Tension Development Model on Skeletal Muscles Using States Transition System

Abstract

As nerve impulse arrives at a skeletal muscle, the sarcoplasmic reticulum releases Ca²⁺ into muscle cells. Ca²⁺ concentration ([Ca²⁺]) increases, troponin conformation changes, and then ATP hydrolysis accelerates largely. Using the ATP hydrolysis energy the myosin heads stroke actin filaments, thus tension is developed.
Recently, the stochastic behavior of biological molecules is revealed by single molecule measurements. In this article, using the above knowledge, tension development model at molecular level is developed. First, we propose a model in which a site binds legands, with stochastic state transition. Applying the ligands binding model to four of Ca²⁺ binding sites on troponin, the troponin activation phenomenon is demonstrated. Next, a model in which a myosin head binds ATP is constructed. Using the models, we estimated the occurrence probability of a myosin head stroke, R_stroke. It is shown that estimated R_stroke realizes the time course of muscle tension, of which peak is delayed and broader than that of [Ca²⁺].