Caffeine stimulates ventilation in athletes with exercise-induced hypoxemia.

INTRODUCTION/PURPOSE: Many athletes with exercise-induced hypoxemia (EIH) show an insufficient ventilatory response to exercise and low resting ventilatory responsiveness. The purpose of this project was to determine whether a moderate dosage of caffeine, a common ventilatory stimulant, could augment resting ventilatory responsiveness, exercise ventilation (V E), end-tidal O2 partial pressure (PetO2), and arterial oxyhemoglobin saturation (HbSaO2) in athletes with EIH.

METHODS: Eight highly trained males (V[spacing dot above]O2max, 69.2 +/- 4.0 mL.[kg.min]) who demonstrated EIH at V[spacing dot above]O2max (HbSaO2, 88.0 +/- 1.7%), ingested in a randomized design a placebo or caffeine (CAF, 8 mg.kg body wt) 1 h before testing. Ventilatory responsiveness at rest was assessed via the isocapnic hypoxic and hyperoxic hypercapnic ventilatory responses (HVR and HCVR, respectively). Dependent measures of metabolic variables, ventilation, and saturation were determined during progressive treadmill exercise to exhaustion.

RESULTS: V E was higher at 75%, 80%, and 100% of V[spacing dot above]O2max with CAF (P < 0.05). V E/V O2, PetO2, and HbSaO2 were increased at 75%, 80%, and 90% of [formula: see text] with CAF but were not different at V[spacing dot above]O2max despite an increase in V e. No change in V[spacing dot above]O2max was observed between treatments. HVR and HCVR were not different between the two conditions, indicating that the increased V E likely came from central stimulation or secondary effects of CAF.

CONCLUSION: The failure of HbSaO2 to increase at [formula: see text] despite an increase in V E suggests that mechanisms influencing HbSaO2 other than an inadequate hyperventilatory response may operate to different degrees across individuals as V[spacing dot above]O2max is approached.