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.

Effect of Permissive Dehydration on Induction and Decay of Heat Acclimation, and Temperate Exercise Performance

“…Our primary finding does not support the suggestion that dehydration provides an additional stimulus for the induction of HA (Garrett et al, 2012, 2014; Périard et al, 2015; Akerman et al, 2016). The data from the short-term phase are somewhat at odds with recent work indicating that dehydrating during 90 min daily exercise-heat stress within a 5-day isothermal HA programme facilitated some aspects of HA (Garrett et al, 2014), but the reason for these discrepant findings is unclear.…”

“…However, the fitness of our participants [VO 2max 57(7) mL·kg −1 ·min −1 ; PPO 338(49) W)] was comparable to Garrett et al (2014) [VO 2max 60(7) mL·kg −1 ·min −1 ; PPO 340(30) W] and greater hypohydration lacks ecological validity, could impair some training adaptations (Judelson et al, 2008) and in rodents at least, might impair aspects of the genomic (Schwimmer et al, 2006) and phenotypic (Horowitz et al, 1999) adaptation to heat. A more sustained stimulus might be required to optimize the rebound hypervolemic response (Akerman et al, 2016), but the drinking regimes were virtually identical and earlier, rather than later, carbohydrate-electrolyte fluid replacement is crucial for recovering PV following ~3% body weight loss (Kovacs et al, 2002). Alternatively, because fluid consumption may need to exceed fluid losses by ~50% to restore euhydration in a hypohydrated individual (Shirreffs and Maughan, 1998), the ad libitum intake of fluid, electrolyte and protein following the permissive dehydration may have been insufficient to enable any additional hypervolemic adaptation (Kay et al, 2005), but this is not supported by the stable daily baseline body mass and (euhydrated) urine osmolality and while there was some evidence for reduced blood volume change in HA De , this appeared to be during the decay, rather than induction, phase.…”

“…Likewise, baseline plasma osmolality was within the normative range (Cheuvront et al, 2010) and was maintained in HA Eu , but increased in HA De to a level consistent with mild dehydration (Cheuvront et al, 2010), although this was not measured in all ISO sessions. Nevertheless, assuming a constant sweating rate, hypohydration (body mass change >−2%) will only have been achieved for the final ~23 min of each ISO and maintained for a further 10 min rest period before fluid consumption, which may have been insufficient to influence the fluid-regulatory mechanisms that are hypothesized to be integral to any effects on HA (Garrett et al, 2012, 2014; Périard et al, 2015; Akerman et al, 2016), although once dehydration is achieved [aldo] p does not appear to further increase with time (Kenefick et al, 2007). Nevertheless, the increased plasma osmolality in HA De did not surpass the threshold 2% increase in osmolality that may be obligatory for compensatory renal water conservation (Cheuvront and Kenefick, 2014) and although [aldo] p was increased by the exercise-heat stress, this was not affected by permissive dehydration, at least within ISO1.…”

“…Although passive approaches have sometimes been employed (Beaudin et al, 2009), the increased thermal strain is often achieved through a combination of environmental heat-stress and increased metabolic heat-production through exercise (e.g., Lorenzo et al, 2010; Gibson et al, 2014, 2015; Keiser et al, 2015). More recently, it has been suggested that dehydration, the process of losing fluid and achieving a state of hypohydration (lower-than-normal body water volume), may also represent an important stimulus for facilitating HA (Garrett et al, 2012, 2014; Périard et al, 2015; Akerman et al, 2016), although this may be controversial (Horowitz et al, 1999; Schwimmer et al, 2006) and in contrast to traditional guidelines for maintaining fluid and electrolyte balance (Armstrong and Maresh, 1991; Bergeron et al, 2012). …”

“…Whilst impaired thermoeffector activity might possibly be maladaptive in terms of sudomotor and vasomotor function, the resultant increased tissue-temperature is important; for T C s between 37.3°C and 38.5°C the magnitude of HA is proportional to the thermal forcing-function (Fox et al, 1963), although increasing T C beyond 38.5°C may not confer any additional benefit (Gibson et al, 2014, 2015). Indeed, because dehydration and heat are often inter-linked in their causation and the strain they induce, demarcating their individual effects can be difficult (Akerman et al, 2016). Recent research employing an isothermal strain (target rectal temperature ( T re ) = 38.5°C) HA programme suggests that dehydration can provide a thermally-independent adaptation stimulus (Garrett et al, 2014).…”