How many of you hit the gym over the weekend? That’s great; exercise and getting in shape should be a top priority on everyone’s list. But how many of you also hit the bar to drink over the weekend? You see, that’s bad, but not for the reasons typically spouted at you.

Let’s face it, if I just told you that alcohol consumption disrupts mood and behavior, damages your liver, and suppresses your immune system, you probably wouldn’t listen because you can’t physically see those ramifications.[1] So instead I’m going to focus on what will grab your attention, muscles and body fat.

I’m willing to bet the majority of you train with weights to get stronger, faster, and look good naked. Ladies, we all know you want those toned legs and to make heads turn in that outfit you’ve been saving. What do all these goals have in common? Muscle growth and fat loss.

Brief Overview of Muscular Hypertrophy and Fat Loss

Muscle growth is fundamentally a two-step process. First, you need to damage the muscle and give your body a reason to put some effort into growing the muscles, which is where weight training shines. Second, and more importantly, you need to provide rest and nutrients to those muscles so that they can recover. Both of these help boost a process called muscle protein synthesis (MPS).

MPS typically lasts up to 48-72 hours after a resistance training bout, depending on the intensity of the exercise.[2] When you push hard in the gym before going out to get hammered at the bar, you do your muscles and your body composition goals a great disservice (more on this in the next section).

Fat loss, on the contrary, antagonizes MPS through an enzyme called AMPk (adenosine monophosphate-activated protein kinase), which is expressed in a multitude of tissues throughout the body. AMPk increases breakdown of body fat (lipolysis), boosts oxidation of fatty acids, enhances insulin sensitivity, and inhibits body fat synthesis (lipogenesis).[3] Essentially, it’s the “metabolic switch” for fat loss. Inversely, MPS tends to suppress AMPk expression, thereby reducing the body’s ability to burn fat.

AMPk is activated when the cell is deprived of energy, signaling ADP has increased and ATP has dropped significantly. This occurs primarily when the body is glucose-deprived and when exercising intensely. Certain drugs also increase AMPk, such as metformin/glucophage.[4] Conversely, things that increase the cell’s ATP-to-ADP ratio, like excessive glycogen levels and overeating, blunt AMPk actions.  

MPA Supps Products

Effect of Alcohol on Muscle Protein Synthesis, Muscle Fiber Composition, and Fat Loss

Acute alcohol intoxication (i.e. getting drunk) has been shown to decrease muscle protein synthesis by 28% and these effects appear to be tissue specific, primarily affecting fast-twitch muscles and the heart.[5],[6] It goes without saying this is pretty bad for your health and body composition. You see, every muscle is composed of two types of fibers – fast-twitch and slow-twitch, which are also known as type-II and type-I fibers, respectively.

The fast-twitch fibers are more responsive to growth and are far stronger and larger than their slow-twitch counterparts. When lifting heavy weights, they are the primary responders. Yet, drinking alcohol diminishes all that hard work by nearly a third. Oh, and this doesn’t include the fact that alcohol consumption is also associated with decreased skeletal muscle weight.[7]

Furthermore, acute alcohol consumption has been shown to inactivate AMPk and activate malonyl-CoA, which stimulates the creation of new fat in the body.[8] In short, your body readily holds onto the fat your already have and adds to it when alcohol and excess energy intake are combined.

The Acute, Deleterious Effects of Alcohol Consumption

Okay, so you decide you will just train the day after you drink. Well, aside from the hangover, mental fog, and difficulty actually getting to the gym, alcohol’s effects persist beyond the good times. A review of the effects of alcohol on athletic performance conducted by researchers at Deakin University, Australia gives insight into common symptoms linked to acute alcohol ingestion.[9] They found that alcohol ingestion led to decreased strength, greater degrees of muscle tissue damage, increased fluid loss, and decreased work tolerance.

It has also been shown that alcohol disrupts many metabolic processes, adversely affecting the skeletal muscle’s ability to produce energy.7 In other words, your workout will suffer and you will likely feel worse than if you just stuck to the cup of coffee.

Bottom line; ethanol is a great energy source…if you’re not human. Don’t drink too much alcohol, if any at all, if you’re looking to improve athletic performance or aesthetics.



[1] NIAAA. Alcohol’s Effects on the Body. n.d. (accessed March 27, 2017).

[2] McLester, J R, et al. “A series of studies–a practical protocol for testing muscular endurance recovery.” J Strength Cond Res. 17, no. 2 (2003): 259-273.

[3] Ruderman NB et. al. Minireview: Malonyl CoA, AMP-activated protein kinase, and adiposity. Endocrinology (2003) 144: 5166-5171.

[4] Zhang, Yaya, et al. "Metformin interacts with AMPK through binding to γ subunit." Molecular and cellular biochemistry 368.1-2 (2012): 69-76.

[5] Vary, Thomas C, and Charles H Lang. “Assessing Effects of Alcohol Consumption on Protein Synthesis in Striated Muscles.” Methods Mol Biol., 2008: 343-355.

[6] Lang, Charles H, Anne M Pruznak, Gerald J Nystrom, and Thomas C Vary. “Alcohol-induced decrease in muscle protein synthesis associated with increased binding of mTOR and raptor: Comparable effects in young and mature rats.” Nutr Metab (Lond) 6 (January 2009):

[7] El-Sayed, Mahmoud S, Nagia Ali, and Zeinab El-Sayed Ali. “Interaction between alcohol and exercise: physiological and haematological implications.” Sports Medicine 35, no. 3 (2005): 257-269.

[8] Lakshman, M. Raj. "Some novel insights into the pathogenesis of alcoholic steatosis." Alcohol 34.1 (2004): 45-48.

[9] Vella, Luke D, and David Cameron-Smith. “Alcohol, Athletic Performance and Recovery.”Nutrients 2, no. 8 (2010): 781-789.