Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

A group of 15 competitive male cyclists [mean peak oxygen uptake, (V) over dot O-2peak 68.5 (SEM 1.5 ml . kg(-1) . min(-1))] exercised on a cycle ergo meter in a protocol which began at an intensity of 150 W and was increased by 25 W every 2 min until the subject was exhausted. Blood samples were tak en from the radial artery at the end of each exercise intensity to determin e the partial pressures of blood gases and oxyhaemoglobin saturation (SaO2) , with all values corrected for rectal temperature. The SaO2 was also monit ored continuously by ear oximetry. A significant decrease in the partial pr essure of oxygen in arterial blood (PaO2) was seen at the first exercise in tensity (150 W, about 40% (V) over dot O-2peak) A further significant decre ase in PaO2 occurred at 200 W, whereafter it remained stable but still sign ificantly below the values at rest, with the lowest value being measured at 350 W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in art erial blood (PaCO2) was unchanged up to an exercise intensity of 250 W wher eafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375 W [34.5 (SEM 0.5) mmHg]. During both the fi rst (150 W and final exercise intensities ((V) over dot O-2peak) PaO2 was c orrelated significantly with both partial pressure of oxygen in alveolar ga s (PAO2, r = 0.81 and r = 0.70, respectively) and alveolar-arterial differe nce in oxygen partial pressure (PA-aO2, r = 0.63 and, = 0.86, respectively) but not with PaCO2. At (V) overdot O-2peak PaO2 was significantly correlat ed with the ventilatory equivalents for both oxygen uptake and carbon dioxi de output (r = 0.58 and r = 0.53, respectively). When both PAO2 and PA-aO2 were combined in a multiple linear regression model, at least 95% of the va riance in PaO2 could be explained at both 150 W and (V) over dot O-2peak. A significant downward trend in SaO2 was seen with increasing exercise inten sity with the lowest value at 375 W [94.6 (SEM 0.3)%]. Oximetry estimates o f SaO2 were significantly higher than blood measurements at all times throu ghout exercise and no significant decrease from rest was seen until 350 W. The significant correlations between PaO2 and PAO2 With the first exercise intensity and at (V) over dot O-2peak led to the conclusion that inadequate hyperventilation is a major contributor to exercise-induced hypoxaemia.