LEG BLOOD-FLOW, METABOLISM AND EXERCISE CAPACITY IN CHRONIC STABLE HEART-FAILURE

Objectives: To assess the metabolic state of skeletal muscle during ex ercise in patients with chronic heart failure (CHF) and relate this to exercise capacity. Background: During exercise in CHF, there is littl e relation between exercise capacity and central haemodynamic function . Skeletal muscle and limb blood flow are abnormal in CHF. We investig ated the relationship between leg blood flow, metabolism and exercise capacity and ventilation in 10 patients (average age 63.3 +/- 6.0 year s; 3 female) with stable CHF. Methods: Patients undertook maximal exer cise testing. Peak oxygen consumption (V over dot O-2) and the slope o f 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, femor al blood flow (FBF) by thermodilution, pulse and blood pressure were r ecorded, and radial arterial and femoral venous blood samples taken fo r 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 sig nificant change thereafter. There was a linear increase in leg V over dot O-2 reaching a plateau towards peak. At peak, femoral venous satur ation was 22.79% +/- 7.20%. Venous lactate and potassium were higher t han arterial (P < 0.001 for each comparison). There was no correlation between exercise performance and any of the measured metabolites eith er in absolute measurements, expressed as change from rest to peak exe rcise 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 i n 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 a naerobic threshold (r = -0.80; P = 0.025). Conclusions: In CHF, exerci se capacity is not determined by individual haemodynamic events, and d oes not seem to be determined by the possible humoral signals we inves tigated. Ventilation is abnormal before anaerobic threshold, and predi cts subsequent lactate rise, suggesting that skeletal muscle is the or igin of excessive ventilation.