Role of potassium and chloride channel during non-fatiguing and fatiguing muscular activity in skeletal muscles

肌肉疲劳的定义是肌肉在重复刺激过程中产生力量或做功的能力下降。它也是一种保护机制，可以防止ATP的大量消耗和胞浆钙的增加，这两个因素已知会导致收缩功能障碍和纤维损伤。疲劳的一个主要机制是钙释放减少，从而减少了力的产生。该实验室广泛研究了膜兴奋性的变化如何导致钙释放减少，主要集中在KATP通道、钠离子和钾离子上。我们提供的证据表明，KATP通道在降低膜兴奋性以保护肌肉免受收缩功能障碍和纤维损伤方面起着至关重要的作用。尽管有充分的证据表明，钠、钾和氢离子对疲劳过程中作用力的减少有贡献，但来自本实验室和其他实验室的新的和令人兴奋的研究也提供了证据，证明在某些条件下，这些离子可以增强作用力或延缓疲劳。

Muscle fatigue is defined as a decreased capacity of muscle to generate force or do work during repetitive stimulation. It is also a protective mechanism that prevents large ATP depletion and increase in cytosolic calcium, two factors known to cause contractile dysfunctions and fiber damage. One major mechanism of fatigue involves a decrease in calcium release resulting in less force generation. This laboratory has extensively studied how changes in membrane excitability can result in less calcium release, and the main focus being on the Katp channel, sodium and potassium ions. We have provided evidence that the Katp channel is crucial in lowering membrane excitability to protect muscle against contractile dysfunctions and fiber damage. Although there is ample evidence for a contribution of sodium, potassium and hydrogen ions to the decrease in force during fatigue, new and exciting studies, from this laboratory and others, have also provided evidence that under some conditions theses same ions can enhance force or delay fatigue.