Five days of heat acclimation improves cardiovascular and thermoregulatory responses without altering renal stress biomarkers in endurance athletes.

Short-term heat acclimation (HA) induces cardiovascular and fluid-regulatory adaptations, but it's impact on markers of renal tubular injury and acute kidney injury risk (AKI) during exercise-heat stress remains unclear. Fourteen healthy endurance-trained male athletes were randomised to five days of isothermic HA (HOT; n = 7; 32 °C, 70% relative humidity; target core temperature ≥38.5 °C), or exercise in thermoneutral conditions (TEMP, n = 7). Heat stress tests (HST; 45 min cycling at 32 °C, 70% RH) were performed pre- and post-intervention. Blood biomarkers of kidney tubular stress (NGAL, KIM-1), fluid-regulation (copeptin, serum osmolality) and sympathetic activity (plasma normetanephrine) were measured at rest and immediately post-HST. HA reduced resting heart rate (-8 ± 5 bpm, p = 0.007, d = 1.0), increased plasma volume (+7.3 ± 5.1%, p = 0.022) and sweat loss (+500 ± 539 mL, p = 0.018, d = 1.1). Copeptin rose during the pre-intervention HST in both groups (HOT: + 11 ± 6; TEMP: + 12 ± 13 pmol·L ⁻ ¹, p < 0.05), but not post-intervention. NGAL increased only in TEMP during HST1 (+45 ± 29 μg·L ⁻ ¹, p = 0.030), while KIM-1 remained unchanged. No group x time interactions were observed for any biomarkers (p > 0.05). Five days of HA improved cardiovascular and thermoregulatory responses but did not alter renal stress markers or fluid-regulatory responses during exercise in the heat. These findings suggest short-term HA enhances heat tolerance but may not attenuate renal biomarker responses associated with early tubular stress under hot, humid conditions.