METABOLIC BASIS FOR INSPIRATORY MUSCLE FATIGUE IN NORMAL HUMANS

Inspiratory muscle fatigue, a common event in patients in the intensiv e care unit, is under multifactorial control. To test the hypothesis t hat systemic oxygenation is a factor in this event, we subjected five healthy males (age 42 +/- 3 yr) to continuous inspiratory pressure (75 % of maximal inspiratory pressure, -95 +/- 5 cmH2O) with the use of a controlled breathing pattern while they breathed normoxic (21% O2), hy peroxic (30% O2), and hypoxic (13% O2) mixtures. Inspiratory muscle en durance (IME; time that pressure could be maintained) and other cardio respiratory parameters were monitored. Room air IME (3.3 +/- 0.4 min) was shortened (P < 0.05) during 13% O2 breathing (1.6 +/- 0.4 min) but was unaffected during 30% O2 breathing (4.0 +/- 0.6 min). Inspiratory loading lowered the respiratory exchange ratio (RER) during the 21 an d 30% O2 trials (1.02 +/- 0.01 to 0.80 +/- 0.03% and 1.05 +/- 0.05 to 0.69 +/- 0.01%, respectively) but not during the 13% O2 trials (1.03 /- 0.03 to 1.06 +/- 0.07%). At the point of fatigue during the 13% O2 trials, RER was lower compared with the same time point during the 21 and 30% O2 trials. A significant relationship was observed between IME and RER (r = -0.73, P = 0.002) but not between IME and any of the oth er measured variables. We conclude that 1) hypoxemia impairs the abili ty of the inspiratory muscles to sustain a mechanical challenge and 2) substrate utilization of the respiratory muscles shifts toward a grea ter reliance on lipid metabolism when O2 is readily available; this sh ift was not observed when the O2 supply was reduced.