BioSimulation Center, Krakow, Poland.
Pulmonary and Critical Care Physiology and Medicine, The Lundquist Institute for Biomedical Innovation Medical Center, Torrance, California.
J Appl Physiol (1985). 2021 Feb 1;130(2):498-507. doi: 10.1152/japplphysiol.00745.2020. Epub 2020 Nov 19.
Computer simulations, using the "P double-threshold" mechanism of muscle fatigue postulated previously (the first threshold initiating progressive reduction in work efficiency and the second threshold resulting in exercise intolerance), demonstrated that several parameters of the skeletal muscle bioenergetic system can affect maximum oxygen consumption (V̇O), critical power (CP), and oxygen consumption (V̇O) on-kinetics in skeletal muscle. Simulations and experimental observations together demonstrate that endurance exercise training increases oxidative phosphorylation (OXPHOS) activity and/or each-step activation (ESA) intensity, the latter, especially in the early stages of training. Here, new computer simulations demonstrate that an endurance training-induced increase in OXPHOS activity and decrease in peak P (Pi), at which exercise is terminated because of exercise intolerance, result in increased V̇O and CP, speeding of the primary phase II of V̇O on-kinetics, and decreases V̇O slow component magnitude, consistent with their observed behavior in vivo. It is possible, but remains unknown, whether there is a contribution to this behavior of an increase in the critical P (Pi), above which the additional ATP usage underlying the slow component begins, and a decrease in the activity of the additional ATP usage (k). Thus, we offer a mechanism, involving P accumulation, Pi and Pi, of the training-induced adaptations in V̇O, CP, and the primary and slow component phases of V̇O on-kinetics that was absent in the literature. A mechanism of the training-induced changes in V̇O, critical power, and V̇O on-kinetics in skeletal muscle reported in the literature is postulated. It involves the self-driving "P double-threshold" mechanism of muscle fatigue underlying exercise inefficiency, the slow component of the V̇O on-kinetics, and termination of exercise. It is proposed that an increase in OXPHOS activity and decrease in peak P at which exercise terminates are responsible for the training-induced changes in the muscle bioenergetic system.
计算机模拟使用先前提出的肌肉疲劳“P 双重阈值”机制(第一个阈值导致工作效率逐渐降低,第二个阈值导致运动不耐受),表明骨骼肌生物能系统的几个参数可以影响最大摄氧量(V̇O)、临界功率(CP)和骨骼肌摄氧量动力学。模拟和实验观察结果共同表明,耐力运动训练可增加氧化磷酸化(OXPHOS)活性和/或每个步骤的激活强度(ESA),后者尤其是在训练的早期阶段。在这里,新的计算机模拟表明,耐力训练引起的 OXPHOS 活性增加和峰值 P(Pi)降低,由于运动不耐受而导致运动终止,这会导致 V̇O 和 CP 增加,V̇O 动力学的主要第二阶段加速,以及 V̇O 缓慢成分幅度降低,与体内观察到的行为一致。有可能,但尚不清楚,是否由于以下原因导致这种行为的增加:临界 P(Pi)增加,超过该值开始使用额外的 ATP,用于缓慢成分;以及额外的 ATP 使用(k)的活性降低。因此,我们提出了一种机制,涉及 V̇O、CP 和 V̇O 动力学的主要和缓慢成分阶段的训练诱导适应中的 P 积累、Pi 和 Pi,这在文献中是不存在的。提出了一种文献中报道的骨骼肌 V̇O、临界功率和 V̇O 动力学的训练诱导变化的机制。它涉及运动效率低下、V̇O 动力学的缓慢成分和运动终止的肌肉疲劳的自驱动“P 双重阈值”机制。提出增加 OXPHOS 活性和降低运动终止时的峰值 P 是导致肌肉生物能系统训练诱导变化的原因。