Effects of intermittent hypoxia on SaO₂, cerebral and muscle oxygenation during maximal exercise in athletes with exercise-induced hypoxemia

In a placebo-controlled study, the effects of intermittent hypoxic exposures (IHE) or a placebo control for 10 days, were examined on the extent of exercise-induced hypoxemia (EIH), cerebral and muscle oxygenation (near-infrared spectroscopy) and \(\dot V{\text{O}}_{2{\text{peak}}}.\) Eight athletes who had previously displayed EIH (fall in saturation of arterial oxygen (SaO₂) of >4% from rest) during an incremental maximal exercise test, volunteered for the present research. Prior to (baseline), and 2 days following (post) the IHE or placebo, an incremental maximal exercise test was performed whilst SaO₂, heart rate, cerebral and muscle oxygenation and respiratory gas exchange were measured continuously. After IHE, but not placebo, EIH was less pronounced at \(\dot V{\text{O}}_{2{\text{peak}}} \) (IHE group, SaO₂ at \(\dot V{\text{O}}_{2{\text{peak}}} :\) baseline 91.23 ± 1.10%, post 94.10 ± 2.19%; P < 0.01, mean ± SD). This reduction was reflected in an increased ventilation (NS), a lower end-tidal CO₂ (P < 0.01), and lowered cerebral TOI during heavy exercise \( (90\% \,\dot V{\text{O}}_{2{\text{peak}}} : - 6.1 \pm 6.0\,\Updelta \% ,{\text{ }}P = 0.04). \) Conversely, muscle tHb at maximal exercise, was increased (2.4 ± 1.8 ΔμM, P = 0.01, mean ± 95 CL) following IHE, whilst de-oxygenated Hb at 90% of \(\dot V{\text{O}}_{2{\text{peak}}} \) was reduced (−0.9 ± 0.8 ΔμM, P = 0.02). These data indicate that exposure to IHE can attenuate the degree of EIH. Despite a potential compromise in cerebral oxygenation, exposure to IHE may induce some positive physiological adaptations at the muscle tissue level. We speculate that the unchanged \(\dot V{\text{O}}_{2{\text{peak}}} \) following IHE might reflect a balance between these central (cerebral) and peripheral (muscle) adaptations.