Osmotic stimulation of vasopressin acutely impairs glucose regulation: a counterbalanced, crossover trial.

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.

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.