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Mechanisms of residual force enhancement in skeletal muscle: insights from experiments and mathematical models

机译:骨骼肌残余力增强的机制:来自实验和数学模型的见解

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摘要

A skeletal muscle that is stretched while contracting will produce more force at steady state than if it is stretched passively and then stimulated to contract. This phenomenon is known as residual force enhancement and has been widely studied since its description more than 60 years ago. The idea that the mechanical properties of a muscle are governed not just by its present length but also by its length at earlier time points has far reaching implications since muscles stretch and shorten routinely in normal use. In this review, we present the experimental and theoretical advances that have been made toward understanding the mechanisms that underlie residual force enhancement. In the past 10 years, experiments and models have focused on essentially three candidate mechanisms for residual force enhancement: (half-) sarcomere inhomogeneity, activity of so-called ‘passive’ mechanical elements in the sarcomere (titin), and the intrinsic properties of myosin crossbridges. Evidence, both computational and experimental, is accumulating for each of these mechanisms such that a final description of the phenomenon seems attainable in the near future. We conclude that computational models that incorporate more than one putative mechanism may ultimately facilitate reconciliation of the growing number of ideas and experimental data in this field.
机译:与被动拉伸然后再刺激收缩相比,在收缩时拉伸的骨骼肌在稳态时会产生更多的力。这种现象被称为残余力增强,自从60多年前对其进行描述以来,已经得到了广泛的研究。肌肉的机械性能不仅取决于其当前长度,还取决于其在较早时间点的长度,这一思想具有深远的意义,因为在正常使用中,肌肉通常会拉伸和缩短。在这篇综述中,我们介绍了在理解残余力增强基础的机制方面取得的实验和理论进展。在过去的十年中,实验和模型主要集中在三种残余力增强的候选机制上:(半)肌小节不均匀性,肌小节(titin)中所谓的``被动''机械元件的活动以及肌球蛋白跨桥。对于这些机制中的每一种,都积累了计算和实验证据,因此在不久的将来似乎可以对现象进行最终描述。我们得出的结论是,包含多个推定机制的计算模型最终可能有助于协调该领域中越来越多的想法和实验数据。

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