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The Effects of Exercise on Ventricular Wall Thickness and Fibrosis in Wild‐Type and Dystrophin‐Deficient Mice
Author(s) -
Plochocki Jeffrey H,
Costas Jeffrey M
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.637.1
Subject(s) - fibrosis , dystrophin , duchenne muscular dystrophy , mdx mouse , medicine , endocrinology , muscular dystrophy , degeneration (medical) , masson's trichrome stain , trichrome stain , myocardial fibrosis , pathology , biology , immunohistochemistry
Dystrophin is a cytoplasmic protein that connects muscle cells to the extracellular matrix. When absent, muscle degeneration and fibrosis occurs that resembles the histopathological presentation of Duchenne muscular dystrophy. In mice that lack dystrophin (Mdx mice), there is muscle degeneration and regeneration in the first few months of life, with fibrosis increasing after that. In this study, we evaluated the relationship between exercise and lateral ventricular wall thickness (LVT) in wild‐type and Mdx mice aged 11 weeks. Degree of cardiac fibrosis was assessed using a trichrome stain. Sedentary Mdx mice exhibited significantly larger LVT than wild‐type mice (P < 0.05). Exercise treated wild‐type mice had larger LVT than sedentary wild‐type mice on average, but this difference was not statistically significant. The LVT of sedentary Mdx mice was 28% larger than that of exercise treated Mdx mice (P < 0.05). Exercised treated Mdx mice were the only group that exhibited any noticeable fibrosis in the lateral aspect of the heart. Our findings suggest that exercise within the normal physiological range can accelerate degeneration and fibrosis of the lateral ventricular wall in Mdx mice.