Gordon T, Stein R B
Department of Pharmacology, University of Alberta, Edmonton, Canada.
Muscle Nerve. 1988 Aug;11(8):819-27. doi: 10.1002/mus.880110804.
Isometric force and stiffness of fast- and slow-twitch muscles of affected and normal mice of the 129/ReJ dy/dy strain were studied at rest and during active contraction at a variety of lengths. Dystrophic muscles developed less force in response to stimulation, but the resting stiffness was not reduced as much, particularly at long muscle lengths. This is consistent with the replacement of muscle fibers by connective tissue that is considerably less elastic. When second and third stimuli are superimposed on the rising phase of a twitch in a normal muscle, a less-than-linear summation of force and stiffness generation (early depression) is followed by a more-than-linear summation (later facilitation). Dystrophic muscles showed a smaller early depression and a greater later facilitation of force and active muscle stiffness. Many of these phenomena can be predicted from a simple model of Ca2+ release and binding to troponin.
对129/ReJ dy/dy品系患病和正常小鼠的快肌和慢肌在静息状态以及不同长度下主动收缩时的等长力和刚度进行了研究。营养不良的肌肉在受到刺激时产生的力较小,但静息刚度降低幅度没那么大,尤其是在肌肉长度较长时。这与弹性小得多的结缔组织替代肌纤维的情况一致。当在正常肌肉的单收缩上升期叠加第二个和第三个刺激时,力和刚度产生呈现小于线性的总和(早期抑制),随后是大于线性的总和(后期易化)。营养不良的肌肉早期抑制较小,后期力和主动肌肉刚度的易化较大。其中许多现象可以从Ca2+释放并与肌钙蛋白结合的简单模型预测出来。