title: Eccentric contraction injury in dystrophic canine muscle.
abstract: OBJECTIVE
  To test the hypothesis that eccentric contractions induce greater injury in dystrophic compared with normal canine muscle.
  
  
  METHODS
  Blinded cohort study.
  
  
  METHODS
  Animal laboratory.
  
  
  METHODS
  Ten dogs with a homologue to Duchenne muscular dystrophy (Golden retriever muscular dystrophy [GRMD]) and 10 normal littermates.
  
  
  METHODS
  Contractions induced in tibiotarsal flexors and extensors by sciatic nerve stimulation. Because more powerful extensors overrode flexors, eccentric contractions occurred in flexors. Concentric contractions were induced in contralateral flexors by peroneal nerve stimulation.
  
  
  METHODS
  Tibiotarsal flexion force 3 days after contractions. Muscle was examined for injury (esterase activity, Evans blue dye penetration) and regeneration (embryonic myosin isoform expression).
  
  
  RESULTS
  Mean force deficit after eccentric flexor contractions was 43.3%+/-25.7% in GRMD dogs compared with 25.0%+/-18.4% in controls (P=.04, Wilcoxon rank-sum test). Concentric contractions induced force deficits in GRMD but not normal dogs; however, the difference between the 2 groups was not significant (P=.08, Wilcoxon rank-sum test). After concentric contractions in controls, force decrements correlated with esterase activity measured by area (r=.794, P=.006) and intensity (r=.697, P=.025, Spearman rank correlation). No other significant correlation was detected between force and biopsy data.
  
  
  CONCLUSIONS
  Force data support the hypothesis that eccentric contractions induce greater injury in dystrophic compared with normal canine muscle. Phenotypic features of the dystrophic canine model used here are similar to those of humans with Duchenne's.
authors.affiliation: Departments of Physical Medicine and Rehabilitation, College of Veterinary Medicine, University of Missouri-Columbia, One Hospital Drive, Columbia, MO 65212, USA. childersmk@health.missouri.edu
authors.forename: Martin K
authors.initials: MK
authors.lastname: Childers
authors.forename: Carol S
authors.initials: CS
authors.lastname: Okamura
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Bogan
authors.forename: Janet R
authors.initials: JR
authors.lastname: Bogan
authors.forename: Gregory F
authors.initials: GF
authors.lastname: Petroski
authors.forename: Kerry
authors.initials: K
authors.lastname: McDonald
authors.forename: Joe N
authors.initials: JN
authors.lastname: Kornegay
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D001706:Biopsy; D016022:Case-Control Studies; D004195:Disease Models, Animal; D004283:Dog Diseases / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D004285:Dogs; D016189:Dystrophin / Q000235:genetics; D004558:Electric Stimulation; D007537:Isometric Contraction; D009137:Muscular Dystrophy, Animal / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D020388:Muscular Dystrophy, Duchenne / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D009154:Mutation / Q000235:genetics; D009210:Myofibrils / Q000473:pathology; D009336:Necrosis; D010543:Peroneal Nerve; D010641:Phenotype; D011897:Random Allocation; D016059:Range of Motion, Articular; D012584:Sciatic Nerve; D016037:Single-Blind Method; D018709:Statistics, Nonparametric
chemical_list: D016189:Dystrophin