HYPOXIC EFFECTS ON EXERCISE-INDUCED DIAPHRAGMATIC FATIGUE IN NORMAL HEALTHY HUMANS

We examined the effects of hypoxia on exercise-induced diaphragmatic fatigue. Eleven subjects with a mean maximal O-2 uptake of 52.4 +/- 0.7 ml.kg(-1).min(-1) completed one normoxic (arterial O-2 saturation 96-94%) and one hypoxic (inspiratory O-2 fraction = 0.15; arterial O-2 saturation 83-77%) exercise test at 85% maximal O-2 uptake to exhaustion on separate days. Supramaximal bilateral phrenic nerve stimulation (BPNS) was used to determine the pressure generation of the diaphragm pre- and postexercise at 1, 10, and 20 Hz. There was increased flow limitation during hypoxic vs. normoxic exercise. There was a decrease in hypoxic exercise time (normoxic 24.9 +/- 0.7 min vs. hypoxic 15.8 +/- 0.8 min; P < 0.05). After exercise the BPNS transdiaphragmatic pressure (Pdi) was significantly reduced at 1 and 10 Hz after both exercise tests. The BPNS Pdi was recovered to control values by 60 min postnormoxic exercise but was still reduced 90 min posthypoxic exercise. The mean percent fall in the stimulated BPNS Pdi was similar (normoxic -24.8 +/- 4.7%; hypoxic -18.8 +/- 3.0%) after both exercise conditions. Experiencing the same amount of diaphragm fatigue in a shorter time period in hypoxic exercise may have been due to 1) the increased expiratory flow limitation and diaphragmatic muscle work, 2) decreased O-2 transport to the diaphragm , and/or 3) increased levels of circulating metabolites.