Biomimetics Laboratory, Instituto de Biotecnología (IBUN), and Numerical Methods and Modeling Research Group (GNUM), Universidad Nacional de Colombia, Bogotá, Colombia.
Biomimetics Laboratory, Instituto de Biotecnología (IBUN), and Numerical Methods and Modeling Research Group (GNUM), Universidad Nacional de Colombia, Bogotá, Colombia; Computational Modeling of Natural Systems Research Group (COMMONS), Mechanical Engineering Department, Universidad Central, Bogotá, Colombia.
Biosystems. 2021 Apr;202:104355. doi: 10.1016/j.biosystems.2021.104355. Epub 2021 Jan 14.
Physical activity produces a change in skeletal-muscle size by activating synthesis or degradation of protein, which are outcomes of stimulating the IGF1-AKT signaling pathway. In this work, we propose a mathematical model that predicts the variation in muscle size under different activity conditions. The IGF1-AKT pathway was modeled using its 4 main molecules as variables in a dynamical system. We checked the stability of the system; we defined exercise training as a function of intensity, duration, and frequency; and we tested the model under four scenarios: first, we considered the daily low-intensity activity that should not promote atrophy nor hypertrophy (steady state); second, we simulated the effects of physical therapy in spinal cord injury patients (atrophy); third, we simulated exercise training in healthy subjects (hypertrophy); and fourth, we considered the effects of suspending a training program in healthy subjects (recovery after hypertrophy). Results showed that: protein synthesis and degradation are inactive, thus the size of the muscle stays stable in the first scenario; the muscle decreases only 10% of its initial size after 84 days of therapy every two days in the second scenario; training frequency produces rapid hypertrophy (11% after 25 days) when training every day, to no hypertrophy when training every 5 days in the third scenario; and a reduction of 50% the gain of the training program in the fourth scenario. By comparing our results to experimental reports, we found a remarkable agreement; therefore, our model is suitable for the development of training and therapeutic protocols.
体力活动通过激活蛋白质的合成或降解来改变骨骼肌大小，而蛋白质的合成或降解是刺激 IGF1-AKT 信号通路的结果。在这项工作中，我们提出了一个数学模型，该模型可预测在不同活动条件下肌肉大小的变化。IGF1-AKT 通路使用其 4 种主要分子作为变量在动力系统中建模。我们检查了系统的稳定性；我们将运动训练定义为强度、持续时间和频率的函数；并在四种情况下对模型进行了测试：首先，我们考虑了不会促进萎缩或肥大的日常低强度活动（稳态）；其次，我们模拟了脊髓损伤患者物理治疗的影响（萎缩）；第三，我们模拟了健康受试者的运动训练（肥大）；第四，我们考虑了在健康受试者中暂停训练计划的影响（肥大后的恢复）。结果表明：蛋白质的合成和降解都不活跃，因此在第一种情况下肌肉的大小保持稳定；在第二种情况下，每隔两天进行 84 天的治疗后，肌肉仅减少其初始大小的 10%；在第三种情况下，每天训练时，训练频率会导致快速肥大（25 天后增加 11%），而每 5 天训练时则不会导致肥大；在第四种情况下，训练计划的收益减少了 50%。通过将我们的结果与实验报告进行比较，我们发现了惊人的一致性；因此，我们的模型适合开发训练和治疗方案。
