ADRENERGIC CONTROL OF POSTEXERCISE METABOLISM

After strenuous exercise there is a sustained increase in resting O-2 consumption. The magnitude and duration of the excess post-exercise O- 2 consumption (EPOC) is a function of exercise intensity and exercise duration. Some of the mechanisms underlying the rapid EPOC component ( <1 h) are well defined, while the mechanisms causing the prolonged EPO C component (<1 h) are not-fully understood. It has been suggested tha t beta-adrenergic stimulation is of importance for the prolonged compo nent. There is an increased level of plasma adrenaline and noradrenali ne during exercise, and it is shown that catecholamines stimulate ener gy expenditure through beta-adrenoceptors. After exercise an increased fat oxidation and an increased rate of triglyceride fatty acid (TG-FA ) cycling may account for a significant part of the prolonged EPOC com ponent. These processes may be stimulated by catecholamines. However, the return of plasma concentration of catecholamines to resting levels after exercise is more rapid than the return of O-2 uptake. But plasm a concentration of catecholamines may be an insensitive indicator of s ympathetic activity, since the clearance rate of catecholamines is hig h. Also, the sensitivity to catecholamines may be increased after exer cise. A decreased post-exercise O-2 uptake has been shown when beta-bl ockade is administered in dogs before the exercise bout. In a pilot st udy in humans, administration of beta-antagonist after exercise did no t seem to change EPOC.