Effect of beta-adrenoceptor blockade on postexercise oxygen consumption and triglyceride/fatty acid cycling.
In the recovery period after strenuous exercise, there is increased O2 uptake, termed the excess postexercise O2 consumption (EPOC). One of the mechanisms suggested to explain EPOC is activation of the triglyceride/fatty acid (TG/FA) cycle by catecholamines. The purpose of this study was to determine the effect of selective beta1- and nonselective beta-adrenoceptor blockade on EPOC and the TG/FA cycle. Seven healthy young men each participated in three control and three exercise experiments in a randomized and balanced sequence. In the exercise experiments, subjects exercised for 90 minutes at 58% +/- 2% (mean +/- SD) of maximal O2 uptake on a cycle ergometer, followed by a 4.5-hour bedrest. The control experiments followed the same protocol, but without exercise. In one control and one exercise experiment, the selective beta1-adrenoceptor antagonist atenolol (0.062 mg.kg(-1) body weight) was administered intravenously immediately after the exercise (EXAT) and at the corresponding time in the rest-control experiment (REAT). In a second set of control and exercise experiments, the nonselective beta-adrenoceptor antagonist propranolol (0.15 mg.kg(-1) body weight) was administered (REPRO and EXPRO). In a third set of rest and exercise experiments, an injection of saline was given instead of beta-antagonist (RE and EX). TG/FA cycling was calculated by combining results obtained with a two-stage glycerol infusion and indirect calorimetry. O2 uptake was significantly increased above control levels throughout the recovery period after exercise with the nonselective beta-adrenoceptor antagonist, beta1-adrenoceptor antagonist, and saline. However, there was no difference between the time course or magnitude of EPOC in the three situations. After 4.5 hours of bedrest, the mean increase in O2 uptake was 8% to 9% in all three conditions. TG/FA cycling was increased after exercise, but no effects of beta-antagonists were observed. We conclude that EPOC and the rate of TG/FA cycling are not attenuated by selective beta1- or nonselective beta-adrenoceptor blockade after an acute prolonged exercise protocol.
Børsheim
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Norwegian University of Sport and Physical Education, Oslo.
Bahr
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Høstmark
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AT
Knardahl
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D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000328:Adult; D001262:Atenolol / Q000494:pharmacology; D002395:Catecholamines / Q000097:blood; D004734:Energy Metabolism / Q000502:physiology*; D015444:Exercise / Q000502:physiology*; D005227:Fatty Acids / Q000378:metabolism*; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007328:Insulin / Q000097:blood; D008297:Male; D010084:Oxidation-Reduction; D010101:Oxygen Consumption / Q000187:drug effects*; D011433:Propranolol / Q000494:pharmacology; D012016:Reference Values; D014280:Triglycerides / Q000378:metabolism*
D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D005227:Fatty Acids; D007328:Insulin; D014280:Triglycerides; D001262:Atenolol; D011433:Propranolol; D006854:Hydrocortisone