Abstract
Previous work suggests that exercise-induced arterial hypoxaemia (EIAH), causing only moderate arterial oxygen desaturation (SaO2 : 92 +/- 1%), does not exaggerate diaphragmatic fatigue exhibited by highly trained endurance athletes. Since changes in arterial O2 tension have a significant effect on the rate of development of locomotor muscle fatigue during strenuous exercise, the present study investigated whether hypoxia superimposed on EIAH exacerbates the exercise-induced diaphragmatic fatigue in these athletes. Eight trained cyclists (VO2max : 67.0 +/- 2.6 ml kg(-1) min(-1); mean +/- S.E.M.) completed in balanced order four 5 min exercise tests leading to different levels of end-exercise SaO2 (64 +/- 2, 83 +/- 1, 91 +/- 1 and 96 +/- 1%) via variations in inspired O2 fraction (FiO2 : 0.13, 0.17, 0.21 and 0.26, respectively). Measurements were made at corresponding intensities (65 +/- 3, 80 +/- 3, 85 +/- 3 and 90 +/- 3% of normoxic maximal work rate, respectively) in order to produce the same tidal volume, breathing frequency and respiratory muscle load at each FiO2. The mean pressure time product of the diaphragm did not differ across the four exercise tests and ranged between 312 +/- 28 and 382 +/- 22 cmH2O s min(-1). Ten minutes into recovery, twitch transdiaphragmatic pressure (P(di,tw)) determined by bilateral phrenic nerve stimulation, was significantly (P = 0.0001) reduced after all tests. After both hypoxic tests (FiO2 : 0.13, 0.17) the degree of fall in P(di,tw) (by 26.9 +/- 2.7 and 27.4 +/- 2.6%, respectively) was significantly greater (P < 0.05) than after the normoxic test (by 20.1 +/- 3.4%). The greater amount of diaphragmatic fatigue in hypoxia at lower leg work rates (presumably requiring smaller leg blood flow compared with normoxia at higher leg work rates), suggests that when ventilatory muscle load is similar between normoxia and hypoxia, hypoxia exaggerates diaphragmatic fatigue in spite of potentially greater respiratory muscle blood flow availability.
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