It was the aim of the study to assess the maximal pressure generated by the inspiratory muscles (MIP) during exposure to different levels of altitude (i.e., hypobaric hypoxia). Eight lowlanders (2 females and 6 males), aged 27 - 46 years, participated in the study. After being evaluated at sea level, the subjects spent seven days at altitudes of more than 3000 metres. On the first day, they rode in a cable car from 1200 to 3200 metres and performed the first test after 45 - 60 minutes rest; they then walked for two hours to a mountain refuge at 3600 metres, where they spent three nights (days 2 - 3); on day 4, they walked for four hours over a glacier to reach Capanna Regina Margherita (4559 m), where they spent days 5 - 7. MIP, flow-volume curve and SpO (2) % were measured at each altitude, and acute mountain sickness (Lake Louise score) was recorded. Increasing altitude led to a significant decrease in resting SpO (2) % (from 98 % to 80 %) and MIP (from 134 to 111 cmH (2)O) (baseline to day 4: p < 0.05); there was an improvement in SpO (2) % and a slight increase in MIP during the subsequent days at the same altitude. Expiratory (but not inspiratory) flows increased, and forced vital capacity and FEF (75) decreased at higher altitudes. We conclude that exposure to high altitude hypoxia reduces the strength of the respiratory muscles, as demonstrated by the reduction in MIP and the lack of an increase in peak inspiratory flows. This reduction is more marked during the first days of exposure to the same altitude, and tends to recover during the acclimatisation process.

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.

The oxygen saturation values reported in the high altitude literature are usually taken during a few minutes of measurement either at rest or during exercise. We aimed to investigate the daily hypoxic profile by monitoring oxygen saturation for 24 h in 8 lowlanders (4 females, ages 26 to 59) during trekking from Lukla (2850 m) to the Pyramid Laboratory (5050 m). Oxygen saturation was measured (1) daily at each altitude (sm), (2) for 24-h during ascent to 3500 m, 4200 m, and on day 1 at 5050 m (lm), and (3) during a standardized exercise (em). Results: (1) the sm and lm values were 90.9% (+/-0.5) and 86.4% (+/-1.1) at 3500 m; 85.2%(+/-1.1), and 80% (+/-1.9) at 4200 m; 83.8%(+/-1) and 77% (+/-1.7) at 5050 m (p < or = 0.05); (2) the daily time spent with oxygen saturation < or =90% was 56.5% at 3500 m, 81% at 4200 m, and 95.5% at 5050 m; (3) during exercise, oxygen saturation decreased by 10.58%, 13.43%, and 11.24% at 3500, 4200, and 5050 m, respectively. In conclusion, our data show that the level of hypoxemia during trekking at altitude is more severe than expected on the basis of a short evaluation at rest and should be taken into account.

The lungs play a pivotal role in adaptation to high altitude. The increase in ventilation and the rise in pulmonary artery pressure are the first features of lung response to hypoxic exposure. At high altitude the lungs can also be affected by high-altitude pulmonary oedema, a severe form of acute mountain sickness. In healthy subjects the ascent to high altitude is also associated with alterations in lung function, which have been in part interpreted as an effect of extra vascular lung fluid accumulation. The patterns of respiratory function changes at high altitude are discussed, taking into account the body fluid movement and the increase in endothelial permeability induced by hypoxic exposure. As the problem of “respiratory” patients at high altitude is very important, a short summary of the guidelines for altitude exposure of asthmatic and COPD patients is reported at the end of the chapter.