Factors determining training-induced changes in V̇O_2max, critical power, and V̇O₂ on-kinetics in skeletal muscle

Computer simulations, using the "P_i 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_2max), critical power (CP), and oxygen consumption (V̇O₂) 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_i (Pi_peak), at which exercise is terminated because of exercise intolerance, result in increased V̇O_2max and CP, speeding of the primary phase II of V̇O₂ on-kinetics, and decreases V̇O₂ 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_i (Pi_crit), above which the additional ATP usage underlying the slow component begins, and a decrease in the activity of the additional ATP usage (k_add). Thus, we offer a mechanism, involving P_i accumulation, Pi_crit and Pi_peak, of the training-induced adaptations in V̇O_2max, CP, and the primary and slow component phases of V̇O₂ on-kinetics that was absent in the literature.NEW & NOTEWORTHY A mechanism of the training-induced changes in V̇O_2max, critical power, and V̇O₂ on-kinetics in skeletal muscle reported in the literature is postulated. It involves the self-driving "P_i double-threshold" mechanism of muscle fatigue underlying exercise inefficiency, the slow component of the V̇O₂ on-kinetics, and termination of exercise. It is proposed that an increase in OXPHOS activity and decrease in peak P_i at which exercise terminates are responsible for the training-induced changes in the muscle bioenergetic system.