Evaluation of a novel model of skeletal muscle fatigue

骨骼肌疲劳是几个世纪以来一直让科学家们着迷的一种常见体验，但在反复激活过程中和之后影响收缩特性的细胞过程尚不清楚。大多数疲劳理论认为代谢产物的积累和收缩反应的抑制。这与已知的疲劳的主要机制：抑制兴奋-收缩偶联(E-CC)不一致。现在是时候研究E-CC是如何受损的了。对肌肉疲劳提出了一种创新的解释：疲劳是E-CC细胞调节的结果，以保存肌肉中的能量电荷。文中提出了实验来检验这一理论以及其他理论。建议在生理温度下使用单纤维、纤维束和整体肌肉进行实验。已有研究表明，在生理温度下，常温下的疲劳机制与疲劳无关。拟议研究的第二个创新和实用方面是，正在考虑的宫缩将是次极大的，就像普通运动中的自然宫缩一样。

Skeletal muscle fatigue, is a common experience that has fascinated scientists for centuries, yet the cellular processes impacting contractile properties during and following repeated activations are not understood. Most theories of fatigue considered build-up of products of metabolism and inhibition of the contractile response. This is not consistent with the known primary mechanism of fatigue: inhibition of excitation-contraction coupling (E-CC). It is time to study how E-CC is impaired. An innovative explanation for muscle fatigue is proposed: fatigue is a consequence of cellular regulation of E-CC to preserve energy charge in the muscle. Experiments are proposed to test this theory as well as alternative theories. Experiments are proposed using: single fibre, fibre bundles and whole muscle at physiological temperature. It has been demonstrated that fatigue mechanisms at room temperature are not relevant at physiological temperature. A second innovative and practical aspect of the proposed studies is contractions under consideration will be sub maximal, like natural contractions in common movements.