Koppes Ryan A, Swank Douglas M, Corr David T
Department of Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, New York; and.
Department of Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, New York; and Department of Biological Sciences and Center for Biotechnology and Interdisciplinary Study, Rensselaer Polytechnic Institute, Troy, New York.
Am J Physiol Cell Physiol. 2015 Oct 15;309(8):C551-7. doi: 10.1152/ajpcell.00202.2015. Epub 2015 Aug 19.
The increase in steady-state force after active lengthening in skeletal muscle, termed force enhancement (FE), has been observed for nearly one century. Although demonstrated experimentally at various structural levels, the underlying mechanism(s) remain unknown. We recently showed that the Drosophila jump muscle is an ideal model for investigating mechanisms behind muscle physiological properties, because its mechanical characteristics, tested thus far, duplicate those of fast mammalian skeletal muscles, and Drosophila has the advantage that it can be more easily genetically modified. To determine if Drosophila would be appropriate to investigate FE, we performed classic FE experiments on this muscle. Steady-state FE (FESS), following active lengthening, increased by 3, 7, and 12% of maximum isometric force, with increasing stretch amplitudes of 5, 10, and 20% of optimal fiber length (FLOPT), yet was similar for stretches across increasing stretch velocities of 4, 20, and 200% FLOPT/s. These FESS characteristics of the Drosophila jump muscle closely mimic those observed previously. Jump muscles also displayed typical transient FE characteristics. The transient force relaxation following active stretch was fit with a double exponential, yielding two phases of force relaxation: a fast initial relaxation of force, followed by a slower recovery toward steady state. Our analyses identified a negative correlation between the slow relaxation rate and FESS, indicating that there is likely an active component contributing to FE, in addition to a passive component. Herein, we have established the Drosophila jump muscle as a new and genetically powerful experimental model to investigate the underlying mechanism(s) of FE.
骨骼肌主动拉长后稳态力的增加，即所谓的力增强（FE），已被观察到近一个世纪。尽管在各种结构水平上通过实验得到了证实，但其潜在机制仍然未知。我们最近表明，果蝇跳跃肌肉是研究肌肉生理特性背后机制的理想模型，因为到目前为止所测试的其力学特性与快速哺乳动物骨骼肌的力学特性相符，而且果蝇具有更容易进行基因改造的优势。为了确定果蝇是否适合用于研究力增强，我们对这种肌肉进行了经典的力增强实验。主动拉长后的稳态力增强（FESS），随着最佳纤维长度（FLOPT）的5%、10%和20%的拉伸幅度增加，分别增加了最大等长力的3%、7%和12%，然而对于4%、20%和200%FLOPT/s的不同拉伸速度下的拉伸，FESS相似。果蝇跳跃肌肉的这些FESS特性与先前观察到的特性非常相似。跳跃肌肉还表现出典型的瞬态力增强特性。主动拉伸后的瞬态力松弛符合双指数函数，产生两个力松弛阶段：力的快速初始松弛，随后是向稳态的较慢恢复。我们的分析确定了慢松弛率与FESS之间存在负相关，表明除了被动成分外，可能还有一个主动成分对力增强有贡献。在此，我们已将果蝇跳跃肌肉确立为一种新的且具有强大遗传学功能的实验模型，用于研究力增强的潜在机制。
