Skeletal muscles of mice deficient in muscle creatine kinase lack burst activity

Jan van Deursen, Arend Heerschap, Frank Oerlemans, Wim Rultenbeek, Paul Jap, Henk ter Laak, Bé Wieringa

Research output: Contribution to journalArticlepeer-review

266 Scopus citations


To understand the physiological role of the creatine kinase-phosphocreatine (CK-PCr) system in muscle bioenergetics, a null mutation of the muscle CK (M-CK) gene was introduced into the germline of mice. Mutant mice show no alterations in absolute muscle force, but lack the ability to perform burst activity. Their fast-twitch fibers have an increased intermyofibrillar mitochondrial volume and an increased glycogenolytic/glycolytic potential. PCr and ATP levels are normal in resting M-CK-deficient muscles, but rates of high energy phosphate exchange between PCr and ATP are at least 20-fold reduced. Strikingly, PCr levels decline normally during muscle exercise, suggesting that M-CK-mediated conversion is not the only route for PCr utilization in active muscle.

Original languageEnglish (US)
Pages (from-to)621-631
Number of pages11
Issue number4
StatePublished - Aug 27 1993

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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