Sjøgaard G
Department of Physiology, National Institute of Occupational Health, Copenhagen O, Denmark.
Acta Physiol Scand. 1996 Mar;156(3):257-64. doi: 10.1046/j.1365-201X.1996.207000.x.
A general finding is that muscle activity leads to potassium fluxes across the muscle membrane as well as to muscle fatigue, defined as a reduction in the force-generating capacity of the muscle. However, much controversy exists regarding the causal role of potassium in fatigue development. The experimental model used is decisive in this context, e.g. whether we study intact in vivo organs in situ with voluntary contractions and reflex feedback for cardiorespiratory regulation, or whether we study in vitro isolated muscles or cells-or even skinned fibres. In the latter models, clear evidence has been presented that Ca2+ is the variable significant for force development and that K+ may be ignored. However, in the in situ situation the limiting link in the chain leading to muscle contraction may be one preventing the Ca2+ release from taking place. The sites are the triads, T-tubules, and the surface membrane. The function of the latter two regarding action potential amplitude and propagation depends on [K+] gradients. Again, conflicting results exist regarding the electrophysiological changes and [K+] in fatigue. The activity pattern must then be taken into consideration. During high-intensity (high-frequency) activity the increased interstitial [K+] has been demonstrated to relate to fatigue, while in low-intensity fatiguing protocols, the T-tubule may be the limiting site. This fits with the concept of interstitial [K+] playing an essential role as a regulatory feedback mechanism, e.g. adjusting muscle blood flow to the metabolic load during muscle activity.
一个普遍的发现是，肌肉活动会导致钾离子穿过肌肉膜，同时也会导致肌肉疲劳，肌肉疲劳被定义为肌肉产生力量的能力下降。然而，关于钾在疲劳发展中的因果作用存在很多争议。在这种情况下，所使用的实验模型起着决定性作用，例如，我们是研究完整的体内器官，通过自愿收缩和心肺调节的反射反馈来进行原位研究，还是研究体外分离的肌肉或细胞，甚至是去膜纤维。在后者的模型中，已经有明确的证据表明Ca2+是对力量发展有重要意义的变量，而K+可能被忽略。然而，在原位情况下，导致肌肉收缩的连锁反应中的限制环节可能是阻止Ca2+释放发生的因素。这些部位是三联体、横小管和表面膜。后两者关于动作电位幅度和传播的功能取决于[K+]梯度。同样，关于疲劳时的电生理变化和[K+]也存在相互矛盾的结果。因此必须考虑活动模式。在高强度（高频）活动期间，已证明间质[K+]增加与疲劳有关，而在低强度疲劳方案中，横小管可能是限制部位。这与间质[K+]作为一种调节反馈机制发挥重要作用的概念相符合，例如在肌肉活动期间根据代谢负荷调节肌肉血流量。
