EFFECT OF BETA-ADRENOCEPTOR BLOCKADE ON POSTEXERCISE OXYGEN-CONSUMPTION

In the recovery period after strenous exercise, there is an increase in O2 uptake termed the excess post-exercise O2 consumption (EPOC), consisting of a rapid and a prolonged component. Mechanisms regulating the prolonged component of EPOC are not completely understood, but an effect of catecholamines has been suggested. The purpose of this study was to investigate the effect of β-adrenoceptor blockade on EPOC. Six healthy young men were randomized to one control experiment and two exercise experiments, one with and one without nonselective β-adrenoceptor blockade. In the exercise experiments, they exercised for 60 minutes at 78% ± 3% (mean ± SD) of maximal O2 uptake (Vo2max) on a cycle ergometer followed by 6.5 hours' bedrest. In the β-adrenoceptor blockade experiment, propranolol (0.1 mg · kg-1 body weight [BW]) was administered intravenously immediately after the exercise bout and again 3.5 hours after exercise. The control experiment was performed without exercise or β-adrenoceptor blockade. EPOC was calculated as the difference in O2 uptake between the exercise and control experiments. A supplementary study on 15 subjects showed resting O2 uptake to be unaffected by propranolol. O2 uptake was significantly increased during the recovery period after exercise when no β-adrenoceptor blocker was administered. After 6.5 hours of bedrest, the mean increase (±SE) in O2 uptake was 19 ± 4 mL · min-1. In contrast, when propranolol was administered during recovery from exercise, O2 uptake was significantly increased for only the first 2 hours. Propranolol decreased total EPOC (±SE) by about one third, from 14.4 ± 1.9 to 9.5 ± 2.5 L. This reduction affected mainly the prolonged EPOC component. We conclude that β-adrenergic stimulation is of major importance for the mechanisms causing the prolonged component of EPOC. © 1994.