This study was supported by the National Institutes of Health (R01 NS045195 to C.L.J. and DK095210 to R.W.W.).
Androgen receptors in muscle fibers induce rapid loss of force but not mass: Implications for spinal bulbar muscular atrophy
Article first published online: 30 APR 2013
Copyright © 2013 Wiley Periodicals, Inc.
Muscle & Nerve
Volume 47, Issue 6, pages 823–834, June 2013
How to Cite
Oki, K., Wiseman, R. W., Breedlove, S. M. and Jordan, C. L. (2013), Androgen receptors in muscle fibers induce rapid loss of force but not mass: Implications for spinal bulbar muscular atrophy. Muscle Nerve, 47: 823–834. doi: 10.1002/mus.23813
- Issue published online: 23 MAY 2013
- Article first published online: 30 APR 2013
- Accepted manuscript online: 8 FEB 2013 07:31AM EST
- Manuscript Accepted: 3 FEB 2013
- Kennedy disease;
- motor dysfunction;
- muscle dysfunction;
- neuromuscular disease;
- skeletal muscle;
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.
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.
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.
These results suggest calcium-handling mechanisms in muscle fibers are defective in motor-impaired mice. Muscle Nerve 47: 823–834, 2013