Nielsen Bjørn Gilbert
Quantum Protein Centre (QuP), Department of Physics, Technical University of Denmark, Bldg. 309, 2800 Lyngby, Denmark.
Eur Biophys J. 2009 Feb;38(2):159-73. doi: 10.1007/s00249-008-0364-2. Epub 2008 Aug 27.
This work presents a novel structural model of skeletal muscle activation, providing a physiologically based account of frequency-dependent muscle responses like the catch-like effect. Numerous Ca2+ reservoirs within muscle fibers are considered, and a simplified analysis of the allocation of Ca2+ resources and the dynamics of calcium transport is proposed. The model correctly accounts for catch-like effects in slow and fast-twitch fibers during long-train stimulations and force-frequency relations in different muscle types. Results obtained from the model compare favorably to experiments showing that prolonged increases in force characteristic of the catch-like effect are not accompanied by sustained increases in free myoplasmic Ca2+. Also, in agreement with early experiments, the interspike interval in catch-inducing doublets is seen to be an important parameter for regulating the precise onset amplitude of the catch-like effect. This suggests that a plausible physiological function for the inclusion of doublets or the exclusion of individual spikes within a regular motor-neuronal spike-train is to rapidly bring skeletal muscles to predefined target forces according to prespecified motor programs in the central nervous system. This is a potentially very useful property directly mediated by the catch-like process modeled here. One further prediction of the model is that the slope of the frequency-tension profile of a given muscle is highly sensitive to changes in the efficiency and temporal characteristics of the dihydropyridine-ryanodine receptor complex. Interestingly, this is consistent with findings made on cardiac muscles, and might incidentally explain some instances of cardiac failure.
这项工作提出了一种新颖的骨骼肌激活结构模型,为诸如捕捉样效应等频率依赖性肌肉反应提供了基于生理学的解释。考虑了肌肉纤维内众多的Ca2+储存库,并对Ca2+资源的分配和钙转运动力学进行了简化分析。该模型正确地解释了长串刺激期间慢肌纤维和快肌纤维中的捕捉样效应以及不同肌肉类型中的力-频率关系。从该模型获得的结果与实验结果相比非常有利,实验表明捕捉样效应的特征性力的长时间增加并不伴随着游离肌浆Ca2+的持续增加。此外,与早期实验一致,诱捕双脉冲中的峰间间隔被视为调节捕捉样效应精确起始幅度的重要参数。这表明在规则的运动神经元放电序列中包含双脉冲或排除单个尖峰的一个合理的生理功能是根据中枢神经系统中的预定运动程序将骨骼肌迅速带到预定义的目标力。这是此处建模的捕捉样过程直接介导的潜在非常有用的特性。该模型的另一个预测是,给定肌肉的频率-张力曲线的斜率对二氢吡啶-雷诺丁受体复合物的效率和时间特征的变化高度敏感。有趣的是,这与在心肌上的发现一致,并且可能顺便解释一些心力衰竭的情况。