期刊
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
卷 316, 期 3, 页码 R189-R198出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00351.2018
关键词
chronic kidney disease; dehydration; exercise; heat stress; soda
类别
The purpose of this study was to test the hypothesis that consuming a soft drink (i.e., a high-fructose, caffeinated beverage) during and following exercise in the heat elevates biomarkers of acute kidney injury (AKI) in humans. Twelve healthy adults drank 2 liters of an assigned beverage during 4 h of exercise in the heat [35.1 (0.1)degrees C, 61 (5)% relative humidity] in counterbalanced soft drink and water trials, and >= 1 liter of the same beverage after leaving the laboratory. Stage 1 AKI (i.e., increased serum creatinine >= 0.30 mg/dl) was detected at postexercise in 75% of participants in the Soft Drink trial compared with 8% in Water trial (P = 0.02). Furthermore, urinary neutrophil gelatinase-associated lipocalin (NGAL), a biomarker of AKI, was higher during an overnight collection period after the Soft Drink trial compared with Water in both absolute concentration [6 (4) ng/dl vs. 5 (4) ng/dl, P < 0.04] and after correcting for urine flow rate [6 (7) (ng/dl)/(ml/min) vs. 4 (4) (ng/dl)/(ml/min), P = 0.03]. Changes in serum uric acid from preexercise were greater in the Soft Drink trial than the Water trial at postexercise (P < 0.01) and 24 h (P = 0.05). There were greater increases from preexercise in serum copeptin, a stable marker of vasopressin, at postexercise in the Soft Drink trial (P < 0.02) than the Water trial. These findings indicate that consuming a soft drink during and following exercise in the heat induces AKI, likely via vasopressin-mediated mechanisms.
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