Campbell K B, Razumova M V, Kirkpatrick R D, Slinker B K
Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman, Washington 99163, USA.
Biophys J. 2001 Oct;81(4):2278-96. doi: 10.1016/S0006-3495(01)75875-4.
To investigate the role of nonlinear myofilament regulatory processes in sarcomeric mechanodynamics, a model of myofilament kinetic processes, including thin filament on-off kinetics and crossbridge cycling kinetics with interactions within and between kinetic processes, was built to predict sarcomeric stiffness dynamics. Linear decomposition of this highly nonlinear model resulted in the identification of distinct contributions by kinetics of recruitment and by kinetics of distortion to the complex stiffness of the sarcomere. Further, it was established that nonlinear kinetic processes, such as those associated with cooperative neighbor interactions or length-dependent crossbridge attachment, contributed unique features to the stiffness spectrum through their effect on recruitment. Myofilament model-derived sarcomeric stiffness reproduces experimentally measured sarcomeric stiffness with remarkable fidelity. Consequently, characteristic features of the experimentally determined stiffness spectrum become interpretable in terms of the underlying contractile mechanisms that are responsible for specific dynamic behaviors.
为了研究非线性肌丝调节过程在肌节力学动态中的作用，构建了一个肌丝动力学过程模型，包括细肌丝开关动力学和横桥循环动力学以及动力学过程内部和之间的相互作用，以预测肌节的刚度动态。对这个高度非线性模型进行线性分解，从而确定了募集动力学和变形动力学对肌节复杂刚度的不同贡献。此外，还证实了非线性动力学过程，如与协同相邻相互作用或长度依赖性横桥附着相关的过程，通过其对募集的影响为刚度谱贡献了独特的特征。肌丝模型推导的肌节刚度以极高的保真度再现了实验测量的肌节刚度。因此，实验确定的刚度谱的特征可以根据负责特定动态行为的潜在收缩机制来解释。
