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pubmed-article:1997813pubmed:dateCreated1991-4-4lld:pubmed
pubmed-article:1997813pubmed:abstractTextFunctional overloading of skeletal muscle induces a compensatory hypertrophy as an adaptive response to increased functional demand. Overload of the extensor digitorum longus (EDL) muscle (129 ReJ strain male mouse) was induced by unilateral surgical removal of a synergistic muscle, tibialis anterior (TA). Response of the EDL to overload for 7, 21, and 42 d was analyzed for changes in 1) muscle weight, 2) myofiber type distribution, 3) myofiber cross-sectional area by fiber type, 4) speed of contraction and relaxation of the muscle, 5) force of contraction, and 6) myofiber morphologic integrity. The weight of the EDL significantly increased. The overload caused no impairment of muscle contractility and did not have a significant effect on isometric twitch contraction time to peak tension or the time to one-half relaxation of the twitch. Overloaded muscles demonstrated a transient shift in fiber type profile with preferential hypertrophy of Type IIA fibers that occurred in the early phase of overload while type IIB fibers were recruited by 42 d. No significant increase in myofiber number in overloaded muscles occurred. Some morphologic changes in over-loaded muscles parallel those found in patients with neurogenic muscular disorders. However, overloaded muscle did not exhibit a significant occurrence of fiber branching from controls in the midbelly region of the muscle.lld:pubmed
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pubmed-article:1997813pubmed:issn0195-9131lld:pubmed
pubmed-article:1997813pubmed:authorpubmed-author:JohnsonT LTLlld:pubmed
pubmed-article:1997813pubmed:authorpubmed-author:KlueberK MKMlld:pubmed
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pubmed-article:1997813pubmed:volume23lld:pubmed
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pubmed-article:1997813pubmed:pagination49-55lld:pubmed
pubmed-article:1997813pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:1997813pubmed:year1991lld:pubmed
pubmed-article:1997813pubmed:articleTitleSkeletal muscle following tonic overload: functional and structural analysis.lld:pubmed
pubmed-article:1997813pubmed:affiliationMedical Sciences Program, Indiana University School of Medicine, Bloomington 47405.lld:pubmed
pubmed-article:1997813pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:1997813pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed