Compromised pressure-generating capacity of diaphragmatic muscle and its interaction with the lower rib cage at high lung volume during airway occlusion

The pressure-generating capacity of the diaphragm is generally thought to be compromised at high lung volume either due to loss of curvature or loss of its membrane tension. At a state of hyperinflation during airway occlusion at total lung capacity, the diaphragmatic muscle is forced to contract from an initial shorter length, the zone of apposition narrows, insertional force on the chest wall is reduced, and abdominal compliance falls. We hypothesize that these altered mechanical conditions at high lung volume lead to a loss of the pressure-generating capacity that is mediated by excessive muscle shortening rather than loss of curvature of its muscle fibers. Using a biplane fluoroscopy, locations of radiopaque markers attached to the diaphragm muscle fibers and the lower three ribs of 10 beagle dogs weighing between 7 and 10.5 kg were determined. Such measurements were conducted during quiet spontaneous breathing and during forceful inspiratory efforts against an occluded airway at three lung volumes spanning the vital capacity from functional residual capacity (FRC) to total lung capacity (TLC). Our data show that transdiaphragmatic pressure (Pdi) at TLC was reduced by nearly 80% and surface area of the midcostal diaphragm muscle at contracted state during airway occlusion at TLC reduced by nearly 35% from its value at end of expiration. In addition, muscle fiber curvature was essentially maintained during the entire vital capacity of airway occlusion. Our data demonstrate that during airway occlusion at high lung volume, the pressure-generating capacity of the diaphragm is compromised primarily due to a mechanism that involved a combined mechanical effect of hyperinflation and excessive muscle contraction rather than a significant loss of curvature of its muscle fibers.<b>NEW & NOTEWORTHY</b> Data from the current study support the hypothesis that the pressure-generating capacity of the diaphragm at high lung volume is compromised primarily due to a mechanism that involves a combined mechanical effect of hyperinflation and substantial muscle contraction rather than a significant loss of its muscle fiber curvature.