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Junglee NA, Di Felice U, Dolci A, Fortes MB, Jibani MM, Lemmey AB, Walsh NP, Macdonald JH. Exercising in a hot environment with muscle damage: effects on acute kidney injury biomarkers and kidney function. Am J Physiol Renal Physiol 305: F813-F820, 2013. First published July 3, 2013; doi:10.1152/ajprenal.00091.2013.--Unaccustomed strenuous physical exertion in hot environments can result in heat stroke and acute kidney injury (AKI). Both exercise-induced muscle damage and AKI are associated with the release of interleukin- 6, but whether muscle damage causes AKI in the heat is unknown. We hypothesized that muscle-damaging exercise, before exercise in the heat, would increase kidney stress. Ten healthy euhydrated men underwent a randomized, crossover trial involving both a 60-min downhill muscle-damaging run (exercise-induced muscle damage; EIMD), and an exercise intensity-matched non-muscle-damaging flat run (CON), in random order separated by 2 wk. Both treatments were followed by heat stress elicited by a 40-min run at 33°C. Urine and blood were sampled at baseline, after treatment, and after subjects ran in the heat. By design, EIMD induced higher plasma creatine kinase and interleukin-6 than CON. EIMD elevated kidney injury biomarkers (e.g., urinary neutrophil gelatinase-associated lipocalin (NGAL) after a run in the heat: EIMD-CON, mean difference [95% CI]: 12 [5, 19] ng/ml) and reduced kidney function (e.g., plasma creatinine after a run in the heat: EIMD-CON, mean difference [95% CI]: 0.2 [0.1, 0.3] mg/dl), where CI is the confidence interval. Plasma interleukin-6 was positively correlated with plasma NGAL (r 0.9, P 0.001). Moreover, following EIMD, 5 of 10 participants met AKIN criteria for AKI. Thus for the first time we demonstrate that muscle-damaging exercise before running in the heat results in a greater inflammatory state and kidney stress compared with non-muscle-damaging exercise. Muscle damage should therefore be considered a risk factor for AKI when performing exercise in hot environments. [ABSTRACT FROM AUTHOR]

This research compared thermal and perceptual adaptations, endurance capacity, and overreaching markers in men after 3, 6, and 12 days of post-exercise hot water immersion (HWI) or exercise heat acclimation (EHA) with a temperate exercise control (CON), and examined thyroid hormones as a mechanism for the reduction in resting and exercising core temperature ( T re ) after HWI. HWI involved a treadmill run at 65% V̇o 2peak at 19°C followed by a 40°C bath. EHA and CON involved a work-matched treadmill run at 65% V̇o 2peak at 33°C or 19°C, respectively. Compared with CON, resting mean body temperature ( T b ), resting and end-exercise T re , T re at sweating onset, thermal sensation, and perceived exertion were lower and whole-body sweat rate (WBSR) was higher after 12 days of HWI (all P ≤ 0.049, resting T b : CON -0.11 ± 0.15°C, HWI -0.41 ± 0.15°C). Moreover, resting T b and T re at sweating onset were lower after HWI than EHA ( P ≤ 0.015, resting T b : EHA -0.14 ± 0.14°C). No differences were identified between EHA and CON ( P ≥ 0.157) except WBSR that was greater after EHA ( P = 0.013). No differences were observed between interventions for endurance capacity or overreaching markers (mood, sleep, Stroop, P ≥ 0.190). Thermal adaptations observed after HWI were not related to changes in thyroid hormone concentrations ( P ≥ 0.086). In conclusion, 12 days of post-exercise hot water immersion conferred more complete heat acclimation than exercise heat acclimation without increasing overreaching risk, and changes in thyroid hormones are not related to thermal adaptations after post-exercise hot water immersion.