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

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.

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.

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.

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.