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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., (Copyright © American Society for Nutrition 2019.)

Purpose: The aim of the present study was to examine the effect of dehydration on exercise performance independently of thirst with subjects blinded of their hydration status., Methods: Seven male cyclists (weight, 72 ± 9 kg; body fat, 14% ± 6%; peak oxygen uptake, 59.4 ± 6 mL·kg·min) exercised for 2 h on a cycle ergometer at 55% peak oxygen uptake, in a hot-dry environment (35°C, 30% relative humidity), with a nasogastric tube under euhydrated-non-thirst (EUH-NT) and dehydrated-non-thirst (DEH-NT) conditions. In both trials, thirst was matched by drinking 25 mL of water every 5 min (300 mL·h). In the EUH-NT trial, sweat losses were fully replaced by water via the nasogastric tube (calculated from the familiarization trial). After the 2 h of steady state, the subjects completed a 5-km cycling time trial at 4% grade., Results: Body mass loss for the EUH-NT and DEH-NT after the 2 h was -0.2% ± 0.6% and -2.2% ± 0.4%, whereas after the 5-km time trial, it was -0.7% ± 0.5% and 2.9% ± 0.4%, respectively. Thirst (35 ± 30 vs 42 ± 31 mm) and stomach fullness (46 ± 21 vs 35 ± 20 mm) did not differ at the end of the 2 h of steady state between EUH-NT and DEH-NT trials (P > 0.05). Subjects cycled faster during the 5-km time trial in the EUH-NT trial compared with the DEH-NT trial (23.2 ± 1.5 vs 22.3 ± 1.8 km·h, P < 0.05), by producing higher-power output (295 ± 29 vs 276 ± 29 W, P < 0.05). During the 5-km time trial, core temperature was higher in the DEH-NT trial (39.2°C ± 0.7°C) compared with the EUH-NT trial (38.8°C ± 0.2°C; P > 0.05)., Conclusions: These data indicated that hypohydration decreased cycling performance and impaired thermoregulation independently of thirst, while the subjects were unaware of their hydration status.