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      Factors determining training-induced changes in V̇O 2max, critical power, and V̇O 2 on-kinetics in skeletal muscle

      1 , 2 , 3
      Journal of Applied Physiology
      American Physiological Society

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          Abstract

          A mechanism of the training-induced changes in V̇O 2max, critical power, and V̇O 2 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 V̇O 2 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.

          Abstract

          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 (V̇O 2) 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 V̇O 2 on-kinetics, and decreases V̇O 2 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 V̇O 2 on-kinetics that was absent in the literature.

          NEW & NOTEWORTHY A mechanism of the training-induced changes in V̇O 2max, critical power, and V̇O 2 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 V̇O 2 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.

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          Exceeding a “critical” muscle Pi: implications for \(\dot{\text{V}}\text{O}_{2}\) and metabolite slow components, muscle fatigue and the power–duration relationship

          The consequences of the assumption that the additional ATP usage, underlying the slow component of oxygen consumption ([Formula: see text]) and metabolite on-kinetics, starts when cytosolic inorganic phosphate (Pi) exceeds a certain "critical" Pi concentration, and muscle work terminates because of fatigue when Pi exceeds a certain, higher, "peak" Pi concentration are investigated.
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            Author and article information

            Contributors
            (View ORCID Profile)
            Journal
            Journal of Applied Physiology
            Journal of Applied Physiology
            American Physiological Society
            8750-7587
            1522-1601
            February 01 2021
            February 01 2021
            : 130
            : 2
            : 498-507
            Affiliations
            [1 ]BioSimulation Center, Krakow, Poland
            [2 ]Pulmonary and Critical Care Physiology and Medicine, The Lundquist Institute for Biomedical Innovation Medical Center, Torrance, California
            [3 ]Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom
            Article
            10.1152/japplphysiol.00745.2020
            8530701
            33211591
            073de2ac-35e1-424d-9008-51965c943e73
            © 2021
            History

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