Linked Life Data

1997813

Source:http://linkedlifedata.com/resource/pubmed/id/1997813

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1991-4-4
pubmed:abstractText
Functional 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0195-9131
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
49-55
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Skeletal muscle following tonic overload: functional and structural analysis.
pubmed:affiliation
Medical Sciences Program, Indiana University School of Medicine, Bloomington 47405.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't