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dc.contributor.authorRaastad, Truls
dc.contributor.authorOwe, Simen Gylterud
dc.contributor.authorPaulsen, Gøran
dc.contributor.authorEnns, Deborah
dc.contributor.authorOvergaard, Kristian
dc.contributor.authorCrameri, Regina
dc.contributor.authorKiil, Steinar
dc.contributor.authorBelcastro, Angelo
dc.contributor.authorBergersen, Linda Hildegard
dc.contributor.authorHallén, Jostein
dc.date.accessioned2011-01-12T13:52:47Z
dc.date.available2011-01-12T13:52:47Z
dc.date.issued2010-01
dc.identifierSeksjon for fysisk prestasjonsevne / Department of Physical Performance
dc.identifier.citationMedicine & Science in Sports & Exercise. 2010, 42(1), 86-95en_US
dc.identifier.issn0195-9131
dc.identifier.urihttp://hdl.handle.net/11250/170663
dc.descriptionI Brage finner du siste tekst-versjon av artikkelen, og den kan inneholde ubetydelige forskjeller fra forlagets pdf-versjon. Forlagets pdf-versjon finner du på www.ovid.com: http://dx.doi.org/10.1249/MSS.0b013e3181ac7afa / In Brage you'll find the final text version of the article, and it may contain insignificant differences from the journal's pdf version. The original publication is available at www.ovid.com: http://dx.doi.org/10.1249/MSS.0b013e3181ac7afaen_US
dc.description.abstractPurpose: The aim of this study was to investigate changes in muscle function, muscle structure, and calpain activity after high-force eccentric exercise. Methods: Eleven healthy males performed 300 maximal voluntary eccentric actions with knee extensors in one leg. Maximal force-generating capacity was measured before exercise and regularly during the next 7 d. Biopsies from musculus vastus lateralis were taken in both control and exercised legs 0.5, 4, 8, 24, 96, and 168 h after exercise for evaluation of myofibrillar structure, extracellular matrix proteins, and calpain activity. Results: In the exercised leg, peak torque was reduced by 47 ± 5% during exercise and was still 22 ± 5% lower than baseline 4 d after the exercise. Calpain activity was three times higher in the exercised leg compared with the control leg 30 min after exercise. Myofibrillar disruptions were observed in 36 ± 6% of all fibers in exercised muscle and in 2 ± 1% of fibers in control muscle. The individual reductions in peak torque correlated with the proportion of fibers with myofibrillar disruptions (r = 0.89). The increase in calpain activity was not correlated to the proportion of fibers with myofibrillar disruptions. Nevertheless, the characteristics of the myofibrillar disruptions mimicked calpain-mediated degradation of myofibrils. Tenascin-C and the N-terminal propeptide of procollagen type III showed increased staining intensity on cross-sections 4-7 d after the exercise. Conclusions: Myofibrillar disruptions seem to be a main cause for the long-lasting reduction in force-generating capacity after high-force eccentric exercise. The increase in calpain activity, but the lack of a relationship between calpain activity and the amount of muscle damage, suggests multiple roles of calpain in the damage and repair process.en_US
dc.language.isoengen_US
dc.publisherLWWen_US
dc.subjectanalysis of variance
dc.subjectbiopsy
dc.subjectcalpain
dc.subjectexercise
dc.subjectimmunohistochemistry
dc.subjectleg
dc.subjectmuscle contraction
dc.subjectmuscle fatigue
dc.subjectmuscle, skeletal
dc.subjectmyofibrils
dc.subjecttorque
dc.titleChanges in calpain activity, muscle structure, and function after eccentric exerciseen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US
dc.subject.nsiVDP::Social science: 200::Social science in sports: 330::Other subjects within physical education: 339en_US
dc.source.pagenumber86-95en_US


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