Skeletal muscles of mice deficient in muscle creatine kinase lack burst activity.
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.
van Deursen
J
J
Department of Cell Biology and Histology, Faculty of Medical Sciences, University of Nijmegen, The Netherlands.
Heerschap
A
A
Oerlemans
F
F
Ruitenbeek
W
W
Jap
P
P
ter Laak
H
H
Wieringa
B
B
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003402:Creatine Kinase / Q000172:deficiency* / Q000235:genetics* / Q000378:metabolism; D004734:Energy Metabolism; D005260:Female; D006003:Glycogen / Q000378:metabolism; D006019:Glycolysis; D006651:Histocytochemistry; D007537:Isometric Contraction; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D008854:Microscopy, Electron; D008931:Mitochondria, Muscle / Q000378:metabolism; D009132:Muscles / Q000378:metabolism / Q000502:physiology* / Q000648:ultrastructure; D016296:Mutagenesis; D010725:Phosphocreatine / Q000378:metabolism
D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D006003:Glycogen; D003402:Creatine Kinase