Ge, Ri-Li, Tony G. Babb, Mark Sivieri, Geir K. Resaland, Trine Karlsen, Jim-Stray-Gundersen,
and Benjamin D. Levine. Urine acid–base compensation at simulated moderate altitude. High
Alt. Med. & Biol. 7:64–71, 2006.—Acute exposure to high altitude elicits respiratory alkalosis, and
this is partially corrected by renal compensation. To determine the time course and magnitude
of renal compensation during short-term moderate altitude exposure, we measured urine gas
tensions and acid–base status in 48 healthy men and women at four levels of simulated altitude
exposures. Each subject was exposed in pseudorandom order to simulated altitudes of 1780,
2085, 2455, and 2800 m in a decompression chamber for 24 h, separated by 1 week at sea level.
Fresh urine was collected anaerobically at sea level and after 6 and 24 h of each altitude exposure.
Urine pH increased significantly (p < 0.01) after 6 h at all altitudes and returned to baseline
values by 24 h at the lowest altitudes. In contrast, urine pH remained elevated at the highest
altitudes. The mean value of urine HCO
at sea level was 1.67 ± 0.25 mmol/L, increased
significantly after 6 h at all altitudes, and then returned to near baseline after 24 h at three lower
altitudes (1780, 2085, and 2455 m). However, it remained elevated at 2800 m. PCO2 in urine was
significantly increased after 6 h and returned to baseline after 24 h at all altitudes. These results
suggest that (1) short-term low to moderate altitude exposure results in a marked HCO
diuresis,
which may be caused by inhibition of the secretion of renal tubular H+, and (2) renal
HCO
compensation was completed by 24 h at low to moderate altitude, but still incomplete at
higher altitude.
