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首页> 外文期刊>Journal of Biomechanics >A cross-bridge based model of force depression: Can a single modification address both transient and steady-state behaviors?
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A cross-bridge based model of force depression: Can a single modification address both transient and steady-state behaviors?

机译：基于跨桥的力降低模型：单个修改可以同时解决瞬态和稳态行为吗？

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Force depression (FD), the reduction of isometric force following active shortening, is a phenomenon of skeletal muscle that has received significant attention in biomechanical and physiological literature, yet the mechanisms underlying FD remain unknown. Recent experiments identified a slower rate of force redevelopment with increasing amounts of steady-state FD, suggesting that FD may be caused, at least in part, by a decrease in cross-bridge binding rate (Corr and Herzog, 2005; Koppes et al., 2014). Herein, we develop a cross-bridge based model of FD in which the binding rate function, f, decreases with the mechanical work performed during shortening. This modification incorporates a direct relationship between steady-state FD and muscle mechanical work (Corr and Herzog, 2005; Herzog et al., 2000; Kosterina et al., 2008), and is consistent with a proposed mechanism attributing FD to stress-induced inhibition of cross-bridge attachments (Herzog, 1998; Marechal and Plaghki, 1979). Thus, for an increase in mechanical work, the model should predict a slower force redevelopment (decreased attachment rate) to a more depressed steady-state force (fewer attached cross-bridges), and a reduction in contractile element stiffness (Ford et al., 1981). We hypothesized that since this modification affects the cross-bridge kinetics, a corresponding model would be able to account for both transient and steady-state FD behaviors. Comparisons to prior experiments (Corr and Herzog, 2005; Herzog et al., 2000; Kosterina et al., 2008) show that both steady-state and transient aspects of FD, as well as the relationship of FD with respect to speed and amplitude of shortening, are well captured by this model. Thus, this relatively simple cross-bridge based model of FD lends support to a mechanism involving the inhibition of cross bridge binding, and indicates that cross-bridge kinetics may play a critical role in FD. (C) 2016 Elsevier Ltd. All rights reserved.
机译：主动压迫（FD）是主动缩短后等轴测力的减小，它是骨骼肌的一种现象，在生物力学和生理学文献中已引起广泛关注，但FD的潜在机制仍然未知。最近的实验发现，随着稳态FD量的增加，力量重建的速度会变慢，这表明FD可能至少部分是由跨桥结合率的降低引起的（Corr and Herzog，2005; Koppes等。 ，2014）。本文中，我们开发了一种基于FD的跨桥模型，其中结合率函数f随着缩短过程中的机械功而降低。这种修饰结合了稳态FD与肌肉机械功之间的直接关系（Corr和Herzog，2005; Herzog等，2000; Kosterina等，2008），并且与将FD归因于压力引起的机制相一致。抑制跨桥连接（Herzog，1998; Marechal和Plaghki，1979）。因此，为了增加机械功，模型应该预测较慢的力再发展（降低的附着率）到更小的稳态力（附着的跨桥更少），以及收缩元件刚度的降低（Ford等。 （1981年）。我们假设，由于这种修改会影响跨桥动力学，因此相应的模型将能够考虑瞬态和稳态FD行为。与先前实验的比较（Corr和Herzog，2005; Herzog等，2000; Kosterina等，2008）表明，FD的稳态和瞬态方面，以及FD与速度和振幅的关系该模型很好地捕获了缩短的时间。因此，这种相对简单的基于FD的跨桥模型为涉及抑制跨桥结合的机制提供了支持，并表明跨桥动力学可能在FD中起关键作用。 （C）2016 Elsevier Ltd.保留所有权利。

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