Departments of Kinesiology and Physical Education, Physiology, Physics, McGill University, Montreal, Quebec, Canada.
Am J Physiol Cell Physiol. 2012 Jan 1;302(1):C240-8. doi: 10.1152/ajpcell.00208.2011. Epub 2011 Oct 12.
When a stretch is imposed to activated muscles, there is a residual force enhancement that persists after the stretch; the force is higher than that produced during an isometric contraction in the corresponding length. The mechanisms behind the force enhancement remain elusive, and there is disagreement if it represents a sarcomeric property, or if it is associated with length nonuniformities among sarcomeres and half-sarcomeres. The purpose of this study was to investigate the effects of stretch on single sarcomeres and myofibrils with predetermined numbers of sarcomeres (n = 2, 3. . . , 8) isolated from the rabbit psoas muscle. Sarcomeres were attached between two precalibrated microneedles for force measurements, and images of the preparations were projected onto a linear photodiode array for measurements of half-sarcomere length (SL). Fully activated sarcomeres were subjected to a stretch (5-10% of initial SL, at a speed of 0.3 μm·s(-1)·SL(-1)) after which they were maintained isometric for at least 5 s before deactivation. Single sarcomeres showed two patterns: 31 sarcomeres showed a small level of force enhancement after stretch (10.46 ± 0.78%), and 28 sarcomeres did not show force enhancement (-0.54 ± 0.17%). In these preparations, there was not a strong correlation between the force enhancement and half-sarcomere length nonuniformities. When three or more sarcomeres arranged in series were stretched, force enhancement was always observed, and it increased linearly with the degree of half-sarcomere length nonuniformities. The results show that the residual force enhancement has two mechanisms: 1) stretch-induced changes in sarcomeric structure(s); we suggest that titin is responsible for this component, and 2) stretch-induced nonuniformities of half-sarcomere lengths, which significantly increases the level of force enhancement.
当对激活的肌肉施加伸展时,会产生一种残余力增强,这种增强会在伸展后持续存在;这种力比相应长度的等长收缩产生的力更高。产生力增强的机制仍然难以捉摸,而且对于它是否代表肌节的特性,或者是否与肌节和半肌节之间的长度不均匀性有关,存在分歧。本研究的目的是研究从兔腰肌中分离出的具有预定肌节数量(n=2、3……8)的单个肌节和肌原纤维对伸展的影响。肌节附着在两个预先校准的微针之间进行力测量,并用线性光电二极管阵列测量准备的半肌节长度(SL)。完全激活的肌节在速度为 0.3 μm·s(-1)·SL(-1)下伸展 5-10%的初始 SL 后,至少保持等长 5 秒,然后再失活。单个肌节显示出两种模式:31 个肌节在伸展后显示出较小的力增强水平(10.46±0.78%),而 28 个肌节没有显示力增强(-0.54±0.17%)。在这些准备中,力增强与半肌节长度不均匀之间没有很强的相关性。当三个或更多串联的肌节被拉伸时,总是会观察到力增强,并且它与半肌节长度不均匀的程度呈线性增加。结果表明,残余力增强有两种机制:1)肌节结构的伸展诱导变化;我们建议肌联蛋白负责此组件,2)伸展诱导的半肌节长度不均匀性,这显著增加了力增强的水平。