Rassier Dilson E
Department of Kinesiology and Physical Education, McGill University, Montreal, Quebec, Canada
Am J Physiol Cell Physiol. 2017 Aug 1;313(2):C134-C145. doi: 10.1152/ajpcell.00050.2017. Epub 2017 May 24.
Muscle contraction is commonly associated with the cross-bridge and sliding filament theories, which have received strong support from experiments conducted over the years in different laboratories. However, there are studies that cannot be readily explained by the theories, showing ) a plateau of the force-length relation extended beyond optimal filament overlap, and forces produced at long sarcomere lengths that are higher than those predicted by the sliding filament theory; ) passive forces at long sarcomere lengths that can be modulated by activation and Ca, which changes the force-length relation; and ) an unexplained high force produced during and after stretch of activated muscle fibers. Some of these studies even propose "new theories of contraction." While some of these observations deserve evaluation, many of these studies present data that lack a rigorous control and experiments that cannot be repeated in other laboratories. This article reviews these issues, looking into studies that have used intact and permeabilized fibers, myofibrils, isolated sarcomeres, and half-sarcomeres. A common mechanism associated with sarcomere and half-sarcomere length nonuniformities and a Ca-induced increase in the stiffness of titin is proposed to explain observations that derive from these studies.
肌肉收缩通常与横桥和肌丝滑行理论相关联，这些理论多年来在不同实验室进行的实验中得到了有力支持。然而，有些研究结果无法用这些理论轻易解释，具体表现为：）力-长度关系的平台期延伸至肌丝最佳重叠长度之外，且在长肌节长度时产生的力高于肌丝滑行理论预测的力；）长肌节长度时的被动力可被激活和钙离子调节，从而改变力-长度关系；）激活的肌肉纤维在拉伸过程中和拉伸后会产生无法解释的高力。其中一些研究甚至提出了“新的收缩理论”。虽然其中一些观察结果值得评估，但许多研究提供的数据缺乏严格的对照，且实验无法在其他实验室重复。本文回顾了这些问题，探讨了使用完整和通透化纤维、肌原纤维、分离的肌节和半肌节进行的研究。提出了一种与肌节和半肌节长度不均匀性以及钙离子诱导的肌联蛋白刚度增加相关的共同机制，以解释这些研究得出的观察结果。
