Oxygen delivery deficit in exercise with rapid ascent to high altitude

This study of high altitude physiology was undertaken during an 11-day expedition to the Himalaya with ascent to Annapurna base camp (4,130 m) reaching it on the sixth day. Fourteen male UK residents (13 aged 16-17 years; 1 adult) measured arterial oxygen saturation (SaO(2)) and heart rate (HR) at rest and at 2 min exercise (30 cm step), daily, after arrival at each altitude. Precision was limited by availability of only one oximeter (CMS50-DLP model, Contec Medical Systems, Qinhuangdao, P.R. China). Mean HR correlated (negatively) with SaO(2) both for rest (HR = -1.7974 × SaO(2)% + 236.33, r = 0.841, p = 0.001) and exercise (HR = -0.8834 × SaO(2)% + 226.14, r = 0.711 p < 0.02). Four subjects individually showed significant HR/SaO(2) correlations at rest (nos. 10, 11, 12 and 13) and one, subject 11, in exercise. SaO2 in exercise was lower than at rest (SaO(2), exercise = 1.5835 × SaO(2), rest - 59.177, r = 0.987, p < 0.001). The product, HR × SaO(2), calculated as a surrogate for oxygen delivery (DO(2), Brierley et al., Adv Exp Med Biol 737:207-212, 2012), from mean values was approximately constant for rest, suggesting good cardiac output (CO) compensation for de-saturation. The HR × SaO(2) for exercise, however, showed a dramatic fall at the highest altitude. Since this deficit occurred at the highest altitude, following 2 days of rapid ascent, there was probably impairment of adequate oxygen delivery (DO(2)) at this point. Correlation, HR versus SaO(2) for exercise, was highly significant, with greater significance (HR = -1.798 × SaO(2) + 281.83, r = 0.769, p = 0.01) on omission of the values for the highest ascent point (4,130 m), where the reduced HR × SaO(2) occurred. In conclusion, oxygen delivery is sustained well here except where there are the extra stresses of rapid ascent and exercise.