Literature DB >> 9550543

Effect of beta-adrenoceptor blockade on postexercise oxygen consumption and triglyceride/fatty acid cycling.

E Børsheim1, R Bahr, A T Høstmark, S Knardahl.   

Abstract

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.

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Year:  1998        PMID: 9550543     DOI: 10.1016/s0026-0495(98)90057-9

Source DB:  PubMed          Journal:  Metabolism        ISSN: 0026-0495            Impact factor:   8.694


  5 in total

Review 1.  Effect of exercise intensity, duration and mode on post-exercise oxygen consumption.

Authors:  Elisabet Børsheim; Roald Bahr
Journal:  Sports Med       Date:  2003       Impact factor: 11.136

Review 2.  Acute effects of physical exercise in type 2 diabetes: A review.

Authors:  Ricardo Yukio Asano; Marcelo Magalhães Sales; Rodrigo Alberto Vieira Browne; José Fernando Vila Nova Moraes; Hélio José Coelho Júnior; Milton Rocha Moraes; Herbert Gustavo Simões
Journal:  World J Diabetes       Date:  2014-10-15

3.  Differential effects of dietary intake of palmitic acid and oleic acid on oxygen consumption during and after exercise.

Authors:  Elisabet Børsheim; C Lawrence Kien; William M Pearl
Journal:  Metabolism       Date:  2006-09       Impact factor: 8.694

4.  Residual effects of prior exercise and recovery on subsequent exercise-induced metabolic responses.

Authors:  Ola Ronsen; Oystein Haugen; Jostein Hallén; Roald Bahr
Journal:  Eur J Appl Physiol       Date:  2004-08       Impact factor: 3.078

5.  High-CHO diet increases post-exercise oxygen consumption after a supramaximal exercise bout.

Authors:  G A Ferreira; R Bertuzzi; F R De-Oliveira; F O Pires; A E Lima-Silva
Journal:  Braz J Med Biol Res       Date:  2016-10-24       Impact factor: 2.590

  5 in total

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