Stretch forces in skeletal muscle myofibrils and myosin molecules

肌肉收缩是生命的基本功能。用来解释肌肉收缩机制的标准理论被称为“跨桥理论”，它是半个世纪前提出的。然而，肌肉收缩的几个方面仍然知之甚少。在这些方面中，在激活的肌纤维拉伸过程中产生的高力不能用交叉桥理论轻易地解释。本提案的目的是研究拉伸力背后的机制，以及它与肌肉收缩的分子基础的联系。我们建议使用新颖而准确的测量方法，包括单个肌原纤维（肌肉纤维的亚细胞成分）和单分子力学来测试已经提出的解释拉伸力的假设。这些假设与收缩蛋白和肌肉纤维内被动成分在收缩过程中的作用有关。拉伸力不仅对理解收缩的基本机制很重要，而且对日常生活的几个方面也很重要，比如拉伸引起的肌肉损伤，以及偏心收缩时的力增强。

Muscle contraction is a basic function of life. The standard theory used to explain the mechanisms of muscle contraction is known as the cross-bridge theory, and was proposed half a century ago. However, several aspects of muscle contraction are still poorly understood. Among these aspects, the high forces produced during stretch of an activated muscle fiber cannot be readily explained by the cross-bridge theory. The goal of this proposal is to investigate the mechanisms behind stretch forces, and its association with the molecular basis of muscle contraction. We propose to use novel and accurate methods of measurement that include single myofibrils (sub-cellular components of muscle fibers) and single molecule mechanics to test hypotheses that have been raised to explain stretch forces. These hypotheses are associated with the role of contractile proteins and passive elements inside muscle fibers during contraction. Stretch forces are important not only to understand the basic mechanisms of contraction, but also several aspects of the everyday life, like stretch-induced muscle damage, and force potentiation during eccentric contractions.