Parsons C, Porter K R
Science. 1966 Jul 22;153(3734):426-7. doi: 10.1126/science.153.3734.426.
Observations of contracting muscle fibrils in cultured cells indicate that the force which restores the resting length of the sarcomere comes from the contractile elements themselves and not from external elasticity, as is now generally accepted. In light of biochemical studies on the contraction-relaxation cycle, it is postulated that the elongating force is one of internal elasticity in the sarcomere, which arises during contraction from the distortion of bonds between filaments and/or structural proteins. This mechanism of restoration may serve to establish optimal sarcomere length for production of maximum contractile force, and in cardiac muscle this mechanism may be a factor in ventricular filling.
对培养细胞中收缩肌原纤维的观察表明,恢复肌节静息长度的力来自收缩元件本身,而非外部弹性,这一点如今已被广泛接受。根据对收缩-舒张周期的生化研究推测,伸长力是肌节内部弹性之一,它在收缩过程中由细丝和/或结构蛋白之间的键扭曲产生。这种恢复机制可能有助于建立产生最大收缩力的最佳肌节长度,在心肌中,这种机制可能是心室充盈的一个因素。