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Muscle function and running activity in mouse models of hereditary muscle dystrophy: Impact of double knockout for dystrophin and the transcription factor MyoD
Author(s) -
Mangner Norman,
Adams Volker,
Sandri Marcus,
Hoellriegel Robert,
Hambrecht Rainer,
Schuler Gerhard,
Gielen Stephan
Publication year - 2012
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.22318
Subject(s) - myod , dystrophin , mdx mouse , soleus muscle , muscular dystrophy , skeletal muscle , endocrinology , medicine , duchenne muscular dystrophy , biology , myogenesis
Mice that lack both the transcription factor MyoD and dystrophin display a more pronounced myopathic phenotype when compared with mdx mice. No data on skeletal muscle function and the impact of exercise training are available. Methods: Six‐month‐old wild‐type, mdx , myoD −/− , mdx:myoD +/− , and mdx : myoD −/− mice were randomly assigned to either 4 weeks of voluntary running or sedentary behavior. The mdx:myoD −/− mice were not able to exercise at all and were kept sedentary. Results: The soleus muscle of sedentary 7‐month‐old mdx:myoD −/− mice showed a significantly lower force development compared with all other mice. Voluntary running beginning at the age of 6 months led to lower force development of soleus muscle in the mdx animals. Conclusions: mdx:myoD −/− is not a suitable model to study exercise‐induced effects on dystrophic muscles. Voluntary exercise in adult mdx mice seems to have detrimental effects on the function of soleus muscle. Muscle Nerve, 2012