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

Abstract

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.

Keywords: acclimatization; adaptation; dehydration; ergogenic; heat; hormesis; hypohydration; performance.

Figure 1.

Heat stress and sweating-induced hypohydration can each cause widespread acute effects, many of which are synergistic. Hypohydration is usually caused by heat stress, but can then oppose heat-induced increases in skin blood flow and sweating to further exacerbate heat strain. Abbreviations: ADH = Anti-diuretic hormone; Aldo = Aldosterone; ANP = Atrial Natriuretic Peptide; BBB = Blood brain barrier; Cats = Catecholamines; LPS = Lipopolysaccharide; ROS = Reactive Oxygen Species.

Figure 2.

Factors that acutely and chronically determine blood volume with repeated training bouts, and the consequential effects on the physiology of exercise. This schematic is based mostly on that developed by Convertino, extended to incorporate subsequent research on the role of central blood volume on renal-, albumin- and EPO- mediated volume expansion. Abbreviations: ADH = Anti-diuretic hormone; Aldo = Aldosterone; AngII = Angiotensin II; ANP = Atrial natrietic peptide; BV = Blood volume; C_Na = sodium clearance; ECFV = Extra cellular fluid volume; EPO = Erythropoietin; GFR = Glomerular filtration rate; PV = plasma volume; RCM = Red cell mass; SNSA = Sympathetic nervous system activity.

Figure 3.

Plasma sodium (A), osmolality (B), and AVP (C) concentration in trained and untrained groups at rest and during exercise (∼70% V̇O_{2 peak}); and thirst as a function of osmolality (D) during the same exercise when receiving 100% rehydration (EUH) or 20% rehydration. Reproduced with permission from ref. .

Figure 4.

Individual responses of resting plasma volume (A), resting body mass (B), end-exercise heart rate (C), and subsequent time-to-exhaustion ((TTE) D) to short-term heat acclimation undertaken with euhydration (EUH) or dehydration (DEH). Mean values are illustrated as a black diamond, offset slightly for visual clarity. The smallest worthwhile difference is shown as a gray band, where able to be calculated. Data for A, C and D are individual responses of data published in ref. .