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

We examined the effects of hypoxia on exercise-induced diaphragmatic f atigue. 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 sa turation 83-77%) exercise test at 85% maximal O-2 uptake to exhaustion on separate days. Supramaximal bilateral phrenic nerve stimulation (B PNS) was used to determine the pressure generation of the diaphragm pr e- and postexercise at 1, 10, and 20 Hz. There was increased flow limi tation during hypoxic vs. normoxic exercise. There was a decrease in h ypoxic 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 te sts. The BPNS Pdi was recovered to control values by 60 min postnormox ic exercise but was still reduced 90 min posthypoxic exercise. The mea n percent fall in the stimulated BPNS Pdi was similar (normoxic -24.8 +/- 4.7%; hypoxic -18.8 +/- 3.0%) after both exercise conditions. Expe riencing 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 transp ort to the diaphragm , and/or 3) increased levels of circulating metab olites.