Oxygen Delivery Deficit in Exercise with Rapid Ascent to High Altitude

Abstract

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 (SaO₂) 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 SaO₂ both for rest (HR = −1.7974 × SaO₂% + 236.33, r = 0.841, p = 0.001) and exercise (HR = −0.8834 × SaO₂% + 226.14, r = 0.711 p < 0.02). Four subjects individually showed significant HR/SaO₂ correlations at rest (nos. 10, 11, 12 and 13) and one, subject 11, in exercise. SaO2 in exercise was lower than at rest (SaO₂, exercise = 1.5835 × SaO₂, rest − 59.177, r = 0.987, p < 0.001). The product, HR × SaO₂, calculated as a surrogate for oxygen delivery (DO₂, 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 × SaO₂ 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 (DO₂) at this point. Correlation, HR versus SaO₂ for exercise, was highly significant, with greater significance (HR = −1.798 × SaO₂ + 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 × SaO₂ occurred. In conclusion, oxygen delivery is sustained well here except where there are the extra stresses of rapid ascent and exercise.