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耐力运动期间的β-肾上腺素能受体阻断与骨骼肌能量代谢

Beta-adrenoceptor blockade and skeletal muscle energy metabolism during endurance exercise.

作者信息

van Baak M A, de Haan A, Saris W H, van Kordelaar E, Kuipers H, van der Vusse G J

机构信息

Department of Human Biology, University of Limburg, Maastricht, The Netherlands.

出版信息

J Appl Physiol (1985). 1995 Jan;78(1):307-13. doi: 10.1152/jappl.1995.78.1.307.

DOI:10.1152/jappl.1995.78.1.307
PMID:7713830
Abstract

Twelve healthy male volunteers cycled to exhaustion at a workload corresponding to 70% of maximal aerobic power after administration of 80 mg of the beta 1+2-adrenoceptor antagonist propranolol and after administration of placebo by mouth. Exercise times until exhaustion were 39 +/- 7 and 86 +/- 7 min in the propranolol and placebo groups, respectively. Muscle inosine 5'-monophosphate content was significantly increased above resting levels at exhaustion after placebo. At exhaustion after propranolol, inosine 5'-monophosphate was not increased significantly and was lower than at exhaustion after placebo. No changes in ATP and the total adenine nucleotide content during exercise were found in the two tests. Muscle glycogen content was significantly reduced at exhaustion after placebo as well as after propranolol, but the levels were still significantly higher at exhaustion after propranolol than after placebo. No evidence for a shift in glycogen utilization among types I, IIa, and IIb fibers after propranolol was found. The results show that neither an imbalance between ATP utilization and ATP regeneration nor premature glycogen depletion, either in the whole muscle or in specific muscle fiber types, provides a satisfactory explanation for the premature fatigue during endurance exercise after propranolol.

摘要

12名健康男性志愿者在口服80毫克β1+2肾上腺素能受体拮抗剂普萘洛尔后以及口服安慰剂后,以相当于最大有氧功率70%的工作量进行骑车运动直至力竭。普萘洛尔组和安慰剂组直至力竭的运动时间分别为39±7分钟和86±7分钟。安慰剂组力竭时肌肉肌苷5'-单磷酸含量显著高于静息水平。普萘洛尔组力竭时,肌苷5'-单磷酸未显著增加且低于安慰剂组力竭时水平。两项测试中运动期间ATP和总腺嘌呤核苷酸含量均未发现变化。安慰剂组和普萘洛尔组力竭时肌肉糖原含量均显著降低,但普萘洛尔组力竭时的水平仍显著高于安慰剂组。未发现普萘洛尔后I型、IIa型和IIb型纤维之间糖原利用发生改变。结果表明,无论是在整个肌肉还是特定肌纤维类型中,ATP利用与ATP再生之间的失衡或糖原过早耗尽,都不能令人满意地解释普萘洛尔后耐力运动期间的过早疲劳。

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