Limited Effect of Dehydrating via Active vs. Passive Heat Stress on Plasma Volume or Osmolality, Relative to the Effect of These Stressors per Se.

The physiological, perceptual, and functional effects of dehydration may depend on how it is incurred (e.g., intense exercise releases endogenous water via glycogenolysis) but this basic notion has rarely been examined. We investigated the effects of active (exercise) heat- vs. passive heat-induced dehydration, and the kinetics of ad libitum rehydration following each method. Twelve fit participants (five females and seven males) completed four trials in randomised order: DEHydration to -3% change in body mass (∆BM) under passive or active heat stress, and EUHydration to prevent ∆BM under passive or active heat stress. In all trials, participants then sat in a temperate-controlled environment, ate a standard snack and had free access to water and sports drink during their two-hour recovery. During mild dehydration (≤2% ∆BM), active and passive heating caused comparable increases in plasma osmolality (Posm: ~4 mOsmol/kg, interaction: p = 0.138) and reductions in plasma volume (PV: ~10%, interaction: p = 0.718), but heat stress per se was the main driver of hypovolaemia. Thirst in DEHydration was comparably stimulated by active than passive heat stress (p < 0.161) and shared the same relation to Posm (r ≥ 0.744) and ∆BM (r ≥ 0.882). Following heat exposures, at 3% gross ∆BM, PV reduction was approximately twice as large from passive versus active heating (p = 0.003), whereas Posm perturbations were approximately twice as large from EUHydration versus DEHydration (p < 0.001). Rehydrating ad libitum resulted in a similar net fluid balance between passive versus active heat stress and restored PV despite the incomplete replacement of ∆BM. In conclusion, dehydrating by 2% ∆BM via passive heat stress generally did not cause larger changes to PV or Posm than via active heat stress. The heat stressors themselves caused a greater reduction in PV than dehydration did, whereas ingesting water to maintain euhydration produced large reductions in Posm in recovery and therefore appears to be of more physiological significance.

Heat stress and dehydration in adapting for performance: Good, bad, both, or neither?

Physiological systems respond acutely to stress to minimize homeostatic disturbance, and typically adapt to chronic stress to enhance tolerance to that or a related stressor. It is legitimate to ask whether dehydration is a valuable stressor in stimulating adaptation per se. While hypoxia has had long-standing interest by athletes and researchers as an ergogenic aid, heat and nutritional stressors have had little interest until the past decade. Heat and dehydration are highly interlinked in their causation and the physiological strain they induce, so their individual roles in adaptation are difficult to delineate. The effectiveness of heat acclimation as an ergogenic aid remains unclear for team sport and endurance athletes despite several recent studies on this topic. Very few studies have examined the potential ergogenic (or ergolytic) adaptations to ecologically-valid dehydration as a stressor in its own right, despite longstanding evidence of relevant fluid-regulatory adaptations from short-term hypohydration. Transient and self-limiting dehydration (e.g., as constrained by thirst), as with most forms of stress, might have a time and a place in physiological or behavioral adaptations independently or by exacerbating other stressors (esp. heat); it cannot be dismissed without the appropriate evidence. The present review did not identify such evidence. Future research should identify how the magnitude and timing of dehydration might augment or interfere with the adaptive processes in behaviorally constrained versus unconstrained humans.