Smith D A
Department of Physics, Monash University, Clayton, Australia.
J Muscle Res Cell Motil. 1991 Oct;12(5):455-65. doi: 10.1007/BF01738330.
Schädler and colleagues (1969, 1971) and Steiger (1977a) have found that tetanized insect fibrillar and cardiac muscles exhibit damped isometric oscillations in tension following a quick stretch. This behaviour cannot be explained by the conventional sliding filament model at full activation, or by including stretch activation in the obvious way. However, it is predicted by a sliding filament model which allows these muscles to be further activated by an increase in thin-filament tension even at high calcium levels (above 10(-5) M), providing the strength gamma of strain-activation coupling exceeds a critical value. Calculations from a comprehensive model of the actin-myosin contraction cycle suggest that this can be achieved if the phosphate release and head rotation steps are both regulated by calcium and thin-filament tension. The model also predicts a delayed tension rise following a quick release for subcritical values of gamma. Current knowledge of sarcomere structure and regulation of contractility in striated muscle indicates that this strain-activation mechanism alone cannot account for all stretch-activation phenomena, although many can be predicted if the regulatory filament is allowed to carry passive tension.
沙德勒及其同事(1969年、1971年)以及施泰格(1977a)发现,强直收缩的昆虫纤维状肌肉和心肌在快速拉伸后会出现张力的阻尼等长振荡。这种行为无法用完全激活时的传统滑动丝模型来解释,也无法通过以明显方式纳入拉伸激活来解释。然而,一个滑动丝模型预测了这种行为,该模型允许这些肌肉即使在高钙水平(高于10⁻⁵ M)下也能通过细肌丝张力的增加而进一步激活,前提是应变激活耦合的强度γ超过临界值。从肌动蛋白 - 肌球蛋白收缩周期的综合模型进行的计算表明,如果磷酸释放和头部旋转步骤都受钙和细肌丝张力调节,就可以实现这一点。该模型还预测,对于γ的亚临界值,快速释放后张力会延迟上升。目前关于肌节结构和横纹肌收缩性调节的知识表明,仅这种应变激活机制不能解释所有的拉伸激活现象,尽管如果允许调节丝承受被动张力,许多现象是可以预测的。