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

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 "P_i double-threshold" mechanism of muscle fatigue, according to which the additional ATP usage appears when (1) inorganic phosphate (P_i) exceeds a critical value (Pi_crit); (2) exercise is terminated because of fatigue, when P_i reaches a peak value (Pi_peak); (3) the P_i increase and additional ATP usage increase mutually stimulate each other.

The endurance-training-induced increase in oxidative phosphorylation (OXPHOS) activity attenuates the reaching of Pi_peak by P_i (and thus of $$ O_2max by $$ 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 1500 m run. Thus, identical total work is performed in a shorter time. Probably, endurance training also lowers Pi_peak, which improves the homeostasis of "bioenergetic" muscle metabolites: ADP, PCr, P_i and H⁺ ions.

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.