In skeletal muscle, Ca²⁺ release from the sarcoplasmic reticulum (SR) triggers contraction. In this study we develop a two compartment model to account for the Ca²⁺ dynamics in frog skeletal muscle fibers. The two compartments in the model correspond to the SR and the cytoplasm, where the myofibrils are placed. We use a detailed model for the several Ca²⁺ binding proteins in the cytoplasm in line with previous models. As a new feature, Ca²⁺ binding sites within the SR, attributed to calsequestrin, are modeled based on experimentally obtained properties. The intra SR Ca²⁺ buffer shows cooperativity, well represented by a Hill equation with parameters that depend on the initial [Ca²⁺] in the SR ([Ca²⁺]_SR). The number of total sites as well as the [Ca²⁺]_SR of half saturation are reduced as the resting [Ca²⁺]_SR is reduced, on the other hand the Hill number is not changed. The buffer power remained roughly constant.

The release process is activated by a voltage dependent mechanism that increases the Ca²⁺ permeability of the SR. We use the permeability time course and amplitude experimentally obtained during a voltage clamp pulse to drive the simulations. This model successfully reproduces the SR and cytoplasmic transients observed.

Additionally, we simulate [Ca²⁺] _SR transients in the case of high concentration of extrinsic Ca²⁺ buffers added to the cytoplasm to explore what properties of the permeability are necessary to account for the experimentally observed [Ca²⁺]_SR transients. The main novelty of the model, the intra SR Ca²⁺ buffer, is crucial for reproducing the experimental observations and it would be of use in future theoretical studies of excitation contraction coupling in skeletal muscle.

在骨骼肌中，从肌质网（SR）释放的Ca ²⁺触发收缩。在这项研究中，我们开发了一个两室模型来解释青蛙骨骼肌纤维中Ca ^2+的动力学。模型中的两个区室分别对应于放置肌原纤维的SR和细胞质。我们使用与以前的模型一致的细胞质中的几个Ca ²⁺结合蛋白的详细模型。作为一项新功能，SR中的Ca ²⁺结合位点（归因于calsequestrin）是根据实验获得的特性进行建模的。内部SR Ca ²⁺缓冲液显示出协同性，用希尔方程很好地表示，其参数取决于初始[Ca ²⁺SR中的[ ] （[Ca ²⁺ ] _SR）。总位点的的[Ca的数量以及²⁺ ] _SR半饱和的减小作为静止的[Ca ²⁺ ] _SR被降低，在另一方面山数目不改变。缓冲功率大致保持恒定。

释放过程由依赖电压的机制激活，该机制增加了SR的Ca ²⁺渗透性。我们使用在电压钳位脉冲期间实验获得的磁导率时间过程和幅度来驱动仿真。该模型成功地再现了观察到的SR和细胞质瞬变。

此外，在高浓度外源Ca ²⁺缓冲液添加到细胞质中的情况下，我们模拟[Ca ²⁺ ] _SR瞬变，以探讨渗透性的哪些特性对于解释实验观察到的[Ca ²⁺ ] _SR瞬变是必需的。该模型的主要新颖之处在于内部SR Ca ²⁺缓冲液对于重现实验结果至关重要，它将在未来骨骼肌兴奋性收缩偶联的理论研究中使用。