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Lateral transmission of force is impaired in skeletal muscles of dystrophic mice and very old rats
Author(s) -
Faulkner John A.,
Ramaswamy Krishnan,
Palmer Mark,
vanderMeulen Jack,
Renoux Abigail,
Kostrominova Tatiana,
Michele Daniel
Publication year - 2011
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.25.1_supplement.1051.37
Subject(s) - tendon , anatomy , dystrophin , muscular dystrophy , extracellular matrix , contraction (grammar) , mdx mouse , duchenne muscular dystrophy , biology , muscle contraction , skeletal muscle , chemistry , endocrinology , medicine , microbiology and biotechnology
In frog muscles, Sibyl Street demonstrated transmission of force laterally from an activated fibre to the surface of the muscle occurs without attenuation, but lateral transmission of force has not been demonstrated in mammalian muscles. The dystrophin‐glycoprotein complex (DGC) provides an essential link from muscle fibre cytoskeleton to the extracellular matrix. In dystrophic humans and mdx mice, mutations in the dystrophin gene disrupt the structure of the DGC causing severe damage to muscle fibres. The lateral transmission of force was measured from the proximal tendon to a unique ‘yoke’ apparatus attached to the surface of muscles midway between the tendons. In muscles of young WT mice and rats, compared over a wide range of longitudinal forces, the forces transmitted laterally showed little or no decrement. In contrast, muscles of mdx mice or very old rats, showed loss or major reductions in the expression of dystrophin and forces transmitted laterally were impaired severely. We conclude that during contractions, forces developed by skeletal muscles of young WT mice and rats are transmitted laterally from fibre to fibre through the DGC without decrement. In contrast, in muscles of dystrophic, or very old animals, disruptions in DGC structure and function impair lateral transmission of force causing instability and increased susceptibility of fibres to contraction‐induced injury.