Five days of heat acclimation improves cardiovascular and thermoregulatory responses without altering renal stress biomarkers in endurance athletes
Abstract
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). 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.
How strong is the evidence?
Evidence Hub reads this as a randomized trial, done in people. Its evidence level is 3 of 5 (Moderate · trial / cohort / secondary analysis). Trials without a large randomized design, cohorts and secondary analyses give moderate evidence. Reported size: 7 participants or records.
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