Abstract
Effects of dehydration may differ depending on how it is induced. For example, ambient heat-induced dehydration might rely on extracellular fluid whereas exercise-induced dehydration might produce and especially release water from within active muscle cells (and liver), thereby causing less homeostatic disruption. The aim of this study therefore was to investigate the physiological and behaviour- mediating effects of exercise- vs heat- induced dehydration. A secondary aim was to investigate the kinetics of ad libitum rehydration following each method of dehydration. Twelve participants (age 33 ± 12 y, height 172 ± 7 cm, body mass 74.4 ± 13.4 kg, V̇O2max 50.7 ± 9.0 mL/kg/min, mean ± SD; 5 females) completed four trials; they 1) dehydrated to a mild extent (3% ∆BM) or 2) rehydrated to prevent ∆BM under passive heat stress (~40˚C, 60% RH; PD, PR) or exercise heat stress (cycling intervals at ~90% V̇O2max in 29˚C, 50% RH; AD, AR). Following trials, participants rehydrated ad libitum for 2 h with water and sports drink. Plasma volume (PV), plasma osmolality (Posm), body mass (BM), thirst, urine indices, rectal core temperate (Tcore), skin temperature (Tskin), thermal sensations and blood pressure were measured at baseline and 1, 2, 3% gross ∆BM, as well as (with the exception of Tcore and Tskin) 1, 2 and 24 h following trials. Respired gas was also measured at 1%, 2%, 3% gross ∆BM to determine rates of substrate oxidation. PV decreased 2.3% more, and Posm rose 0.8 mOsmol/kg more, per % ∆BM in passive vs. exercise-induced dehydration (p=0.003, p=0.087, resp.), however, after controlling for hydration state by subtracting respective changes across the corresponding rehydration trials, these differences were not reliably evident. Specifically, PV reduction was 1.2 vs. 0.4% per % ∆BM during passive heat vs. exercise (p=0.550), while Posm rose by 4 vs 5 mOsmol/kg per % ∆BM (p=0.880). However, ‘full rehydration’ during these stress periods decreased Posm by 8 ± 5 and 11 ± 5 mOsmol/kg below baseline in passive and active trials, respectively (main effect: p<0.001) despite incomplete restoration of PV. Following a 2-h rehydration period, ad libitum fluid intakes following passive and active dehydration restored PV within 2 h, despite incomplete replacement of ∆BM (72% and 75%, resp.). Therefore, PV and Posm are better maintained during exercise-induced dehydration; however, this seems unable to be attributable to endogenous water production or release, but rather a mechanism induced by ‘exercise’ in combination with ‘dehydration’. Full replacement of 3% ∆BM during or immediately after dehydration, causes substantial hypotonicity and thus seems inappropriate. Ad libitum fluid intakes following passive and active dehydration restore PV despite incomplete replacement of ∆BM.