Abstract
Chronic alcohol consumption leads to muscle weakness and atrophy in part by suppressing protein synthesis and mTORC1-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 C57BL/6 adult male mice while the contralateral leg remained intact as the sham control. A nutritionally complete alcohol-containing liquid diet (EtOH) or isocaloric, alcohol-free liquid diet (Con) was provided for 14 days post-surgery. EtOH 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 EtOH-fed mice. OL increased muscle weight (90%) and protein synthesis (125%) in both Con and EtOH mice. The overload-induced increase in mTOR (Ser2448), 4E-BP1 (Thr37/46), S6K1 (Thr389), rpS6 (Ser240/244), and eEF2 (Thr56) were comparable in muscle from Con and EtOH mice. Modulation of signaling upstream of mTORC1 including REDD1 protein expression, Akt (Thr308), PRAS40 (Thr246), and ERK (Thr202/Tyr204) also did not differ between Con and EtOH mice. Markers of autophagy (ULK1, p62, and LC3) 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.
Highlights
Skeletal muscle disease occurs in 40–60% of chronic alcoholics, and is more prevalent than many other myopathies in addition to being of greater incidence than alcohol-induced cirrhosis (Martin et al 1985; Estruch et al 1993)
As there was no corresponding total protein to control for loading of REDD1, it was expressed relative to GAPDH as we found that mechanical overload increased a 2015 The Authors
Consistent with previous work in this model, overload of the plantaris muscle led to significant hypertrophy concomitant with a sustained increase in protein synthesis at 14 days (Bodine et al 2001; Miyazaki et al 2011; Perez-Schindler et al 2013; Baehr et al 2014)
Summary
Skeletal muscle disease occurs in 40–60% of chronic alcoholics, and is more prevalent than many other myopathies in addition to being of greater incidence than alcohol-induced cirrhosis (Martin et al 1985; Estruch et al 1993). Past work related to alcohol-induced skeletal muscle disease has primarily focused on determining the mechanism(s) through which alcohol decreases skeletal muscle size and function; while to our knowledge, no reports exist investigating whether alcohol hinders muscle growth. This information would prove important to the treatment of alcohol-induced muscle disease as interventional therapies to prevent, offset or reverse the loss of muscle mass, and strength resulting from prolonged alcohol intake are lacking. Muscle mass is regulated by the balance (or lack thereof) between rates of protein synthesis and protein breakdown Both acute and chronic alcohol consumption inhibits synthesis to a greater extent than degradation (Lang et al 2001).
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