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

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 "P double-threshold" mechanism of muscle fatigue, according to which the additional ATP usage appears when (1) inorganic phosphate (P) exceeds a critical value (Pi); (2) exercise is terminated because of fatigue, when P reaches a peak value (Pi); (3) the P 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 Pi by P (and thus of O by O) 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, which improves the homeostasis of "bioenergetic" muscle metabolites: ADP, PCr, P 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.