I. M. Egner and J. C. Bruusgaard contributed equally to this work.
A cellular memory mechanism aids overload hypertrophy in muscle long after an episodic exposure to anabolic steroids
Article first published online: 22 NOV 2013
© 2013 The Authors. The Journal of Physiology © 2013 The Physiological Society
The Journal of Physiology
Volume 591, Issue 24, pages 6221–6230, December 2013
How to Cite
Egner, I. M., Bruusgaard, J. C., Eftestøl, E. and Gundersen, K. (2013), A cellular memory mechanism aids overload hypertrophy in muscle long after an episodic exposure to anabolic steroids. The Journal of Physiology, 591: 6221–6230. doi: 10.1113/jphysiol.2013.264457
- Issue published online: 19 DEC 2013
- Article first published online: 22 NOV 2013
- Accepted manuscript online: 27 OCT 2013 04:37AM EST
- (Received 30 August 2013; accepted after revision 21 October 2013; first published online 28 October 2013)
- • Training studio folklore suggests that previous strength training, with or without the use of anabolic steroids facilitates re-acquisition of muscle mass even after long intervening periods of inactivity. This ‘muscle memory’ has previously been attributed to motor learning, but our data suggest the existence of a cellular memory residing in the muscle fibres themselves.
- • Muscle fibres have multiple nuclei, and the number of nuclei increases when muscle mass increases.
- • When mice were briefly treated with steroids the muscle mass and number of nuclei increased. The drug was subsequently withdrawn for 3 months and the muscle mass returned to normal, but the excess cell nuclei persisted. When such muscles were subjected to overload they grew by 30% over 6 days while controls grew insignificantly.
- • Our data suggest that previous strength training might be beneficial later in life, and that a brief exposure to anabolic steroids might have long lasting performance-enhancing effects.
Abstract Previous strength training with or without the use of anabolic steroids facilitates subsequent re-acquisition of muscle mass even after long intervening periods of inactivity. Based on in vivo and ex vivo microscopy we here propose a cellular memory mechanism residing in the muscle cells. Female mice were treated with testosterone propionate for 14 days, inducing a 66% increase in the number of myonuclei and a 77% increase in fibre cross-sectional area. Three weeks after removing the drug, fibre size was decreased to the same level as in sham treated animals, but the number of nuclei remained elevated for at least 3 months (>10% of the mouse lifespan). At this time, when the myonuclei-rich muscles were exposed to overload-exercise for 6 days, the fibre cross-sectional area increased by 31% while control muscles did not grow significantly. We suggest that the lasting, elevated number of myonuclei constitutes a cellular memory facilitating subsequent muscle overload hypertrophy. Our findings might have consequences for the exclusion time of doping offenders. Since the ability to generate new myonuclei is impaired in the elderly our data also invites speculation that it might be beneficial to perform strength training when young in order to benefit in senescence.