Paterson D J
University Laboratory of Physiology, University of Oxford, UK.
Acta Physiol Scand. 1996 Mar;156(3):287-94. doi: 10.1046/j.1365-201X.1996.190000.x.
In exercise, potassium (K+) is released from contracting muscle predominately through K+ channels associated with the repolarization phase of the action potential. Increases in extracellular K+ are directly related to increases in metabolic rate and may reach concentrations as high as 8-9 mM in the arterial blood during exhaustive work. Exercise-induced hyperkalaemia has been implicated in several physiological processes, in particular skeletal muscle fatigue, hyperaemia, pressor reflex, arterial chemosensitivity and myocardial stability. There is no direct evidence to show that hyperkalaemia causes muscle fatigue, although raised extracellular [K+] may contribute to fatigue during prolonged tetani by depressing the propagation of the action potential down the t-tubule system, thus impairing the release of Ca2+ from the sarcoplasmic reticulum. The vasodilating properties of K+ may transiently contribute to the early phase of exercise hyperaemia and interact synergistically with other vasoactive substances to cause relaxation by hyperpolarizing K+ channels in vascular smooth muscle. Hyperkalaemia has been implicated in the regulation of arterial blood pressure through activation of the muscle afferent reflex where potassium-depolarized C fibres may contribute to a reflex increase in arterial blood pressure. K+ can also increase ventilation and the sensitivity of the ventilatory response to hypoxia through direct excitation of the arterial chemoreceptors. Finally, to maintain myocardial electrical stability in exercise, there is a beneficial interaction between raised K+ and catecholamines on the heart, so that when they combine, each offsets the other's deleterious effects.
在运动过程中,钾离子(K+)主要通过与动作电位复极化阶段相关的钾通道从收缩的肌肉中释放出来。细胞外钾离子的增加与代谢率的增加直接相关,在力竭运动期间,动脉血中的钾离子浓度可能高达8 - 9 mM。运动诱导的高钾血症与多种生理过程有关,特别是骨骼肌疲劳、充血、压力反射、动脉化学敏感性和心肌稳定性。虽然细胞外[K+]升高可能通过抑制动作电位沿横管系统的传播,从而损害肌浆网中Ca2+的释放,在长时间强直收缩期间导致疲劳,但尚无直接证据表明高钾血症会导致肌肉疲劳。钾离子的血管舒张特性可能会暂时促进运动性充血的早期阶段,并与其他血管活性物质协同作用,通过使血管平滑肌中的钾通道超极化来引起舒张。高钾血症通过激活肌肉传入反射参与动脉血压的调节,其中钾离子去极化的C纤维可能导致动脉血压反射性升高。钾离子还可以通过直接刺激动脉化学感受器来增加通气量以及通气对缺氧反应的敏感性。最后,为了在运动中维持心肌电稳定性,升高的钾离子与儿茶酚胺在心脏上存在有益的相互作用,因此当它们结合时,彼此抵消对方的有害影响。