These data indicated that hypohydration decreased cycling performance and impaired thermoregulation independently of thirst, while the subjects were unaware of their hydration status.

Nationally representative data from the National Health and Nutrition Examination Survey (NHANES) indicate that over 65% of adults aged 51–70 years in the U.S. do not meet hydration criteria. They have hyponatremia (serum sodium < 135 mmol/L) and/or underhydration (serum sodium >145 mmol/L, spot urine volume <50 mL, and/or spot urine osmolality ≥500 mmol/kg). To explore potential public health implications of not meeting hydration criteria, data from the NHANES 2009–2012 and National Center for Health Statistics Linked Mortality Files for fasting adults aged 51–70 years (sample n = 1200) were used to determine if hyponatremia and/or underhydration were cross-sectionally associated with chronic health conditions and/or longitudinally associated with chronic disease mortality. Underhydration accounted for 97% of the population group not meeting hydration criteria. In weighted multivariable adjusted Poisson models, underhydration was significantly associated with increased prevalence of obesity, high waist circumference, insulin resistance, diabetes, low HDL, hypertension, and metabolic syndrome. Over 3–6 years of follow-up, 33 chronic disease deaths occurred in the sample, representing an estimated 1,084,144 deaths in the U.S. Alongside chronic health conditions, underhydration was a risk factor for an estimated 863,305 deaths. Independent of the chronic health conditions evaluated, underhydration was a risk factor for 128,107 deaths. In weighted multivariable Cox models, underhydration was associated with 4.21 times greater chronic disease mortality (95% CI: 1.29–13.78, p = 0.019). Zero chronic disease deaths were observed for people who met the hydration criteria and did not already have a chronic condition in 2009–2012. Further work should consider effects of underhydration on population health.

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Background Epidemiological studies in humans show increased concentrations of copeptin, a surrogate marker of arginine vasopressin (AVP), to be associated with increased risk for type 2 diabetes. Objectives To examine the acute and independent effect of osmotically stimulated AVP, measured via the surrogate marker copeptin, on glucose regulation in healthy adults. Methods Sixty subjects (30 females) participated in this crossover design study. On 2 trial days, separated by ≥7 d (males) or 1 menstrual cycle (females), subjects were infused for 120 min with either 0.9% NaCl [isotonic (ISO)] or 3.0% NaCl [hypertonic (HYPER)]. Postinfusion, a 240-min oral-glucose-tolerance test (OGTT; 75 g) was administered. Results During HYPER, plasma osmolality and copeptin increased (P < 0.05) and remained elevated during the entire 6-h protocol, whereas renin-angiotensin-aldosterone system hormones were within the lower normal physiological range at the beginning of the protocol and declined following infusion. Fasting plasma glucose did not differ between trials (P > 0.05) at baseline and during the 120 min of infusion. During the OGTT the incremental AUC for glucose from postinfusion baseline (positive integer) was greater during HYPER (401.5 ± 190.5 mmol/L·min) compared with the ISO trial (354.0 ± 205.8 mmol/L·min; P < 0.05). The positive integer of the AUC for insulin during OGTT did not differ between trials (HYPER 55,850 ± 36,488 pmol/L·min compared with ISO 57,205 ± 31,119 pmol/L·min). Baseline values of serum glucagon were not different between the 2 trials; however, the AUC of glucagon during the OGTT was also significantly greater in HYPER (19,303 ± 3939 ng/L·min) compared with the ISO trial (18,600 ± 3755 ng/L·min; P < 0.05). Conclusions The present data indicate that acute osmotic stimulation of copeptin induced greater hyperglycemic responses during the oral glucose challenge, possibly due to greater glucagon concentrations. This study was registered at clinicaltrials.gov as NCT02761434.

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, VO 2peak : 64.9 ± 5.6 mL/kg/min, body fat: 12.0 ± 5.8%, Power max : 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 steadystate 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 (T re ) 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. K E Y W O R D Scycling, heat stress, time trial, water intake