Abstract
PurposeWhilst 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.MethodsAfter 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).ResultsPost-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).ConclusionThese 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.
Highlights
The incidence of acute kidney injury (AKI; diagnosed using changes in serum creatinine) following prolonged endurance events is variable (Lipman et al 2014; Hoffman and Weiss 2016; Mansour et al 2017; Poussel et al 2020), but has been reported to be as high as 85% (Kao et al 2015), with some severe cases resulting in temporary dialysis (Hodgson et al 2017).Whilst these studies are likely to have overestimated AKI incidence, due to issues with measuring serum creatinine in close proximity to exercise (Hodgson et al 2017), rises in serum creatinine following these events have been accompanied by rises in urinary neutrophil gelatinase-associated lipocalin and urinary kidney injury molecule-1
The aim of the present study was to investigate the effect of manipulating hydration status during high-intensity intermittent running in temperate conditions on urinary neutrophil gelatinase-associated lipocalin (uNGAL) and urinary kidney injury molecule-1 (uKIM-1) concentrations
The aim of the present study was to investigate the effect of manipulating hydration status during high-intensity intermittent running on biomarkers of renal injury
Summary
The incidence of acute kidney injury (AKI; diagnosed using changes in serum creatinine) following prolonged endurance events (i.e. marathons and ultramarathons) is variable (Lipman et al 2014; Hoffman and Weiss 2016; Mansour et al 2017; Poussel et al 2020), but has been reported to be as high as 85% (Kao et al 2015), with some severe cases resulting in temporary dialysis (Hodgson et al 2017).Whilst these studies are likely to have overestimated AKI incidence, due to issues with measuring serum creatinine in close proximity to exercise (Hodgson et al 2017), rises in serum creatinine following these events have been accompanied by rises in urinary neutrophil gelatinase-associated lipocalin (uNGAL) and urinary kidney injury molecule-1 (uKIM-1) (McCullough et al. Vol.:(0123456789)European Journal of Applied Physiology2011; Lippi et al 2012; Mansour et al 2017; Poussel et al 2020), which are both novel biomarkers that indicate renal tubular injury (Kashani et al 2017). The rise in biomarkers of renal injury reported following prolonged endurance events is likely due to several factors, including increases in sympathetic activity and body temperature, as well as muscle damage and hypohydration (Poortmans 1984; Junglee et al 2013; Hoffman and Weiss 2016; Chapman et al 2020). Of these factors, hypohydration may be of particular interest in the pathophysiology of exercise-associated renal injury, as whilst it is commonly seen during prolonged endurance events (Cheuvront and Haymes 2001), it can be mitigated with fluid consumption. Though there is observational evidence to suggest that hypohydration may contribute to AKI after a marathon (Mansour et al 2019), causation cannot be inferred from such data, and whether hydration status influences renal injury during exercise in temperate conditions remains unknown and warrants investigation
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