Viscoelastic properties of dystrophin-deficient mouse skeletal muscles are resilient to isometric fatiguing exercise.

Exercise prescription for Duchenne muscular dystrophy (DMD) is complicated by the susceptibility of unstable skeletal muscle to contraction-induced damage. Although evidence suggests that isometric contractions can confer molecular and physiological benefits to DMD muscle, their impact on viscoelastic properties has not been assessed in vivo. Given that DMD is characterized by muscular instability due to the absence of dystrophin, we employed "myomechanical profiling"-a custom apparatus compatible with an MCR702e rheometer-to evaluate stiffness, compressibility, and elasticity of the tibialis anterior muscle of male mice following a bout of submaximal isometric fatiguing exercise. Fatigue was standardized to a 50% reduction in strength. Immediately after exercise, both dystrophin-positive (wildtype) and dystrophin-deficient (mdx) muscles exhibited reduced compressibility. Storage and loss moduli, reflecting stiffness and energy dissipation during rotational deformation, increased markedly in fatigued wildtype muscle but remained unchanged in mdx muscle. Conversely, elasticity was unaffected in wildtype muscle but shifted mdx muscle toward a more viscous state. These findings indicate that compressibility, stiffness, and energy storage capacity are not disproportionately affected in dystrophin-deficient muscle compared to wildtype muscle following fatiguing contractions. Thus, metabolically fatiguing, non-lengthening contractions appear not to compromise viscoelastic properties in dystrophin-deficient muscle, supporting their potential clinical use without exacerbating muscle instability.