Exercise-Induced Hypoxemia among Endurance-Trained Athletes

It is well documented that in endurance-trained athletes performing heavy intensity exercise, arterial oxyhemoglobin saturation (SaO2) may fall below resting values. This phenomenon, termed exercise-induced arterial hypoxemia (EIAH), is common among male and female athletes, regardless of age, with prevalence rates reaching up to 70% in certain populations of highly-trained athletes. EIAH is manifested as excessive widening of the alveolar-arterial PO2 difference (D(A-a)O2) due to a substantial fall in arterial partial pressure of O2 (PaO2) and a rightward shift in the haemoglobin-O2 dissociation curve. In athletes, the reduction in PaO2 has been mostly attributed to ventilation-perfusion mismatch, an inadequate hyperventilatory response during exercise, and diffusion limitations such as incomplete pulmonary gas exchange and reduced erythrocyte pulmonary transit time. A 3-4% fall in SaO2 below resting levels has been suggested as a threshold for significant negative effects on aerobic capacity measures such as maximal O2 uptake (VO2max) and time-trial performance. Prevention of EIAH by maintaining Hb-O2 saturation at resting levels has been shown to improve performance, likely by mitigation of locomotor muscle fatigue. Yet, there remains a gap in the literature as to the physiological consequences of EIAH. For example, whether the occurrence of EIAH is associated with more pronounced increases in stress and immune-related markers following a bout of prolonged (20 min), heavy intensity (80-85% VO2max) exercise is yet to be determined. This question is of high relevance for endurance athletes who routinely perform heavy-intensity exercise for 20-30 min (e.g., “tempo runs”) and could experience, on a regular basis, an exaggerated inflammatory and/or stress response.