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1Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs, Connecticut 06269;2United States Army Research Institute of Environmental Medicine, Natick, Massachusetts 01760;3Division of Experimental Medicine, St. Luke's Hospital and Foundation for Medical Education and Research, Kansas City, Missouri 64134; and 4Department of Surgery, University of Arizona Health Sciences Center, Tucson, Arizona 85724
Submitted 18 July 2003 ; accepted in final form 27 August 2003
High-altitude exposure changes the distribution of body water and electrolytes. Arginine vasopressin (AVP) may influence these alterations. The purpose of this study was to examine the effect of a 24-h water deprivation trial (WDT) on AVP release after differing altitude exposures. Seven healthy males (age 22 ± 1 yr, height 176 ± 2 cm, mass 75.3 ± 1.8 kg) completed three WDTs: at sea level (SL), after acute altitude exposure (2 days) to 4,300 m (AA), and after prolonged altitude exposure (20 days) to 4,300 m (PA). Body mass, standing and supine blood pressures, plasma osmolality (Posm), and plasma AVP (PAVP) were measured at 0, 12, 16, and 24 h of each WDT. Urine volume was measured at each void throughout testing. Baseline Posm increased from SL to altitude (SL 291.7 ± 0.8 mosmol/kgH2O, AA 299.6 ± 2.2 mosmol/kgH2O, PA 302.3 ± 1.5 mosmol/kgH2O, P < 0.05); however, baseline PAVP measurements were similar. Despite similar Posm values, the maximal PAVP response during the WDT (at 16 h) was greater at altitude than at SL (SL 1.7 ± 0.5 pg/ml, AA 6.4 ± 0.7 pg/ml, PA 8.7 ± 0.9 pg/ml, P < 0.05). In conclusion, hypoxia appeared to alter AVP regulation by raising the osmotic threshold and increasing AVP responsiveness above that threshold.
acute mountain sickness; antidiuretic hormone; dehydration; fluid regulation; osmotic threshold
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