Androgen receptors in muscle fibers induce rapid loss of force but not mass: implications for spinal bulbar muscular atrophy

Muscle Nerve. 2013 Jun;47(6):823-34. doi: 10.1002/mus.23813. Epub 2013 Apr 30.


Introduction: Testosterone (T) induces motor dysfunction in transgenic (Tg) mice that overexpress wild-type androgen receptor (AR) in skeletal muscles. Because many genes implicated in motor neuron disease are expressed in skeletal muscle, mutant proteins may act in muscle to cause dysfunction in motor neuron disease.

Methods: We examined contractile properties of the extensor digitorum longus (EDL) and soleus (SOL) muscles in vitro after 5 and 3 days of T treatment in motor-impaired Tg female mice.

Results: Both muscles showed deficits in tetanic force after 5 days of T treatment, without losses in muscle mass, protein content, or fiber number. After 3 days of T treatment, only SOL showed a deficit in tetanic force comparable to that of 5 days of treatment. In both treatments, EDL showed slowed twitch kinetics, whereas SOL showed deficits in the twitch/tetanus ratio.

Conclusions: These results suggest calcium-handling mechanisms in muscle fibers are defective in motor-impaired mice.

MeSH terms

  • Androgens / pharmacology*
  • Animals
  • Bulbo-Spinal Atrophy, X-Linked / physiopathology*
  • Disease Models, Animal
  • Female
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Muscle Contraction / drug effects*
  • Muscle Fibers, Skeletal / drug effects*
  • Muscle Fibers, Skeletal / pathology
  • Muscle Strength / drug effects*
  • Organ Size / drug effects
  • Rats
  • Receptors, Androgen / genetics*
  • Testosterone / pharmacology*


  • Androgens
  • Receptors, Androgen
  • Testosterone