Association of Knowledge and Health Habits with Physiological Hydration Status.

The association of hydration knowledge and health habits with hydration status and fluid intake is rarely examined. We sought to determine whether knowledge or physical health behaviors predict physiological hydration status and fluid intake. Ninety-six participants (59 female; 27 ± 10 year) completed the previously validated hydration survey. Participants then recorded total fluids consumed (TFC), collected urine, and tracked void frequency for 24 h. Hydration status was assessed via 24 h urine specific gravity (USG) and osmolality (Uosm). Health behaviors included self-reported physical activity, BMI, smoking, alcoholic drinking, and sleep status. TFC was significantly correlated with 24 h USG (r = -0.390; p < 0.001), Uosm (r = -0.486; p < 0.001), total urine volume (r = 0.675; p < 0.001), and void frequency (r = 0.518; p < 0.001). Hydration knowledge was not correlated with 24 h USG (r = 0.085; p = 0.420), Uosm (r = 0.087; p = 0.419), urine total volume (r = 0.019; p = 0.857), void frequency (r = 0.030; p = 0.771), or TFC (r = 0.027; p = 0.813). Hydration knowledge did not predict 24 h USG (LR+ = 1.10; LR- = 0.90), Uosm (LR+ = 0.81; LR- = 1.35), or TFC (LR+ = 1.00; LR- = 1.00). Health habits did not predict 24 h USG, Uosm, or TFC. In conclusion, self-reported 24 h diet and fluid log recording is comparable to hydration status verification via 24 h urine collection. Hydration knowledge and health habits are not related to, or predictive of, hydration status.

Sports drinks do not increase acute kidney injury risk in males during industrial work in the heat when euhydration is maintained, a randomized crossover trial.

Industrial workers regularly perform physical labor under high heat stress, which may place them at risk for dehydration and acute kidney injury. Current guidelines recommend that workers should consume sports drinks to maintain euhydration during work shifts. However, the impact of fructose sweetened sports drinks on acute kidney injury risk is unknown. The purpose of this study was to investigate the effects of sports drink consumption on markers of acute kidney injury following simulated industrial work in the heat. Twenty males completed two matched 2 h simulated industrial work trial visits in a warm and humid environment (30 °C and 55% relative humidity). During and following the bout of simulated work, participants consumed either a commercially available sports drink or a noncaloric placebo. Urine and blood samples, collected pre-, post-, and 16 h post-work were assayed for markers of hydration (plasma/urine osmolality, and urine specific gravity) and acute kidney injury (KIM-1 and NGAL). There were no differences in physiological or perceptual responses to the bout of work (interaction p > 0.05 for all indices), and markers of hydration were similar between trials (interaction p > 0.05 for all indices). KIM-1 (Placebo: Δ Ln 1.18 ± 1.64; Sports drink: Δ Ln 1.49 ± 1.10 pg/mL; groupwide d = 0.89, p < 0.001) and NGAL (Placebo: Δ Ln 0.44 ± 1.11; Sports drink: Δ Ln 0.67 ± 1.22 pg/mL; groupwide d = 0.39, p = 0.03) were elevated pre- to post-work, but there were no differences between trials (interaction p > 0.05). These data provide no evidence that consumption of fructose sweetened sports drinks increases the risk of acute kidney injury during physical work in the heat.

Acute Kidney Injury Biomarkers and Hydration Outcomes at the Boston Marathon.

The purpose of our field study was to investigate the effects of running the Boston Marathon on acute kidney injury (AKI) biomarkers. We hypothesized that biomarker values would be elevated immediately post-marathon but would resolve in the 24-h post-marathon. Secondarily, we sought to identify sex differences related to renal stress. Participants were 65 runners who completed the Boston Marathon (46 ± 9 years, 65.4 ± 10.8 kg). Urine samples were collected at three different time points (pre-marathon, post-marathon, and 24-h post-marathon). Blood samples were collected post-marathon and 24-h post-marathon. Urine specific gravity (USG) and AKI biomarkers were evaluated. Pre-marathon USG (1.012 ± 0.007) was significantly less than post-marathon (1.018 ± 0.008) and 24-h post-marathon (1.020 ± 0.009; P < 0.001). Male USG (1.024 ± 0.009) was significantly greater 24-h post-marathon than females (1.017 ± 0.008; P = 0.019). Urinary neutrophil gelatinase-associated lipocalin values were significantly greater over time (P < 0.001), and there was a main effect of sex with female urinary creatinine (UCr) greater than males at all three time points (P = 0.040). Post-marathonUCr (366.24 ± 295.16 mg/dl) was significantly greater than pre-marathon (206.65 ± 145.28.56 mg/dl; p < 0.001) and 24-h post-marathon was significantly lower than other time-points (93.90 ± 125.07 mg/dl; P < 0.001). FemaleUCr values were significantly greater than males 24-h post-marathon (P < 0.001). There was no difference in serum cystatin C (SCys) values post- or 24-h post-marathon (P = 0.178). Serum creatinine (SCr) significantly decreased between post-marathon and 24-h post-marathon, (P < 0.001). We can infer that the characteristics unique to the Boston Marathon may have attributed to prolonged elevations in AKI biomarkers. Sex differences were observed during the Boston Marathon warranting further investigation.

Mild hypohydration impairs cycle ergometry performance in the heat: A blinded study.

The aim of the present study was to observe the effect of mild hypohydration on exercise performance with subjects blinded to their hydration status. Eleven male cyclists (weight 75.8 ± 6.4 kg, VO2peak : 64.9 ± 5.6 mL/kg/min, body fat: 12.0 ± 5.8%, Powermax : 409 ± 40 W) performed three sets of criterium-like cycling, consisting of 20-minute steady-state cycling (50% peak power output), each followed by a 5-km time trial at 3% grade. Following a familiarization trial, subjects completed the experimental trials, in counter-balanced fashion, on two separate occasions in dry heat (30°C, 30% rh) either hypohydrated (HYP) or euhydrated (EUH). In both trials, subjects ingested 25 mL of water every 5 minutes during the steady-state and every 1 km of the 5-km time trials. In the EUH trial, sweat losses were fully replaced via intravenous infusion of isotonic saline, while in the HYP trial, a sham IV was instrumented. Following the exercise protocol, the subjects' bodyweight was changed by -0.1 ± 0.1% and -1.8 ± 0.2% for the EUH and HYP trial, respectively (P < 0.05). During the second and third time trials, subjects averaged higher power output (309 ± 5 and 306 ± 5 W) and faster cycling speed (27.5 ± 3.0 and 27.2 ± 3.1 km/h) in the EUH trial compared to the HYP trial (Power: 287 ± 4 and 276 ± 5 W, Speed: 26.2 ± 2.9 and 25.5 ± 3.3 km/h, all P < 0.05). Core temperature (Tre ) was higher in the HYP trial throughout the third steady-state and 5-km time trial (P < 0.05). These data suggest that mild hypohydration, even when subjects were unaware of their hydration state, impaired cycle ergometry performance in the heat probably due to greater thermoregulatory strain.

Renal stress and kidney injury biomarkers in response to endurance cycling in the heat with and without ibuprofen.

Exercise, especially in the heat, can contribute to acute kidney injury, which can expedite chronic kidney disease onset. The additional stress of ibuprofen use is hypothesized to increase renal stress. OBJECTIVES: To observe the effects of endurance cycling in the heat on renal function. Secondarily, we investigated the effect of ibuprofen ingestion on kidney stress. DESIGN: Randomized, placebo controlled and observational methods were utilized. METHODS: Forty cyclists (52±9y, 21.7±6.5% body fat) volunteered and completed an endurance cycling event (5.7±1.2h) in the heat (33.2±5.0°C, 38.4±10.7% RH). Thirty-five participants were randomized to ingest a placebo (n=17) or 600mg ibuprofen (n=18) pre-event. A blood sample was drawn before and following the event. Serum creatinine was assessed by colorimetric assay. An ELISA was used to measure serum neutrophil gelatinase-associated lipocalin. Fractional excretion of sodium was calculated after urinary and serum electrolyte analyses. RESULTS: Placebo versus ibuprofen groups contributed no significant difference in any variable (p>0.05). Serum creatinine significantly increased from pre- (0.52±0.14mg/dL) to post-event (0.88±0.21mg/dL; p<0.001). Serum neutrophil gelatinase-associated lipocalin significantly increased (pre: 68.51±17.54ng/mL; post: 139.12±36.52ng/mL; p<0.001) and fractional excretion of sodium was significantly reduced from pre- (0.52±0.24%) to post-event (0.27±0.18%; p<0.001). CONCLUSIONS: Changes in renal biomarkers suggest mild acute kidney injury and reduced kidney function during a single bout of endurance cycling in the heat, without influence from moderate ibuprofen ingestion.