08 (+/- 0.03) to 0.22 (+/- 0.06) (P < 0.001) at 3 min, with no further significant change thereafter. There was a liner increase in leg VO2 reaching a plateau towards peak. At peak, femoral venous saturation was 22.79% +/- 7.20%. Venous lactate and potassium were higher than arterial (P < 0.001 for each comparison). There was no correlation between exercise performance and any of the measured metabolites either in absolute measurements, expressed as change from rest to peak exercise or as arterio-venous difference. The closest correlate of leg VO2 was leg hydrogen ion production, V[H+]. Change in femoral venous lactate from rest to peak exercise correlated with VE/VCO2 slope even when calculated from before the anaerobic threshold (r = -0.80; P = 0.025). CONCLUSIONS: In CHF, exercise capacity is not determined by individual haemodynamic events, and does not seem to be determined by the possible humoral signals we investigated. Ventilation is abnormal before anaerobic threshold, and predicts subsequent lactate rise, suggesting that skeletal muscle is the origin of excessive ventilation.