European journal of applied physiology · 2024
Pi-based biochemical mechanism of endurance-training-induced improvement of running performance in humans.
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Korzeniewski Bernard
Аннотация
PURPOSE: Endurance training improves running performance in distances where oxidative phosphorylation (OXPHOS) is the main ATP source. Here, a dynamic computer model is used to assess possible biochemical mechanisms underlying this improvement.
METHODS: The dynamic computer model is based on the "Pi double-threshold" mechanism of muscle fatigue, according to which the additional ATP usage appears when (1) inorganic phosphate (Pi) exceeds a critical value (Picrit); (2) exercise is terminated because of fatigue, when Pi reaches a peak value (Pipeak); (3) the Pi increase and additional ATP usage increase mutually stimulate each other.
RESULTS: The endurance-training-induced increase in oxidative phosphorylation (OXPHOS) activity attenuates the reaching of Pipeak by Pi (and thus of V ˙ O2max by V ˙ O2) at increased power output. This in turn allows a greater work intensity, and thus higher speed, to be achieved before exercise is terminated because of fatigue at the end of the 1500 m run. Thus, identical total work is performed in a shorter time. Probably, endurance training also lowers Pipeak, which improves the homeostasis of "bioenergetic" muscle metabolites: ADP, PCr, Pi and H+ ions.
CONCLUSIONS: The present dynamic computer model generates clear predictions of metabolic changes that limit performance during 1500 m running. It contributes to our mechanistic understanding of training-induced improvement in running performance and stimulates further physiological experimental studies.
METHODS: The dynamic computer model is based on the "Pi double-threshold" mechanism of muscle fatigue, according to which the additional ATP usage appears when (1) inorganic phosphate (Pi) exceeds a critical value (Picrit); (2) exercise is terminated because of fatigue, when Pi reaches a peak value (Pipeak); (3) the Pi increase and additional ATP usage increase mutually stimulate each other.
RESULTS: The endurance-training-induced increase in oxidative phosphorylation (OXPHOS) activity attenuates the reaching of Pipeak by Pi (and thus of V ˙ O2max by V ˙ O2) at increased power output. This in turn allows a greater work intensity, and thus higher speed, to be achieved before exercise is terminated because of fatigue at the end of the 1500 m run. Thus, identical total work is performed in a shorter time. Probably, endurance training also lowers Pipeak, which improves the homeostasis of "bioenergetic" muscle metabolites: ADP, PCr, Pi and H+ ions.
CONCLUSIONS: The present dynamic computer model generates clear predictions of metabolic changes that limit performance during 1500 m running. It contributes to our mechanistic understanding of training-induced improvement in running performance and stimulates further physiological experimental studies.