Delaying task failure in high-intensity exercise: a Pi-afferent-effort framework for targeted sports nutrition.

BACKGROUND

Task failure during high-intensity exercise may reflect the convergence of intramuscular, neural, perceptual, and behavioral boundaries rather than the consequence of a single fatigue mechanism.

METHODS

This hypothesis-generating narrative review proposes the Pi-afferent-effort model of task failure during high-intensity exercise and applies the model to targeted performance nutrition.

RESULTS

Rapid ATP turnover increases inorganic phosphate (Pi), while phosphocreatine breakdown through the creatine kinase reaction buffers ATP availability. As phosphate-linked disturbance progresses, Pi may impair crossbridge function, Ca2+ sensitivity, and excitation-contraction coupling and thereby reduce force capacity. In parallel, interstitial acid-base disturbance and metabolite- and mechanosensitive group III/IV afferent feedback support ventilatory and circulatory regulation, but may also constrain motor output and voluntary activation. Perceived effort and muscle pain are treated as distinct constructs: effort is closely related to central motor command, whereas pain and discomfort reflect nociceptive-affective processing influenced by afferent feedback and context. Nutritional strategies are interpreted according to the model boundary they are most likely to affect. Nitrate may reduce ATP cost and phosphate-linked perturbation in selected tasks; creatine may support PCr availability and between-bout recovery; beta-alanine and sodium bicarbonate may alter intracellular and extracellular acid-base stress; caffeine may affect arousal, motor output, effort appraisal, pain, and tolerance; and carbohydrate is most relevant during prolonged or repeated high-intensity work.

CONCLUSIONS

Future studies should combine metabolic, neuromuscular, perceptual, and performance outcomes to determine whether supplements reduce work-matched strain, increase tolerance of terminal strain, or both.