Pi-based biochemical mechanism of endurance-training-induced improvement of running performance in humans.

Abstract

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. 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. The endurance-training-induced increase in oxidative phosphorylation (OXPHOS) activity attenuates the reaching of Pipeak by Pi (and thus of O2max by 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 1500m 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. The present dynamic computer model generates clear predictions of metabolic changes that limit performance during 1500m running. It contributes to our mechanistic understanding of training-induced improvement in running performance and stimulates further physiological experimental studies.