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 testing ventilatory responsiveness, exercise ventilation (PE), end-tidal 0, partial pressure (PETO2), and arterial oxyhemoglobin saturation (HbSaO(2)) in athletes with EIH. Methods: Eight highly trained males ((V) over dotO(2max), 69.2 +/- 4.0 mL.[kg.min](-1)) who demonstrated EIH at VO2max (HbSaO(2), 88.0 +/- 1.7%), ingested in a randomized design a placebo or caffeine (CAF, 8 mg.kg(-1) body wt) I 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 VO2max with CAF (P < 0.05). V-E/VO2, PETO2, and HbSaO(2) were increased at 75%, 80%, and 90% of VO2max With CA-F but were not different at VO2max, despite an increase in VE. No change in VO2max 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 HbSaO(2) to increase at VO2max despite an increase in V-E suggests that mechanisms influencing HbSaO(2) other than an inadequate hyperventilatory response may operate to different degrees across individuals as VO2max is approached.