Muscle Blood Flow Is Reduced With Maintenance of Arterial Perfusion Pressure

We studied the central hemodynamic, leg blood flow, and metabolic responses to maximal upright bicycle exercise in 30 patients with chronic heart failure attributable to severe left ventricular dysfunction (ejection fraction, 24+8%) and in 12 normal subjects. At peak exercise, patients demonstrated reduced oxygen consumption (15.1±+4.8 vs. 32.1±9.9 ml/kg/min, p <0.001), cardiac output (8.7±3.2 vs. 18.6± 4.4 1/min, p <0.001), and mean systemic arterial blood pressure (116±15 vs. 135±13 mm Hg, p<0.01) compared with normal subjects. Leg blood flow was decreased in patients versus normal subjects at rest and matched submaximal work rates and maximal exercise (2.1±1.9 vs. 6.4±1.4 1/min, all p<0.01). Mean systemic arterial blood pressure was no different in the two groups at rest or at matched submaximal work rates, whereas leg vascular resistance was higher in patients compared with normal subjects at rest, submaximal, and maximal exercise (all p<0.01). Although nonleg blood flow was decreased at rest in patients, it did not decrease significantly during exercise in either group. Peak exercise leg blood flow was related to peak exercise cardiac output in patients (r=0.66, p<0.01) and normal subjects (r=0.67, p<0.01). In patients, leg vascular resistance was not related to mean arterial blood pressure, pulmonary capillary wedge pressure, arterial catecholamines, arterial lactate, or femoral venous pH at rest or during exercise. Compared with normal subjects during submaximal exercise, patients demonstrated increased leg oxygen extraction and lactate production accompanied by decreased leg oxygen consumption. Thus, in patients with chronic heart failure compared with normal subjects, skeletal muscle perfusion is decreased at rest and during submaximal and maximal exercise, and local vascular resistance is increased. Our data indicate that nonleg blood flow and arterial blood pressure were preferentially maintained during exercise at the expense of leg hypoperfusion in our patients. This was associated with decreased leg oxygen utilization and increased leg oxygen extraction when compared to normal subjects, providing further evidence that reduced perfusion of skeletal muscle is important in causing early anaerobic skeletal muscle metabolism during exercise in subjects with this disorder. Although these results do not define the mechanisms responsible for increased leg vascular resistance during exercise in subjects with chronic heart failure, our finding that arterial blood pressure in patients was closely regulated suggests a role for reflex-mediated peripheral vasoconstriction in linking the cardiac output and skeletal muscle blood flow responses to exercise in subjects with this disorder. (Circulation 1989;80:769-781)