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DOI 10.1111/j.1365-2362.1990.tb01913.x

Медицинская библиотека · European journal of clinical investigation · 1990

Exercise-induced hyperkalaemia can be reduced in human subjects by moderate training without change in skeletal muscle Na,K-ATPase concentration.

Kjeldsen K, Nørgaard A, Hau C

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

In 15 conscripts, venous plasma potassium was followed during exercise on a training bicycle before and after 10 weeks of moderate physical training and a putative relationship with skeletal muscle Na,K-ATPase was evaluated. Peak plasma potassium concentration obtained at exhaustion was 6.1 +/- 0.2 and 5.6 +/- 0.2 mmol l-1 (mean +/- SEM, n = 14, P less than 0.05) before and after training, respectively. Throughout the exercise period and within the first minutes of rest plasma potassium concentration was 0.2-0.5 mmol l-1 higher before than after training. Neither peak values nor peak rises in plasma potassium concentration before nor after training were correlated to the 3H-ouabain binding site (Na,K-ATPase) concentration in vastus lateralis muscle. The results indicate that net loss of potassium from the skeletal muscle pool during exercise is reduced after training, that the heart during exercise may be exposed to a smaller rise in plasma potassium concentration after training than before, and that moderate improvement of capacity to clear extracellular potassium during exercise may be due to increased activity of existing Na,K-pumps in resting skeletal muscle fibres. This may reduce muscle fatigue, increase physical performance and explain the paradoxical observation that, despite an increased catecholamine response, there is a reduced risk of cardiac events after training.

Для цитирования: Kjeldsen K, Nørgaard A, Hau C. Exercise-induced hyperkalaemia can be reduced in human subjects by moderate training without change in skeletal muscle Na,K-ATPase concentration.. European journal of clinical investigation. 1990. DOI: 10.1111/j.1365-2362.1990.tb01913.x.

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