THE COMPARATIVE EFFECTS OF ELASTASE-INDUCED EMPHYSEMA ON COSTAL AND CRURAL DIAPHRAGM AND PARASTERNAL INTERCOSTAL MUSCLE CONTRACTILITY

Chronically, hyperinflated human subjects with chronic obstructive pulmonary disease and animals with experimentally induced emphysema generate greater than expected levels of transdiaphragmatic pressure at high lung volume because of adaptive changes in the length-tension relationship of the costal diaphragm. The ability to lower intrathoracic pressure during inspiration depends on the mechanical action of all the inspiratory muscles acting in concert. However, the effect of chronic hyperinflation on the mechanical action of inspiratory muscles other than the costal diaphragm remains unknown. This study compares the effect of chronic hyperinflation in the form of elastase-induced emphysema on the contractile properties of the three major inspiratory muscles of the hamster (i.e., the costal and crural diaphragm and parasternal intercostals). Muscles were studied in vitro 6 months after emphysema was induced by intratracheal injection of elastase. Saline-injected animals served as controls. TLC in the elastase-injected hamsters was significantly greater than in controls (12.5 +/- 0.8 ml versus 9.5 +/- 0.3 ml, p < 0.002). Maximal tetanic tension, time to peak tension, maximal velocity of shortening, and the force-velocity relationship differed among the three muscles but for any given muscle were similar in control and emphysematous animals. In contrast, the fiber length optimal for tension generation (L(o)) not only differed across muscles but was significantly shorter in the costal diaphragm of emphysematous animals compared with control animals. However, L(o), of the parasternal intercostal and crural diaphragm was similar in both groups. These data indicate that chronic hyperinflation has no discernable effect on the velocity of muscle shortening and twitch tension wave form in any of the primary inspiratory muscles and alters the length-tension relationship in muscle specific fashion. We speculate that muscle specific changes in the length-tension relationship of the major inspiratory muscles in response to chronic hyperinflation may be due to alterations in inspiratory muscle precontraction length secondary to regional differences in thoracic volume and/or configuration.