Introduction/Aim High altitude exposure results in acute hypoxia and an increase in the ventilatory drive. This hyperventilatory response is characterised by a worsening breathing efficiency (increased VE/VCO2) and a lower end tidal CO2 (PETCO2) both at rest and during exercise. Whilst the time-course changes in the hyperventilatory response are well-characteristed in acclimated climbers, to date there has been little or no examination of the response during ascent and on return from altitude in a large group of non-acclimated climbers. The aim of the current study was to examine the changes in gas exchange measures in a group of non-acclimated climbers during the ascent of Mt Kilimanjaro and immediately on return from altitude.

Methods 27 (age: 44±15, range 22-66yrs) individuals ascended Mt Kilimanjaro during an 11-day climb. Exercise testing (4-minute step test with gas-exchange) was completed on four occasions at the following altitudes: (1) basecamp, 1850m (PB=690 mmHg); (2) 3500m (PB=505 mmHg); (3) 4840m (PB=428 mmHg) and on return to base camp (4) 2850m (PB=690 mmHg).

Results During the ascent subjects became increasingly hypoxic and there was a decrease in the nadir SpO2 during exercise (nadir SpO2(%): 1850m: 96±2; 3500m: 82±3; 4840m: 73±4). During exercise breathing efficiency worsened (VE/VCO2: 1850m: 28.5±2.9; 3500m: 35.8±4.6; 4840m: 50.7±5.8) and PETCO2 fell (PETCO2 mmHg: 1850m: 37.1±3.6; 3500m: 28.5±2.6; 4840m: 20.8±1.9) as subjects ascended. On return from altitude (2850m) SpO2 normalised (SPO2(%)=97±3 ), however there was persistent evidence of hyperventilation with both breathing efficiency and PETCO2 remaining abnormal during exercise (VE/VCO2: 32.8 +3.2, PETCO2,mmHg: 31.2+3.0; p<0.01 vs 1850m) and at rest.

Conclusion With high altitude exposure there is an increased ventilatory drive. Following high altitude exposure and once SpO2 normalises, gas exchange remains altered. We hypothesise that this altered gas exchange may be due to a sustained alkalosis with the central chemoreceptors remaining reset to defend a lower PCO2 established during high altitude exposure.