Journal of Applied Physiology, Vol 75, Issue 5 2188-2194, Copyright © 1993 by American Physiological Society
Metabolic basis for inspiratory muscle fatigue in normal humans
E. T. Mannix, T. Y. Sullivan, P. Palange, I. R. Dowdeswell, F. Manfredi, P. Galassetti and M. O. Farber
Indiana University Department of Medicine, Indianapolis.
Inspiratory muscle fatigue, a common event in patients in the intensive
care unit, is under multifactorial control. To test the hypothesis that
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), hyperoxic (30%
O2), and hypoxic (13% O2) mixtures. Inspiratory muscle endurance (IME; time
that pressure could be maintained) and other cardiorespiratory 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 and 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 other measured variables. We conclude that 1) hypoxemia impairs
the ability of the inspiratory muscles to sustain a mechanical challenge
and 2) substrate utilization of the respiratory muscles shifts toward a
greater reliance on lipid metabolism when O2 is readily available; this
shift was not observed when the O2 supply was reduced.
