Exertional heat stress and sodium balance: Leaders, followers, and adaptations

Exertional heat stress presents a different acute challenge to salt balance compared to at rest. Sodium (Na⁺) and chloride (Cl⁻) losses during exercise are overwhelmingly driven by eccrine sweat glands (the “leader”), with minimal urinary excretion. Total salt losses are therefore largely influenced by thermoregulatory need, although adaptations from prior heat exposure or altered dietary intake influences sweat gland ion reabsorption, and therefore sweat Na⁺ ([Na⁺]_sweat) and Cl⁻ concentrations. The hypotheses that body Na⁺ and Cl⁻ conservation, or their release from osmotically inactive stores, can occur during the timeframe of a single bout of exertional heat stress, has not been studied to date. The consequences of unreplaced Na⁺ and Cl⁻ losses during exertional heat stress appear limited primarily to their interactions with water balance. However, the water volume ingested is substantially more influential than salt intake on total body water, plasma volume, osmolality, and thermoregulation during exercise. Acute salt and water loading 1–3 h prior to exercise can induce isosmotic hyperhydration in situations where this is deemed beneficial. During exercise, only scenarios of whole body [Na⁺]_sweat > 75th centile, combined with fluid replacement >80% of losses, are likely to require significant replacement to prevent hyponatremia. Post-exercise, natriuresis resumes as the main regulator of salt losses, with the kidneys (the “follower”) working to restore salt balance incurred from any exercise-induced deficit. If such a deficit exceeds usual dietary intake, and rapid restoration of hydration status is desirable, a deliberate increase in salt intake may assist in volume restoration.