title: Effects of mechanical over-loading on the properties of soleus muscle fibers, with or without damage, in wild type and mdx mice.
abstract: Effects of mechanical over-loading on the characteristics of regenerating or normal soleus muscle fibers were studied in dystrophin-deficient (mdx) and wild type (WT) mice. Damage was also induced in WT mice by injection of cardiotoxin (CTX) into soleus muscle. Over-loading was applied for 14 days to the left soleus muscle in mdx and intact and CTX-injected WT mouse muscles by ablation of the distal tendons of plantaris and gastrocnemius muscles. All of the myonuclei in normal muscle of WT mice were distributed at the peripheral region. But, central myonuclei were noted in all fibers of WT mice regenerating from CTX-injection-related injury. Further, many fibers of mdx mice possessed central myonuclei and the distribution of such fibers was increased in response to over-loading, suggesting a shift of myonuclei from peripheral to central region. Approximately 1.4% branched fibers were seen in the intact muscle of mdx mice, although these fibers were not detected in WT mice. The percentage of these fibers in mdx, not in WT, mice was increased by over-loading (∼51.2%). The fiber CSA in normal WT mice was increased by over-loading (p<0.05), but not in mdx and CTX-injected WT mice. It was suggested that compensatory hypertrophy is induced in normal muscle fibers of WT mice following functional over-loading. But, it was also indicated that muscle fibers in mdx mice are susceptible to mechanical over-loading and fiber splitting and shift of myonuclei from peripheral to central region are induced.
authors.affiliation: Graduate School of Frontier Biosciences, Osaka University, Toyonaka City, Osaka, Japan.
authors.forename: Masahiro
authors.initials: M
authors.lastname: Terada
authors.forename: Fuminori
authors.initials: F
authors.lastname: Kawano
authors.forename: Takashi
authors.initials: T
authors.lastname: Ohira
authors.forename: Naoya
authors.initials: N
authors.lastname: Nakai
authors.forename: Norihiro
authors.initials: N
authors.lastname: Nishimoto
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Ohira
mesh_terms: D000818:Animals; D054715:Cardiotoxins / Q000633:toxicity; D016189:Dystrophin / Q000172:deficiency; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018101:Mice, Inbred mdx; D009119:Muscle Contraction / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000473:pathology / Q000502:physiology*; D018482:Muscle, Skeletal / Q000187:drug effects / Q000503:physiopathology*; D009137:Muscular Dystrophy, Animal / Q000503:physiopathology*; D012038:Regeneration; D013314:Stress, Mechanical
chemical_list: D054715:Cardiotoxins; D016189:Dystrophin