Exercise-induced hypoxemia: fact or fallacy?

Abstract

Whereas the prevalence of exercise-induced hypoxemia (EIH) in endurance athletes is commonly reported as approximately 50%, most previous studies have not corrected PaO2 for exercise-induced hyperthermia. Furthermore, although a detrimental effect on aerobic performance has been assumed, no study has measured arterial oxygen content (CaO2) in this context. To determine the effect of temperature-correcting PaO2 values for rectal, arterial blood, esophageal, and exercising muscle temperatures during exercise on CaO2 and the prevalence of EIH. Twenty-three trained males (age 26 +/- 5 yr; VO2peak 65.2 +/- 1.6 mL x kg-1 x min-1) performed incremental treadmill exercise to exhaustion with PaO2 corrected for simultaneous temperature measurements at all four sites. EIH was defined as DeltaPaO2 >or= 10 mm Hg. : With no temperature correction, DeltaPaO2 was -20.8 +/- 5.0 mm Hg and prevalence was 96% (n = 23), but when corrected for rectal temperature, DeltaPaO2 was -14.7 +/- 7.8 mm Hg and prevalence was 73% (n = 20); for arterial blood temperature, DeltaPaO2 was -7.7 +/- 6.5 mm Hg and prevalence was 35% (n = 20); and for esophageal temperature, DeltaPaO2 was -8.1 +/- 7.7 mm Hg and prevalence was 48% (n = 23), although when corrected for active muscle temperature, DeltaPaO2 was +8.2 +/- 7.8 mm Hg and prevalence was 0% (n = 10). There were no significant changes in CaO2 except for uncorrected values, and there was no correlation between DeltaPaO2 and VO2peak. Although the prevalence of EIH depends on the temperature correction applied to PaO2 values, in no case is there a significant change in CaO2 or any relationship with maximal aerobic power.