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

钾和氯离子通道在骨骼肌非疲劳和疲劳肌肉活动中的作用

• 批准号: 120524-2009
• 负责人: Renaud, JeanMarc
• 金额: $ 2.4万
• 依托单位: University of Ottawa
• 依托单位国家: 加拿大
• 项目类别: Discovery Grants Program - Individual
• 财政年份: 2013
• 资助国家: 加拿大
• 起止时间: 2013-01-01 至 2014-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=522104
• 关键词: Role; potassium; chloride; channel; during

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.

肌肉疲劳被定义为在重复刺激期间肌肉产生力或做功的能力降低。它也是一种保护机制，可以防止大量ATP消耗和胞质钙增加，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涉及钙释放的减少，导致产生的力减少。 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，主要关注Katp通道，钠离子和钾离子。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至关重要。虽然有足够的证据表明钠、钾和氢离子对疲劳期间力的下降有贡献，但来自该实验室和其他实验室的新的令人兴奋的研究也提供了证据，证明在某些条件下，这些相同的离子可以增强力或延迟疲劳。