Ad libitum drinking does not mitigate acute kidney injury risk nor elevations in markers of oxidative stress and inflammation during simulated occupational heat stress

This study tested the hypothesis that ad libitum fluid intake during a 2-h occupational heat stress simulation attenuates increases in renal oxidative stress, inflammation, and acute kidney injury (AKI) risk compared with fluid restriction. Thirteen healthy adults (5 women) completed two 2-h occupational heat stress simulations consisting of eight circuits of treadmill walking and rowing exercise in a wet bulb globe temperature of 33.1 ± 0.2°C. In the drinking trial (Drink), participants were provided 237 mL of a noncaloric sport drink every 15 min and drank ad libitum. In the fluid restriction trial (No Drink), no fluid was provided. Urine and blood samples were analyzed for markers of oxidative stress (thioredoxin-1, TRX-1), inflammation (monocyte chemotactic protein-1, MCP-1), and AKI risk ([IGFBP7·TIMP-2]). During Drink, ad libitum fluid intake was 1,394 ± 316 mL, and reductions in body weight were greater in No Drink (1.3 ± 0.8% vs. 2.8 ± 0.9%, <i>P</i> < 0.001). Peak core temperature was not different between Drink (38.5 ± 0.4°C) and No Drink [38.6 ± 0.4°C, mean difference (upper, lower CI): 0.1 (0.4, -0.1)°C; <i>P</i> = 0.346]. Urine, but not serum TRX-1 (<i>P</i> = 0.254), was elevated at postrecovery and recovery (<i>P</i> < 0.001) but not different between trials (<i>P</i> = 0.743). Serum and urine MCP-1 were elevated at postrecovery and recovery (<i>P</i> < 0.001) but not different between trials (<i>P</i> ≥ 0.407). Urine [IGFBP7·TIMP-2] was elevated at postrecovery and recovery (<i>P</i> < 0.001) but not different between trials (<i>P</i> ≥ 0.096). Ad libitum fluid intake during a 2-h occupational heat stress simulation does not modify biomarkers of systemic and renal oxidative stress and inflammation, nor AKI risk, compared with when fluid is restricted.<b>NEW & NOTEWORTHY</b> Ad libitum fluid intake, consistent with occupational hydration recommendations, does not attenuate renal oxidative stress, inflammation, or acute kidney injury risk during simulated heat stress. These findings challenge the assumption that current hydration recommendations are protective, suggesting that additional strategies are needed to mitigate heat-induced kidney injury in occupational settings.