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1 University of Florida
2 University of Pennsylvania
* To whom correspondence should be addressed. E-mail: tclanton{at}hhp.ufl.edu.
The diaphragm and other respiratory muscles undergo extensive remodeling in both animal models of emphysema and in human COPD, but the nature of the remodeling is different in many respects. One common feature is a shift towards improved endurance characteristics and increased oxidative capacity. Furthermore, both animals and man respond to chronic hyperinflation by diaphragm shortening. Though in rodent models this clearly arises by deletion of sarcomeres in series, the mechanism has not been proven conclusively in human COPD. Unique characteristics of the adaptation in human diaphragms includes shifts to more predominant slow, Type I fibers, expressing slower MHC isoforms and Type I and Type II fiber atrophy. Though some laboratories report reductions in specific force, this may be accounted for by decreases in myosin heavy chain content as the muscles become more oxidative and more efficient. More recent findings have reported reductions in Ca+2 sensitivity and reduced myofibrillar elastic recoil. In contrast, in rodent models of disease, there is no consistent evidence for loss of specific force, no consistent shift in fiber populations, and atrophy is predominantly seen only in fast, Type IIX fibers. This review challenges the hypothesis that the adaptations in human diaphragm represent a form of dysfunction, secondary to systemic disease, and suggest that most findings can as well be attributed to adaptive processes of a complex muscle responding to unique alterations in its working environment
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