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 (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.
To King’s School Grantham for their encouragement and help in money raising activities and to Kevin Adams (staff member and mountaineer) and guide on the trek.