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Recent insights into the molecular basis of muscular fatigue

机译：对肌肉疲劳分子基础的最新见解

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The cause of muscle fatigue has been studied for more than 100 yr, yet its molecular basis remains poorly understood. Prevailing theories suggest that much of the fatigue-induced loss in force and velocity can be attributed to the inhibitory action of metabolites, principally phosphate (Pi) and hydrogen ions (H, i.e., acidosis), on the contractile proteins, but the precise detail of how this inhibition occurs has been difficult to visualize at the molecular level. However, recent technological developments in the areas of biophysics, molecular biology, and structural biology are enabling researchers to directly observe the function and dysfunction of muscle contractile proteins at the level of a single molecule. In fact, the first direct evidence that high levels of H and Pi inhibit the function of muscle's molecular motor, myosin, has recently been observed in a single molecule laser trap assay. Likewise, advances in structural biology are taking our understanding further, providing detail at the atomic level of how some metabolites might alter the internal motions of myosin and thereby inhibit its ability to generate force and motion. Finally, new insights are also being gained into the indirect role that muscle regulatory proteins troponin (Tn) and tropomyosin (Tn) play in the fatigue process. In vitro studies, incorporating TnTm, suggest that a significant portion of the decreased force and motion during fatigue may be mediated through a disruption of the molecular motions of specific regions within Tn and Tm. These recent advances are providing unprecedented molecular insight into the structure and function of the contractile proteins and, in the process, are reshaping our understanding of the process of fatigue.
机译：肌肉疲劳的原因已经研究了100多年，但其分子基础仍然知之甚少。普遍的理论表明，疲劳引起的力和速度的损失大部分可以归因于代谢产物（主要是磷酸盐（Pi）和氢离子（H，即酸中毒））对收缩蛋白的抑制作用，但确切的细节这种抑制作用的发生机理很难在分子水平上观察到。但是，生物物理学，分子生物学和结构生物学领域的最新技术发展使研究人员能够直接观察到单个分子水平的肌肉收缩蛋白的功能和功能障碍。事实上，最近首次在单分子激光阱测定中观察到了高水平的H和Pi抑制肌肉分子分子肌球蛋白功能的直接证据。同样，结构生物学的进步使我们进一步了解，在原子水平上提供了一些代谢物可能如何改变肌球蛋白内部运动从而抑制其产生力和运动能力的详细信息。最后，关于肌肉调节蛋白肌钙蛋白（Tn）和肌钙蛋白（Tn）在疲劳过程中发挥的间接作用也获得了新的见解。纳入TnTm的体外研究表明，疲劳过程中很大一部分力和运动的降低可能是通过破坏Tn和Tm内特定区域的分子运动来介导的。这些最新进展为收缩蛋白的结构和功能提供了前所未有的分子洞察力，并在此过程中重塑了我们对疲劳过程的理解。

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