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 (V over dot O-2) and the slope of the relationship between ventilation and carbon dioxide production (V over dot E/V over dot CO2 slope) were derived. During a supine cycle exercise test, cardiac output (GO) 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 V over dot O-2 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 linear increase in leg V over dot O-2 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 V over dot O-2 was leg hydrogen ion production, V over dot[H+]. Change in femoral venous lactate from rest to peak exercise correlated with V over dot E/V over dot CO2 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.