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Am J Physiol Regul Integr Comp Physiol 283: R583-R590, 2002. First published May 23, 2002; doi:10.1152/ajpregu.00080.2002
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Vol. 283, Issue 3, R583-R590, September 2002

Diaphragm contractile dysfunction in MyoD gene-inactivated mice

Jessica L. Staib1, Steven J. Swoap2, and Scott K. Powers1,3

1 Departments of Exercise and Sport Sciences and 3 Physiology Center for Exercise Science, University of Florida, Gainesville, Florida 32611; and 2 Department of Biology, Williams College, Williamstown, Massachusetts 01267

MyoD is one of four myogenic regulatory factors found exclusively in skeletal muscle. In an effort to better understand the role that MyoD plays in determining muscle contractile properties, we examined the effects of MyoD deletion on both diaphragmatic contractile properties and myosin heavy chain (MHC) phenotype. Regions of the costal diaphragm from wild-type and MyoD knockout [MyoD (-/-)] adult male BALB/c mice (n = 8/group) were removed, and in vitro diaphragmatic contractile properties were measured. Diaphragmatic contractile measurements revealed that MyoD (-/-) animals exhibited a significant (P < 0.05) downward shift in the force-frequency relationship, a decrement in maximal specific tension (Po; -33%), a decline in maximal shortening velocity (Vmax; -37%), and concomitant decrease in peak power output (-47%). Determination of MHC isoforms in the diaphragm via gel electrophoresis revealed that MyoD elimination resulted in a fast-to-slow shift (P < 0.05) in the MHC phenotype toward MHC types IIA and IIX in MyoD (-/-) animals. These data indicate that MyoD deletion results in a decrease in diaphragmatic submaximal force generation and Po, along with decrements in both Vmax and peak power output. Hence, MyoD plays an important role in determining diaphragmatic contractile properties.

myogenic regulatory factors; myosin heavy chain; maximal specific tension; maximal shortening velocity; oxidative capacity


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