The effect of hyperinflation on respiratory muscle work in acute induced asthma.

To examine the relationship between end-expiratory lung volume and respiratory muscle work during acute bronchoconstriction, we measured the work of breathing in nine asthmatic subjects, in whom bronchoconstriction was induced with histamine aerosol. When the forced expiratory volume in one second (FEV1) fell below 60% of the control value, work was measured at the spontaneously hyperinflated lung volume (VLS), at a volume equivalent to the control functional residual capacity (FRC) and at a volume 30% of vital capacity (VC) above the control FRC. Hyperinflation to VLS caused a 39% decrease in the total positive work per breath from 2.8 +/- 0.4 to 1.7 +/- 0.1 J, entirely due to a decrease in expiratory work per breath from 1.6 +/- 0.4 to 0.10 +/- 0.05 J. Inspiratory work did not change at any lung volume, because the increase in inspiratory elastic work due to hyperinflation was offset by the decrease in flow resistive work. Breathing above VLS did not alter the total positive muscle work, but did increase the negative work of the inspiratory muscles from 0.4 +/- 0.1 to 0.8 +/- 0.1 J.breath. We conclude that during induced asthma spontaneous hyperinflation minimizes the total respiratory muscle work and may constitute a mechanism for minimizing energy expenditure.