Abstract
Cell hydration is integral to endocrine, immune, neural, cardiovascular, gastrointestinal, muscle, and skeletal function. Acute cell dehydration is associated with a wide variety of adverse outcomes under extreme conditions and in critical illness. Biomarkers of chronic cell hydration are needed to test for longer‐term effects under daily life conditions. In vitro, cells adapt to chronic cell dehydration by increasing protein breakdown to increase intracellular concentrations and counter the osmotic gradient. Once adapted, cells overswell if exposed to hypoosmotic conditions, and release accumulated amino acids. In vivo, in chronically stressed animals, hypoosmotic amino acid efflux is measurable in urine. This study explored for changes in cell hydration and urinary amino acid excretion in 5 healthy men (20–25y) with habitually low total water intake (<2L/d) who increased water intake to 3.5L/d over 4 wks by drinking water. Each week, urine was collected after a 750ml bolus of drinking water. Higher water intake was associated with increased urine volume, decreased urine ADH and osmolality, a downward shift in the distribution of red cell deformability over the osmolality range, and altered post‐bolus urinary amino acid excretion. More work is needed on amino acid efflux as a possible biomarker of chronic cell hydration.Funded by Danone Research, NIH #UL1 RR024131 & #5UL1RR024131‐05, and RAS #A106017.
Published Version
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