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.

Hydration pertains simplistically to body water volume. Functionally, however, hydration is one aspect of fluid regulation that is far more complex, as it involves the homeostatic regulation of total body fluid volume, composition and distribution. Deliberate or pathological alteration of these regulated factors can be disabling or fatal, whereas they are impacted by exercise and by all environmental stressors (e.g. heat, immersion, gravity) both acutely and chronically. For example, dehydration during exercising and environmental heat stress reduces water volume more than electrolyte content, causing hyperosmotic hypohydration. If exercise continues for many hours with access to food and water, composition returns to normal but extracellular volume increases well above baseline (if exercising upright and at low altitude). Repeating bouts of exercise or heat stress does likewise. Dehydration due to physical activity or environmental heat is a routine fluid-regulatory stress. How to gauge such dehydration and — more importantly—what to do about it, are contested heavily within sports medicine and nutrition. Drinking to limit changes in body mass is commonly advocated (to maintain ≤2% reduction), rather than relying on behavioural cues (mainly thirst) because the latter has been deemed too insensitive. This review, as part of the series on moving in extreme environments, critiques the validity, problems and merits of externally versus autonomously controlled fluid-regulatory behaviours, both acutely and chronically. Our contention is that externally advocated hydration policies (especially based on change in body mass with exercise in healthy individuals) have limited merit and are extrapolated and imposed too widely upon society, at the expense of autonomy. More research is warranted to examine whether ad libitum versus avid drinking is beneficial, detrimental or neither in: acute settings; adapting for obligatory dehydration (e.g. elite endurance competition in the heat), and; development of chronic diseases that are associated with an extreme lack of environmental stress.

Exercise induces arterial flow patterns that promote functional and structural adaptations, improving functional capacity and reducing cardiovascular risk. While heat is produced by exercise, local and whole-body passive heating have recently been shown to generate favorable flow profiles and associated vascular adaptations in the upper limb. Flow responses to acute heating in the lower limbs have not yet been assessed, or directly compared to exercise, and other cardiovascular effects of lower-limb heating have not been fully characterized. Lower-limb heating by hot-water immersion (30 min at 42°C, to the waist) was compared to matched-duration treadmill running (65-75% age-predicted heart rate maximum) in 10 healthy, young adult volunteers. Superficial femoral artery shear rate assessed immediately upon completion was increased to a greater extent following immersion (mean ± SD: immersion +252 ± 137% vs. exercise +155 ± 69%, interaction: p = 0.032), while superficial femoral artery flow-mediated dilation was unchanged in either intervention. Immersion increased heart rate to a lower peak than during exercise (immersion +38 ± 3 beats·min^-1 vs. exercise +87 ± 3 beats·min^-1, interaction: p < 0.001), whereas only immersion reduced mean arterial pressure after exposure (−8 ± 3 mmHg, p = 0.012). Core temperature increased twice as much during immersion as exercise (+1.3 ± 0.4°C vs. +0.6 ± 0.4°C, p < 0.001). These data indicate that acute lower-limb hot-water immersion has potential to induce favorable shear stress patterns and cardiovascular responses within vessels prone to atherosclerosis. Whether repetition of lower-limb heating has long-term beneficial effects in such vasculature remains unexplored.