Shimizu H, Fujita T, Ishiwata S
Department of Physics, School of Science and Engineering, Waseda University, Tokyo, Japan.
Biophys J. 1992 May;61(5):1087-98. doi: 10.1016/S0006-3495(92)81918-5.
The length of sarcomeres in isolated myofibrils fixed at both ends spontaneously oscillates when MgADP and Pi coexist with MgATP in the absence of Ca2+ (Okamura, N., and S. Ishiwata, 1988. J. Muscle Res. Cell. Motil. 9:111-119). Here, we report that MgADP and Pi function as an activator and an inhibitor, respectively, of tension development of single skeletal muscle fibers in the absence of Ca2+ and the coexistence of MgADP and Pi with MgATP induces spontaneous tension oscillation. First, the isometric tension sharply increased when the concentration of MgADP became higher than approximately 3x that of MgATP and saturated at approximately 90% of the tension obtained under full Ca2+ activation; in parallel with this sigmoidal increase of tension, MgATPase activity appeared. The inhibition of contraction by the regulatory system seems to be desuppressed by the allosteric effect of actomyosin-ADP complex, similarly to so-called rigor complex. The ADP-induced tension was decreased along a reversed sigmoidal curve by the addition of Pi; actomyosin-ADP-Pi complex, which has no desuppression function, may be formed by exogenous Pi; accompanying the decline of tension, spontaneous oscillations of tension and sarcomere length appeared. It is suggested that the length oscillation of each (half) sarcomere would occur through the transition of cross-bridges between force-generating (on) and non-force-generating (off) states, which may be regulated by the mechanical states (strain) of cross-bridges and/or thin filaments.
在没有Ca2+的情况下，当MgADP和Pi与MgATP共存时，两端固定的分离肌原纤维中肌节的长度会自发振荡（冈村，N.，和S.石渡，1988。《肌肉研究与细胞运动杂志》9:111 - 119）。在此，我们报告在没有Ca2+的情况下，MgADP和Pi分别作为单根骨骼肌纤维张力发展的激活剂和抑制剂，并且MgADP和Pi与MgATP共存会诱导自发的张力振荡。首先，当MgADP的浓度高于MgATP浓度约3倍时，等长张力急剧增加，并在完全Ca2+激活下获得的张力的约90%处达到饱和；与这种张力的S形增加同时出现的是MgATP酶活性。调节系统对收缩的抑制似乎被肌动球蛋白 - ADP复合物的变构效应解除抑制，类似于所谓的强直复合物。通过添加Pi，ADP诱导的张力沿着反向S形曲线下降；没有解除抑制功能的肌动球蛋白 - ADP - Pi复合物可能由外源性Pi形成；随着张力的下降，张力和肌节长度出现自发振荡。有人提出，每个（半）肌节的长度振荡将通过横桥在产生力（接通）和不产生力（断开）状态之间的转变而发生，这可能由横桥和/或细肌丝的机械状态（应变）调节。
