Herzog W, Schachar R, Leonard T R
University of Calgary, 2500 University Drive NW, Calgary, AB T2N 1N4, Canada.
J Exp Biol. 2003 Oct;206(Pt 20):3635-43. doi: 10.1242/jeb.00645.
The mechanisms causing the steady-state force enhancement following active skeletal muscle stretching are not well understood. Recently, we found direct evidence that part of the force enhancement is associated with the engagement of a passive component. In this study, we reproduced the conditions that give consistent passive force enhancement and evaluated the mechanical properties of this passive force enhancement so as to gain insight into its source. The three primary results were that (1). the passive force enhancement is long lasting (>25 s), (2). passive force enhancement was reduced in a dose-dependent manner by the amount of shortening preceding active muscle stretching, and (3). passive force enhancement could be abolished 'instantaneously' by shortening-stretching the passive muscle by an amount equivalent to the active stretch magnitude. Together with the remaining results, we conclude that the source of the passive force enhancement must be arranged in parallel with the contractile force, it must consist of a viscoelastic molecular spring whose stiffness characteristic can be reset by shortening, and it must have a characteristic length that is governed by the length of the contractile components, possibly the sarcomeres. Based on these results, the molecular spring titin emerges as a possible candidate for the passive component of the steady-state force enhancement observed in this and previous studies.
主动拉伸骨骼肌后导致稳态力增强的机制尚未完全明确。最近,我们发现了直接证据,表明部分力增强与被动成分的参与有关。在本研究中,我们重现了能产生一致的被动力增强的条件,并评估了这种被动力增强的力学特性,以便深入了解其来源。三个主要结果是:(1)被动力增强持续时间长(>25秒);(2)主动肌肉拉伸前的缩短量会使被动力增强以剂量依赖的方式降低;(3)通过将被动肌肉缩短拉伸至与主动拉伸幅度相当的量,可以“瞬间”消除被动力增强。结合其他结果,我们得出结论,被动力增强的来源必须与收缩力并联排列,它必须由一个粘弹性分子弹簧组成,其刚度特性可通过缩短来重置,并且它必须具有一个由收缩成分(可能是肌节)的长度所决定的特征长度。基于这些结果,分子弹簧肌联蛋白成为在本研究及之前研究中观察到的稳态力增强的被动成分的一个可能候选者。