Herzog W, Lee E J, Rassier D E
University of Calgary, 2500 University Dr. N.W., Calgary, AB, Canada T2N 1N4.
J Physiol. 2006 Aug 1;574(Pt 3):635-42. doi: 10.1113/jphysiol.2006.107748. Epub 2006 May 18.
Residual force enhancement has been observed consistently in skeletal muscles following active stretching. However, its underlying mechanism(s) remain elusive, and it cannot be explained readily within the framework of the cross-bridge theory. Traditionally, residual force enhancement has been attributed to the development of sarcomere length non-uniformities. However, recent evidence suggests that this might not be the case. Rather, it appears that residual force enhancement has an active and a passive component. The active component is tentatively associated with changes in the cross-bridge kinetics that might be reflected in decreased detachment rates following active muscle stretching, while the passive component possibly originates from a structural protein, such as titin, whose stiffness might be regulated by calcium.
在主动拉伸后,骨骼肌中持续观察到残余力增强现象。然而,其潜在机制仍然难以捉摸,并且在横桥理论的框架内无法轻易解释。传统上,残余力增强归因于肌节长度不均匀性的发展。然而,最近的证据表明情况可能并非如此。相反,残余力增强似乎有一个主动成分和一个被动成分。主动成分初步与横桥动力学的变化有关,这可能反映在主动肌肉拉伸后解离速率的降低,而被动成分可能源自一种结构蛋白,如肌联蛋白,其刚度可能受钙调节。