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1 Department of Medicine (AH/NH), University of Melbourne, Heidelberg, Australia
2 Department of Physiology, University of Melbourne, Parkville, Australia
3 Department of Medicine (RMH), University of Melbourne, Parkville, Australia
4 ANZAC Research Institute, University of Sydney, Concord, New South Wales, Australia
* To whom correspondence should be addressed. E-mail: hmaclean{at}unimelb.edu.au.
Androgens promote anabolism in skeletal muscle; however, effects on subsequent muscle function are less well defined because of a lack of reliable experimental models. We have established a rigorous model of androgen withdrawal and administration in male mice, and assessed androgen regulation of muscle mass, structure and function. Adult C57Bl/6J male mice were orchidectomized (Orx) or sham-operated (Sham) and received 10 weeks continuous testosterone (T) or control treatment (C) via intraperitoneal implants. Mass, fiber cross-sectional area (CSA), and in vitro contractile function were assessed for fast-twitch extensor digitorum longus (EDL) and slow-twitch soleus (SOL) muscles. Following 10 weeks, Orx+C mice had reduced body weight gain (p < 0.05), seminal vesicle mass (p < 0.01), and levator ani muscle mass (p < 0.001) compared to Sham+C mice, and these effects were prevented with testosterone treatment. Orx+T mice had greater EDL (p < 0.01) and SOL (p < 0.01) muscle mass compared to Orx+C, however, median fiber CSA was not significantly altered in these muscles. EDL and SOL muscle force was greater in Sham+T compared to Orx+C mice (p < 0.05) in proportion to muscle mass. Unexpectedly, Orx+T mice had increased fatigue resistance of the SOL muscle compared to Orx+C mice (p < 0.001). We have used a rigorous model of androgen withdrawal and administration in male mice to demonstrate an essential role of androgens in the maintenance of muscle mass and force. In addition, we have shown that testosterone treatment increases resistance to fatigue of slow- but not fast-twitch muscle.
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