We tested the hypothesis that the individual ventilatory adaptation to high altitude (HA, 5050 m) may influence renal water excretion in response to water loading. In 8 healthy humans (33+/-4 S.D. years) we studied, at sea level (SL) and at HA, resting ventilation (VE), arterial oxygen saturation (SpO2), urinary output after water loading (WL, 20 mL/kg), and total body water (TBW). Ventilatory response to HA was defined as the difference in resting VE over SpO2 (DeltaVE/DeltaSpO2) from SL to HA. At HA, a significant increase in urinary volume after the first hour from WL (%WLt0-60) was observed. Significant correlations were found between DeltaVE/DeltaSpO2 versus %WLt0-60 at HA and versus changes in TBW, from SL to HA. In conclusion, in healthy subjects the ventilatory response to HA influences water balance and correlates with kidney response to WL. A higher ventilatory response at HA, allowing a more efficient water renal handling, is likely to be a protective mechanisms from altitude illness.

For the evaluation of a respiratory test at high altitude, several factors must be taken into account: the decreased barometric pressure, the decreased density of air and the degree of acclimatization which is related to the altitude and to the length of exposure. Several studies have shown a reduction in forced vital capacity (FVC) at high altitude and using simulated conditions, mainly related to an increase in pulmonary blood volume and development of interstitial edema. To assess the daily spirometric patterns during ascending to high altitudes we studied 17 healthy subjects at both Capanna Regina Margherita on the Italian Alps (4,559 m) and the Pyramid Laboratory in Nepal (5,050 m). Respiratory function tests were performed every day. Peak expiratory flow values significantly increased. The mean percent increase was 15% at 3,200 and 3,600 m and 26% at 4,559 m. FVC and MEF25 values showed a significant decrease (p < 0.005) during the first days above 3,500 m and improved only after several days spent above this altitude. For each subject the maximal reductions in FVC and maximal expiratory flow (MEF) at 25% of FVC however were found on different days. In our opinion, these data support the hypothesis that at high altitude the respiratory function can be affected by the presence of an increased pulmonary blood volume and/or the development of interstitial edema. The observed changes in forced expiration curves at high altitude seem to reflect the degree of acclimatization that is related to the individual susceptibility, to the altitude reached and to the duration of the exposure. These changes are transient and resolve after returning to sea level.

We tested the hypothesis that the individual ventilatory adaptation to high altitude (HA, 5050 m) may influence renal water excretion in response to water loading. In 8 healthy humans (33+/-4 S.D. years) we studied, at sea level (SL) and at HA, resting ventilation (VE), arterial oxygen saturation (SpO2), urinary output after water loading (WL, 20 mL/kg), and total body water (TBW). Ventilatory response to HA was defined as the difference in resting VE over SpO2 (DeltaVE/DeltaSpO2) from SL to HA. At HA, a significant increase in urinary volume after the first hour from WL (%WLt0-60) was observed. Significant correlations were found between DeltaVE/DeltaSpO2 versus %WLt0-60 at HA and versus changes in TBW, from SL to HA. In conclusion, in healthy subjects the ventilatory response to HA influences water balance and correlates with kidney response to WL. A higher ventilatory response at HA, allowing a more efficient water renal handling, is likely to be a protective mechanisms from altitude illness.