Titins are mainly responsible for passive mechanical properties of a single muscle fiber, which, however, can be compromised by the change in molecular structures of titins occurring in some muscle-related diseases. Based on molecular structures of titins within a sarcomere unit, we have developed a constitutive theory for the passive elasticity of a single muscle fiber with the utilization of the virtual work principal. The number density of titins, domain composition of titins, the kinetics of folded domains within titins, the interaction between the water and molecular chains, the sarcomere length, etc., can all be considered in the theory. The predicted stress-strain curves based on the theory are in agreement with experiment. We also demonstrate that abnormal structural parameters of titins from patients with chronic obstructive pulmonary disease or muscle atrophy caused by long-term disuse can be extracted with the theory. We then suggest that this constitutive theory may potentially facilitate the molecular diagnosis of muscle diseases exhibiting abnormality in the passive elasticity.

Titins 主要负责单条肌肉纤维的被动机械特性，然而，在一些肌肉相关疾病中发生的 Titins 分子结构的变化可能会损害这些特性。基于肌节单元内肌动蛋白的分子结构，我们利用虚拟功原理开发了单条肌纤维被动弹性的本构理论。肌动蛋白的个数密度、肌动蛋白的结构域组成、肌动蛋白内折叠结构域的动力学、水与分子链的相互作用、肌节长度等都可以在理论中加以考虑。基于该理论预测的应力-应变曲线与实验一致。我们还证明了该理论可以提取慢性阻塞性肺疾病或长期废用引起的肌肉萎缩患者的肌动蛋白结构参数异常。然后，我们建议这种本构理论可能有助于对表现出被动弹性异常的肌肉疾病的分子诊断。.