残余力增强是由骨骼和心脏肌原纤维中的titin调节的

N. Shalabi, A. Cornachione, F. de Souza Leite, S. Vengallatore, D. Rassier
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引用次数: 32

摘要

当骨骼肌在收缩时被拉伸时,肌肉产生的力比在相同长度的等距收缩时产生的力要大得多:这种现象被称为残余力增强。残余力的增强是令人困惑的,因为它不能直接解释经典的力-长度关系和滑动丝收缩理论,这是肌肉领域的主要范式。我们使用定制的仪器来测量骨骼肌原纤维的剩余力增强,并首次测量了心脏肌原纤维。我们的数据报告,残余力增强存在于骨骼肌中,但不存在于心肌中,并由titin蛋白细丝的不同同工型调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Residual force enhancement is regulated by titin in skeletal and cardiac myofibrils
When a skeletal muscle is stretched while it contracts, the muscle produces a relatively higher force than the force from an isometric contraction at the same length: a phenomenon referred to as residual force enhancement. Residual force enhancement is puzzling because it cannot be directly explained by the classical force–length relationship and the sliding filament theory of contraction, the main paradigms in the muscle field. We used custom‐built instruments to measure residual force enhancement in skeletal myofibrils, and, for the first time, in cardiac myofibrils. Our data report that residual force enhancement is present in skeletal muscles, but not cardiac muscles, and is regulated by the different isoforms of the titin protein filaments.
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