Open AccessModerate alcohol consumption does not impair overload‐induced muscle hypertrophy and protein synthesis
Author(s) -
Steiner Jennifer L.,
Gordon Bradley S.,
Lang Charles H.
Publication year - 2015
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.12333
Subject(s) - muscle hypertrophy , endocrinology , medicine , mtorc1 , anabolism , autophagy , muscle atrophy , ampk , protein kinase b , soleus muscle , p70 s6 kinase 1 , chemistry , atrophy , pi3k/akt/mtor pathway , myocyte , skeletal muscle , protein kinase a , kinase , phosphorylation , biochemistry , signal transduction , apoptosis
Chronic alcohol consumption leads to muscle weakness and atrophy in part by suppressing protein synthesis and mTORC 1‐mediated signaling. However, it is unknown whether moderate alcohol consumption also prevents overload‐induced muscle growth and related anabolic signaling. Hypertrophy of the plantaris muscle was induced by removal of a section of the gastrocnemius and soleus muscles from one leg of C57 BL /6 adult male mice while the contralateral leg remained intact as the sham control. A nutritionally complete alcohol‐containing liquid diet (Et OH ) or isocaloric, alcohol‐free liquid diet (Con) was provided for 14 days post‐surgery. Et OH intake was increased progressively (day 1–5) before being maintained at ~20 g/day/kg BW . The plantaris muscle from the sham and OL leg was removed after 14 days at which time there was no difference in body weight between Con and Et OH ‐fed mice. OL increased muscle weight (90%) and protein synthesis (125%) in both Con and Et OH mice. The overload‐induced increase in mTOR (Ser2448), 4E‐ BP 1 (Thr37/46), S6K1 (Thr389), rpS6 (Ser240/244), and eEF 2 (Thr56) were comparable in muscle from Con and Et OH mice. Modulation of signaling upstream of mTORC 1 including REDD 1 protein expression, Akt (Thr308), PRAS 40 (Thr246), and ERK (Thr202/Tyr204) also did not differ between Con and Et OH mice. Markers of autophagy ( ULK 1, p62, and LC 3) suggested inhibition of autophagy with overload and activation with alcohol feeding. These data show that moderate alcohol consumption does not impair muscle growth, and therefore imply that resistance exercise may be an effective therapeutic modality for alcoholic‐related muscle disease.