To understand the physiological role of the creatine kinase-phosphocre
atine (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 abili
ty to perform burst activity. Their fast-twitch fibers have an increas
ed intermyofibrillar mitochondrial volume and an increased glycogenoly
tic/glycolytic potential. PCr and ATP levels are normal in resting M-C
K-deficient muscles, but rates of high energy phosphate exchange betwe
en PCr and ATP are at least 20-fold reduced. Strikingly, PCr levels de
cline normally during muscle exercise, suggesting that M-CK-mediated c
onversion is not the only route for PCr utilization in active muscle.