BACKGROUND: Regulating hydration status in active individuals is essential for mitigating losses in performance and physiological function that occur with hypohydration. Many hormonal responses stimulated by physiological stressors are amplified by hypohydration and may impair central nervous system function, cardiovascular responses, perspiration rates, and increase core body temperature. This study aims to assess the cortisol, arginine vasopressin (AVP), and blood lactate (La-) responses to exercise-heat exposure and an oral rehydration regiment. METHODS: Thirty-seven physically active individuals, aged 18 to 50 years (n = 37; MWeight ± SD = 72.10 ± 13.80 kg; MHeight = 172 ± 9.54 cm), entered a heat chamber (30°C, 45% relative humidity) and completed two, 45-minute bouts of running on a treadmill at a 2% grade. The protocol mimicked demands of a soccer match to control for extraneous variables (environment, opponent, travel, player position, etc.). During a 15-min break between treadmill bouts and at PE, participants consumed fluids equal to their total body mass loss. Venous blood was drawn from the antecubital space and was analyzed for La-, AVP, and cortisol at pre-exercise (PRE), immediately post-exercise (PE), and 1-hour post-exercise (PE1). Body mass (BM) was measured at PRE, PE, and PE1. Using a linear mixed effects model, significant main effects were followed up with post hoc pairwise comparisons using the Holm correction method. RESULTS: AVP showed a significant main effect of time (p = 0.03). Post hoc testing revealed significantly lower values at PRE (0.80 ± 0.45 pmol/L) and PE1 (1.33 ± 0.39 pmol/L), compared to PE (3.28 ± 0.46 pmol/L, p = 0.05). Total cortisol had a significant main effect of time of (p < 0.01). Post hoc testing revealed significantly higher values at PRE (14.52 ± 1.04 µg/dL) than at PE (11.58 ± 1.05 µg/dL, p = 0.09), and PE1 (9.98 ± 1.05 µg/dL, p < 0.01). There was a significant main effect of time for La- (p < 0.01). Post hoc testing revealed that PRE values (1.41 ± 0.20 mmol/L) were significantly lower than at PE (2.12 ± 0.12 mmol/L, p = 0.02). There was a significant main effect of time for BM (p < 0.01). Post hoc testing revealed significantly lower values at PE (71.40 ± 2.32 kg, p < 0.01) and PE1 (71.80 ± 2.32 kg, p < 0.01) in comparison to PRE (72.20 ± 2.32 kg, p < 0.01). CONCLUSION: AVP was elevated significantly at PE but values normalized by PE1. BM at PE was significantly lower than PRE, demonstrating some degree of hypohydration, while values at PE1 were higher than PE due to the rehydration protocol. Despite an intensive exercise-heat stress protocol accompanied by significant increases in La- from PRE to PE, cortisol values were significantly less at PE compared to PRE. Therefore, further research is warranted to rationalize or replicate the unexpected decrease in cortisol following exercise-heat stress.

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