Abstract / Summary
Abstract Exogenous ketosis induced by ketone ester (KE) ingestion has attracted growing interest as a potential strategy to enhance physiological tolerance to reduced O 2 availability. Reported benefits arise largely from KE‐induced hyperventilation, which can improve systemic and tissue oxygenation during altitude exposure and hypoxic exercise, potentially complemented by favourable effects on cellular bioenergetics. Whether these responses translate to breath‐hold diving, however, remains unknown. Breath‐hold performance is constrained by the integrated effects of progressive hypoxaemia, CO 2 accumulation, acid–base disturbance, altered cerebrovascular regulation and chemoreflex‐mediated respiratory drive. Because ventilation ceases during apnoea, interventions that alter pre‐apnoeic acid–base status or CO 2 signalling might modify the chemical, neural and perceptual stimuli underlying the urge to breathe without slowing O 2 depletion. Safety therefore depends not only on preserving cerebral O 2 delivery, but also on maintaining the chemoreflex and perceptual warning signals that ordinarily precede hypoxic loss of consciousness. This review evaluates whether the established physiological effects of KE are mechanistically compatible with the unique demands of apnoea, focusing on acid–base regulation, CO 2 ‐dependent cerebrovascular control, autonomic integration and training‐related adaptations in elite freedivers, including reduced chemoreflex sensitivity and enhanced cortical control of respiratory drive. We propose that benefits observed during maintained ventilation might not translate to breath‐hold diving and could create a mechanistic mismatch with uncertain consequences for performance and safety. Direct apnoea‐specific studies are required to determine whether KE supplementation is beneficial, neutral or harmful.