Shorten Paul R, O'Callaghan Paul, Davidson John B, Soboleva Tanya K
AgResearch Limited, Ruakura Research Centre, Private Bag, 3123, Hamilton, New Zealand.
J Muscle Res Cell Motil. 2007;28(6):293-313. doi: 10.1007/s10974-007-9125-6. Epub 2007 Dec 14.
The ability for muscle to repeatedly generate force is limited by fatigue. The cellular mechanisms behind muscle fatigue are complex and potentially include breakdown at many points along the excitation-contraction pathway. In this paper we construct a mathematical model of the skeletal muscle excitation-contraction pathway based on the cellular biochemical events that link excitation to contraction. The model includes descriptions of membrane voltage, calcium cycling and crossbridge dynamics and was parameterised and validated using the response characteristics of mouse skeletal muscle to a range of electrical stimuli. This model was used to uncover the complexities of skeletal muscle fatigue. We also parameterised our model to describe force kinetics in fast and slow twitch fibre types, which have a number of biochemical and biophysical differences. How these differences interact to generate different force/fatigue responses in fast- and slow- twitch fibres is not well understood and we used our modelling approach to bring new insights to this relationship.
肌肉反复产生力量的能力受到疲劳的限制。肌肉疲劳背后的细胞机制很复杂，可能包括兴奋 - 收缩途径上多个点的功能障碍。在本文中，我们基于将兴奋与收缩联系起来的细胞生化事件构建了骨骼肌兴奋 - 收缩途径的数学模型。该模型包括膜电压、钙循环和横桥动力学的描述，并使用小鼠骨骼肌对一系列电刺激的反应特性进行了参数化和验证。这个模型被用来揭示骨骼肌疲劳的复杂性。我们还对模型进行了参数化，以描述快肌纤维和慢肌纤维类型中的力动力学，它们在许多生化和生物物理方面存在差异。这些差异如何相互作用以在快肌纤维和慢肌纤维中产生不同的力/疲劳反应尚未得到充分理解，我们使用建模方法为这种关系带来了新的见解。
