OBJECTIVE: To test the hypothesis that eccentric contractions induce greater injury in dystrophic compared with normal canine muscle. DESIGN: Blinded cohort study. SETTING: Animal laboratory. ANIMALS: Ten dogs with a homologue to Duchenne muscular dystrophy (Golden retriever muscular dystrophy [GRMD]) and 10 normal littermates. INTERVENTIONS: 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. MAIN OUTCOME MEASURE: 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. Copyright 2002 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation
OBJECTIVE: To test the hypothesis that eccentric contractions induce greater injury in dystrophic compared with normal canine muscle. DESIGN: Blinded cohort study. SETTING: Animal laboratory. ANIMALS: Ten dogs with a homologue to Duchenne muscular dystrophy (Golden retriever muscular dystrophy [GRMD]) and 10 normal littermates. INTERVENTIONS: 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. MAIN OUTCOME MEASURE: 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 dystrophiccanine model used here are similar to those of humans with Duchenne's. Copyright 2002 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation
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