Abstract
Many athletes with exercise induced hypoxemia (EIH) show a reduced ventilatory response to exercise, as well as reduced measures of resting peripheral chemoresponsiveness (PC). The purpose of this project was to determine if a moderate dosage of caffeine, a common ventilatory stimulant, could augment resting PC, exercise ventilation (VE), end-tidal O2 partial pressure (PETO2), and arterial O2 saturation(SaO2) in athletes with EIH. Eight highly trained males (VO2 max, 69.2 ± 4.0 ml·kg-1·min-1) who demonstrated EIH at VO2 max (SaO2, 88.0 ± 1.7%), ingested in a randomized, single-blind design, a placebo (PLA) or caffeine (CAF, 8 mg·kg-1 body wt) one hour prior to testing. PC at rest was assessed via the hypoxic and hypercapnic ventilatory responses (HVR and HCVR, respectively). Dependent measures of ventilation and saturation were determined during progressive exercise on a treadmill. Ve was higher at 75%, 80%, and 100% of VO2 max with CAF (p<0.05). HVR and HCVR were not different between the two conditions, indicating that the increased Ve likely came from central stimulation or secondary effects of CAF. Ve/VO2, PETO2 and SaO2 were increased at 75%, 80%, and 90% of VO2max with CAF (p<0.05), but were not different at VO2 max despite an increase in Ve. EIH subjects demonstrated a large inter-individual variance in Ve and SaO2 at VO2 max in response to CAF. This fact, combined with the declining effect of CAF as workload increased, suggests mechanisms other than an inadequate hyperventilatory response may operate to different degrees across individuals as VO2 max is approached.
Published Version
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