Myofiber androgen receptor promotes maximal mechanical overload-induced muscle hypertrophy and fiber type transition in male mice

Arnaud Ferry*, Mélanie Schuh, Ara Parlakian, Takouhie Mgrditchian, Nicolas Valnaud, Pierre Joanne, Gillian Butler-Browne, Onnik Agbulut, Daniel Metzger

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

13 Citations (Scopus)

Abstract

The first aim of this study was to examine the role of myofiber androgen receptor (AR) in male mice on muscle performance gain and remodeling-induced muscle mechanical overloading (OVL) that mimics resistance training. The response of OVL in mice in which AR is selectively ablated in myofibers ( ARskm-/y) was compared with that of wild-type (WT) mice. In addition, we determined whether the synthetic anabolic androgen nandrolone administration affects the OVL response. We found that OVL increased absolute maximal force and fatigue resistance in both mouse genotypes ( P < .05). However, the absolute maximal force increased more in AR skm-/ymice as compared with WT mice ( + 88% vs + 63%) (P < .05). Muscle weight increased less in response to OVL in AR skm-/ymice ( + 54%) than in WT mice ( + 115%) ( P < .05). The fiber number per cross-section similarly increased in both mouse genotypes after OVL ( P < .05). In contrast to WT mice, the diameter of the fibers expressing myosin heavy chain (MHC)-2x decreased after OVL in AR skm-/ymice ( P < .05). The MHC-2b to MHC-2a fiber type transition in response to OVL was reduced in ARskm-/ymice as compared with WT mice (P < .05). Finally, nandrolone administration during OVL did not further improve absolute maximal force and fatigue resistance and markedly alter muscle remodeling in both mouse genotypes. Together, our results indicate that myofiber AR is required for a complete response to OVL and that exogenous androgens do not increase muscle performance during intensive remodeling in male mice.

Original languageEnglish
Pages (from-to)4739-4748
Number of pages10
JournalEndocrinology
Volume155
Issue number12
DOIs
Publication statusPublished - 1 Dec 2014
Externally publishedYes

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