Hypohydration produced by high-intensity intermittent running increases biomarkers of renal injury in males
Loris A. Juett, European Journal of Applied Physiology volume 121, pages3485–3497 (2021)
Purpose
Whilst there is evidence to suggest that hypohydration caused by physical work in the heat increases renal injury, whether this is the case during exercise in temperate conditions remains unknown. This study investigated the effect of manipulating hydration status during high-intensity intermittent running on biomarkers of renal injury.
Methods
After familiarisation, 14 males (age: 33 ± 7 years; V̇O2peak: 57.1 ± 8.6 ml/kg/min; mean ± SD) completed 2 trials in a randomised cross-over design, each involving 6, 15 min blocks of shuttle running (modified Loughborough Intermittent Shuttle Test protocol) in temperate conditions (22.3 ± 1.0 °C; 47.9 ± 12.9% relative humidity). During exercise, subjects consumed either a volume of water equal to 90% of sweat losses (EU) or 75 mL water (HYP). Body mass, blood and urine samples were taken pre-exercise (baseline/pre), 30 min post-exercise (post) and 24 h post-baseline (24 h).
Results
Post-exercise, body mass loss, serum osmolality and urine osmolality were greater in HYP than EU (P ≤ 0.024). Osmolality-corrected urinary kidney injury molecule-1 (uKIM-1) concentrations were increased post-exercise (P ≤ 0.048), with greater concentrations in HYP than EU (HYP: 2.76 [1.72–4.65] ng/mOsm; EU: 1.94 [1.1–2.54] ng/mOsm; P = 0.003; median [interquartile range]). Osmolality-corrected urinary neutrophil gelatinase-associated lipocalin (uNGAL) concentrations were increased post-exercise (P < 0.001), but there was no trial by time interaction effect (P = 0.073).
Conclusion
These results suggest that hypohydration produced by high-intensity intermittent running increases renal injury, compared to when euhydration is maintained, and that the site of this increased renal injury is at the proximal tubules.