Booze and Barbells Part II

By Jordan Feigenbaum MS, Starting Strength Staff, CSCS, HFS, USAW CC

In case you missed part one of this three part series, click here. In today’s blog entry we’re going to talk about how alcohol affects skeletal muscle and the sex steroid, testosterone. Things can get pretty complicated in a hurry here, but what I aim to do is provide some basic science background for my readers as well as how a certain stressor, i.e. alcohol, can alter the internal milieu. I actually just used the words “internal milieu”, which describes the internal environment of the human body just so I could provide the following quote to pay homage to my previous physiology professors:

“The stability of the internal environment [the milieu intérieur] is the condition for the free and independent life”- Claude Bernard

The concept of the internal environment being important for physiological normalcy and a rationale for the human body’s homeostatic underpinnings was later expanded upon by Walter Canon’s characterization of homeostasis in 1932. He [Canon], proposed four characteristics of homeostasis as follows:

1. Constancy in an open system, such as our bodies represent, requires mechanisms that act to maintain this constancy. Cannon based this proposition on insights into the ways by which steady states such as glucose concentrations, body temperature and acid-base balance were regulated.
2. Steady-state conditions require that any tendency toward change automatically meets with factors that resist change. An increase in blood sugar results in thirst as the body attempts to dilute the concentration of sugar in the extracellular fluid.
3. The regulating system that determines the homeostatic state consists of a number of cooperating mechanisms acting simultaneously or successively. Blood sugar is regulated by insulin, glucagons, and other hormones that control its release from the liver or its uptake by the tissues.
4. Homeostasis does not occur by chance, but is the result of organized self-government.

It is important to appreciate the homeostatic mechanisms that the human body possesses in order to maintain an “even keel”, as without redundant pathways in place things can go awry in a hurry. At any rate, while the overall concept of the internal milieu and it’s influences on homeostasis are critically important, further discussion of it would preclude our look at just how alcohol/ethanol can alter skeletal muscle metabolism and testosterone levels. To begin, let’s talk a bit about skeletal muscle.

One of the most common effects of alcohol on striated muscle, i.e. skeletal and cardiac muscle, is fiber atrophy or reduction in size. Skeletal and cardiac muscle are both striated, as they have repeating sarcomeres and appear (under the microscope) to have alternating “light” and “dark” bands.

Smooth muscle on the other hand, which is found in lots of places like the walls of the vascular system and the GI tract, do not appear striated under a microscope because they lack the organized, repeating structure of the sarcomere.

At any rate, striated muscle size is a result of the balance of protein synthesis and protein breakdown. In other words, the net flux of protein reflects the protein being built (synthesized) and deposited minus the protein being broken down and metabolized. If something were to either increase protein synthesis or inhibit (prevent) protein breakdown, their would be a net gain in protein levels. On the other hand, if the rate of protein breakdown is increased OR the synthesis of new protein is inhibited, there will be a net loss of protein. In general, a net gain of protein within muscle tissue results in hypertrophy (increased size) and a net loss of protein in the muscle tissue results in atrophy.

Ethanol tends to decrease striated muscle protein synthesis [1]. Interestingly, the resulting atrophy appears to be greatest in Type IIB fibers, which are a subtype of the fast-twitch muscle fibers that produce high amounts of force, contract rapidly, and are anaerobic. Some researchers actually classify type II muscle fiber atrophy as part of a diagnostic criteria of alcoholic myopathy, however this selective decrease in size also occurs in other issues like calorie malnutrition, neuropathy, etc. Additionally, only about 33% of chronic asymptomatic alcoholics show significant type II fiber atrophy without malnutrition, neuropathy, etc. although other studies report 40-60% of alcoholics presenting with significant atrophy [1]. Urbano et al. goes head to head with Preedy et al in the following quotes:

In fact, it [ethanol] is the most frequent cause of toxicity to striated skeletal and cardiac muscle in adults in dose dependent fashion [1].

“Due to the ethanol-induced reduction of muscle phosphorylase activity, decreased rates of protein synthesis and whole-body protein metabolism by 15–30%, predominantly in type II fast-twitch anaerobic fibers that utilize glycolytic metabolism.Type I fibers were not overly affected and there was no clear decrease in muscle protein breakdown [5].

As far as how this occurs on a cellular level, it appears as though ethanol consumption disrupts the translation of would-be muscle-protein RNA, but not it’s transcription. For background information, muscle protein synthesis signalers (like eating a protein-rich meal or training) increase the transcription of certain DNA to muscle protein RNA. Muscle protein RNA is then translated into muscle protein, which is shuttled to it’s target and deposited as muscle. Through increased binding of a variety of different regulatory sites on the muscle protein RNA, translation is decreased and total muscle protein synthesis decreases [2].

Measuring decreases in total muscle protein synthesis can be tricky in the laboratory settings, as most of the time a total nitrogen balance measurement is used. Remember, protein is the only macronutrient with nitrogen as a component. Therefore, it intuitively makes sense that the amount of nitrogen taken in minus the amount of nitrogen excreted can give insight into the nitrogen balance of a person or animal. Unfortunately, some people take this sort of information as definitive with regards to what is actually happening in the muscle specifically. Remember, all tissues (lungs, gut, kidney, visceral organs, etc.) are made up of protein, which are also turned over regularly and thus influence total body protein and nitrogen balance. Lang et. al. provide a nice quote describing this:

However, whole body measurements represent the sum of many vastly different organ systems (e.g., muscle and nonmuscle protein synthesis and hepatic secretory protein synthesis) and provide little information concerning individual processes or tissues.

So while total body nitrogen balance tells us what’s happening on a body wide or systemic level, it does not tell us what’s happening in just the muscle tissue. Muscle protein turnover, in sum, makes up less than 30% of total body protein turnover anyway [3]. Other studies, however, have shown that with acute alcohol intoxication muscle protein synthesis decreases in skeletal muscle, heart, intestine, bone, and skin. Additionally, chronic ethanol exposure has been demonstrated to decrease skeletal muscle protein synthesis in rats [4, 5]. It appears that ethanol exposure is potentially harmful to overall protein synthesis, as described in the following quote:

“However, experimental and clinical studies have clearly demonstrated that ethanol itself is a direct noxious agent to heart and skeletal muscle in a progressive, cumulative, and dose-dependent manner, an effect independent of nutritional, vitamin, or mineral factors.”-[Nguyen et al. (6)]

There are only a couple of things left to discuss with respect to actual skeletal muscle function and ethanol. First, muscle glycogen concentration tends to increase in chronic alcohol patients because glycogen cannot be degraded as efficiently. This is due to a partial inhibition of the biochemical pathway for glycogenolysis (glycogen breakdown) as well as glycolysis (glucose breakdown) [5]. In contrast, acute alcohol exposures tend to decrease glycogen storage, especially post workout as some of the mechanisms used to store glycogen in skeletal muscle are inhibited and instead fatty acid production is increased. These effects are independent of acetaldehyde toxicity, which was discussed in part one of this series [5].

Ethanol and acetylaldehyde also tend to increase formation of reactive oxygen species due to their effects on vitamin metabolism. Reactive oxygen species (ROS) tend to increase cellular damage and stress in the skeletal muscle, thus increasing damage to cells of the muscles which may increase atrophy.

Moving along, let’s start our discussion about alcohol and testosterone production by covering the general overview of testosterone production in vivo (in the body). This will give us some background to what is normal so we can consider the effects of ethanol on the internal milieu and homeostasis.

Normally, males produce testosterone in the Leydig cells of the testes from cholesterol via increasing leutinizing hormone (LH) activity within the testes. LH increases an enzyme called cholesterol desmolase, which is responsible for converting cholesterol to pregnenolone. Pregnenolone will go on to be converted through various enzymes to testosterone and thus, but first it needs to be formed from cholesterol. Thus, increasing the enzymatic activity of cholesterol desmolase helps to increase testosterone production.

Naturally, one would ask well what increases LH? Gonadotropin releasing hormone (GnRH) is secreted by the hypothalamus in the brain. GnRH is released into blood vessels that carry this peptide to the anterior pituitary gland (hypothalamic-hypophysial portal system). GnRH is normally secreted in a pulsatile fashion, i.e. it is not constant. It acts on certain cells in the anterior lobe of the pituitary gland (gonadotropes) to cause them to manufacture and release LH, which is also released in a pulsatile fashion. LH is released into the systemic (body-wide) circulation where it ends up traveling to the testicles and causing the Leydig cells to pump out testosterone, as described above.

As discussed at the beginning of this post, most, if not all of the body’s pathways are tightly regulated to keep it on an “even-keel”. Let’s explore this now that we know the testosterone-producing pathway. Testosterone produced by the Leydig cells provides what’s known as “negative feedback” on the hypothalamus and cells of anterior lobe of the pituitary, effectively decreasing secretion of GnRH and LH. Thus, when testosterone levels are high, GnRH and LH levels are low. Conversely, when testosterone levels are low, the frequency and amplitude of GnRH pulses are increased. A downstream effect of this is increased LH release and thus, increased signaling to the Leydig cells to produce more testosterone because the negative feedback signaling is removed.

As we’ll see in the upcoming discussion of ethanol’s effects, perturbation at any level of this pathway can result in deleterious effects. So, how does ethanol affect testosterone production and/or signaling?

As it turns out, ethanol exposure appears to lower GnRH levels, which leads to reduced LH secretion from the anterior pituitary and reduced testosterone production by the Leydig cells of the testes [7]. Mechanistically, this occurs because a hormone normally produced in the testes and hypothalamus at very low levels, β-endorphin (an endogenous opiod), normally only slightly suppresses testicular testosterone production and release. In the hypothalamus, β-endorphin results in decreased GnRH release. Adams and Cicero have shown an increase in β-endorphin after acute alcohol exposure [10]. Naltrexone, a treatment currently used in alcoholism to decrease alcohol cravings, blocks B-endorphin activity and may prevent reduced testosterone levels. Three other ways ethanol affects active GnRH levels is through acetalaldehyde, which is toxic, disturbing nerve impulses outside the hypothalamus that signal GnRH production WITHIN the hypothalamus, and finally, ethanol appears to interfere with processing of the inactive GnRH precursor to the active GnRH form according to Uddin et al.

LH levels actually decrease with alcohol exposure, which is not what we’d expect. Harkening back to our homeostatic mechanism discussion, if testosterone production falls, we’d expect GnRH and LH levels to increase to “right the ship”. However, as discussed above GnRH levels actually decrease and so do LH levels. Mechanistically, the decreased LH levels appear to be due to the toxic affect of ethanol directly on the anterior pituitary gland where LH is released by interfering with GnRH’s signaling of LH production in the cells that they act on (gonadotropes). Another effect of ethanol on LH that causes it’s decrease is that alcohol in the blood tends to result in the anterior pituitary gland’s production of less potent LH variants, thus decrease the level of LH in the blood and the quality of LH in the blood too.

A study done by Steiner and colleagues in 1996 found that when males were given a 15-percent alcohol solution that was administered every 3 hours, around the clock, together with a diet replete with protein, vitamins, folic acid, and minerals (total daily alcohol dose was 220g or 3g/kg body weight, which equals 15 drinks) that the testosterone levels in the men’s blood declined 5 days into the study and continued to fall over the entire period. This was attributed to a decrease in testosterone production in the Leydig cells of the testes and increased removal rate of testosterone from the blood via catabolic processes. On the other hand, Southren et al. found that the increased testosterone catabolism or breakdown is only present in men without liver disease, whereas the clearance is decreased in men with liver disease.

Numerous studies in human and animal models have since confirmed reduction in testosterone levels after either acute or long term alcohol exposure. Acute alcohol ingestion appears to result in a significant reduction in testosterone levels that lasted for 96 hours in a rat model [9].

Sarkola and Eriksson actually found that testosterone can increase in men exposed to a low dose of ethanol, although this is a transient effect due to the predomination of decreased liver clearance of testosterone from the blood compared to the decreased testosterone production in the testes. Unfortunately, during the latter stages of elimination of alcohol or when alcohol has been completely eliminated, testosterone production decreases even more. Similarly, in higher doses of alcohol consumption, e.g. 1.5g/kg, the decreased production of testosterone predominates over the transient decreased clearance rate of testosterone. This has been confirmed by experiemental evidence from Välimäki et al in 1990 and Ylikahri et al. in 1974 [10].

Another interesting finding is that alcohol abuse and subsequent impaired testosterone production tends to result in testicular atrophy/shrinkage, which occurs in about 75% of men with advanced cirrhosis [10]. The atrophy most likely results from the toxicity on the testes, decreased LH and FSH production, and other confounding factors causing decreased sperm cells and sperm production.

Finally, and perhaps one of the more important ways alcohol effects testosterone’s activity and blood levels is that ethanol exposure tends to increase aromatization of testosterone and testosterone precursors. Aromatase is an enzyme that converts testosterone to estrogen and thus, increased aromatization results in increased conversion of testosterone to estrogen. Additionally, the immediate precursors to testosterone, androstenedione (Mark McGwire?) can be “aromatized” to another estrogen subtype called estrone. Scientific evidence points to this “increased aromatization” as a byproduct of increased estrogen production and not a decrease in estrogen clearance [10]. Aromatization is not a good thing above physiological normal (homeostatic) levels in men, as the authors conclude:

“In addition to causing breast enlargement, estrogens appear to exert a negative feedback effect on LH and FSH production and may thereby contribute to alcohol’s suppression of those key reproductive hormones.”

While alcohol certainly has some benefits, which we’ll get to I PROMISE, it’s important to know the deleterious effects that alcohol can have on the internal milieu, especially as it pertains to training. Again, I’ll leave you with my favorite axiom related to alcohol consumption and training:

“If you’re drinking enough to get drunk, you’re drinking enough to mess with your results.”

 

Until next time.

-thefitcoach

1)  Urbano-Marquez, A.; Fernandez-Sola, J. Effects of alcohol on skeletal and cardiac muscle. Muscle Nerve 2004, 30, 689-707.

2) Lang, CH, Wu, DQ,  Frost, RA. Inhibition of muscle protein synthesis by alcohol is associated with modulation of eIF2B and eIF4E. American Journal of Physiology-Endocrinology and Metabolism 1999, 277, 268-276.

3) White JP, Baynes JW, Welle SL, Kostek MC, Matesic LE, et al. (2011) The Regulation of Skeletal Muscle Protein Turnover during the Progression of Cancer Cachexia in the Apc^Min/+ Mouse. PLoS ONE 6(9)

4) Preedy V. R.,Peters T. J.,Patel V. B.,Miell J. P. (1994) Chronic alcoholic myopathy: transcription and translational alterations. FASEB J. 8:1146–1151

5) Preedy V. R., Peters T. J. (1990) Changes in protein, RNA, DNA and rates of protein synthesis in muscle-containing tissues of the mature rat in response to ethanol feeding: a comparative study of heart, small intestine and gastrocnemius muscle. Alcohol Alcohol. 25:489–498.

6) Nguyen VA, Le T, Tong M, Silbermann E, Gundogan F, de la Monte SM. Impaired Insulin/IGF Signaling in Experimental Alcohol-Related Myopathy. Nutrients. 2012; 4(8):1058-1075.

7) Vatsalya Vatsalya, Julnar E. Issa, Daniel W. Hommer, and Vijay A. Ramchandani. Pharmacodynamic Effects of Intravenous Alcohol on Hepatic and Gonadal Hormones: Influence of Age and Sex. Alcohol Clin Exp Res. 2012 February; 36(2): 207–213.

8) Sarkola, T. and Eriksson, C. J. P. (2003), Testosterone Increases in Men After a Low Dose of Alcohol. Alcoholism: Clinical and Experimental Research, 27: 682–685

9) Steiner, J., Halloran M.M., Jabamoni K., Emanuele, N.V., Emanuele, M.A. Sustained effects of a single injection of ethanol on the hypothalamic-pituitary-gonadal axis in the male rat. Alcoholism: Clinical and Experimental Research 20:1368–1374, 1996.

10) Emanuele, N.V., Emanuele, M.A. (1998) Alcohol’s Effects on Male Reproduction. The Alcohol and Other Drug Thesaurus. Vol. 22, No.3.

Booze and Barbells Part 1

By Jordan Feigenbaum MS, CSCS, HFS, USAW CC, Starting Strength Staff

And I hate running…

One of the most common questions I get with regards to nutrition and/or training pertains to alcohol and how it effects potential performance, health, or aesthetic outcomes. I get asked this question so often that I’m dedicating an entire chapter of my book to the stuff. Instead of sharing part of the manuscript on here, I thought I’d post up a truncated version of my thoughts and findings on the subject, which will actually be broken up into three separate blog posts on this blog as well as my new website. Consider this advertising for what sort of cool things go on over on that site. You should join, methinks, to get some good information 🙂 Now, let’s talk about booze!

Let’s begin by defining alcohol as a dietary component. An average “drink” has approximately 14 grams of pure alcohol (ethanol) within it, which is in addition to all the other stuff in the drink, i.e. mixers, flavorings, etc. At any rate, a drink is defined by the volume of substance that has 14g of alcohol in it. This metric equates to the following serving sizes:

or equivalently:

• 12-ounces of beer.
• 8-ounces of malt liquor.
• 5-ounces of wine.
• 1.5-ounces or a “shot” of 80-proof distilled spirits or liquor (e.g., gin, rum, vodka, or whiskey)

So now that we have defined our terms of what an actual drink is, what exactly happens to the good stuff when we’re out at happy hour? Orally ingested alcohol is transported through the proximal digestive tract intact, i.e. it is not broken down, metabolized, or otherwise changed until it gets into the stomach. The amount of alcohol that gets to the stomach is very high compared to other parts of the digestive system like the duodenum or other parts of the small intestine. Due to this high concentration, approximately 40% of alcohol is metabolized (broken down) in the stomach within the first hour following initiation of drinking. Within about 2 hours, up to73% of the total alcohol that was ingested has been metabolized in the stomach [1]. Alcohol absorption, on the other hand, takes place in both the stomach (slow) and small intestine (rapid). The total amount of alcohol metabolized and absorbed in the stomach depends on the rate of emptying of the stomach, which is influenced by lots of things. At any rate, the stomach’s metabolism of alcohol in humans plays an important role in First Pass Metabolism.

Some of you science-minded folks might be thinking, Wait, the STOMACH metabolizes and absorbs alcohol? I thought that absorption occurred in the small intestine! Yes Virginia, this is normally correct. However, it has been shown that the stomach’s lining, more appropriately termed the gastric epithelium, contains a version of the enzyme alcohol dehydrogenase (ADH). This version, σ-ADH, is not present in the liver. breaks down ethanol into acetylaldehyde, which is the metabolite in the overall metabolism of ethanol. Different types of alcohol dehydrogenase (ADH isoforms) are present in the liver, but σ-ADH is only found in the gastric epithelium.

So how do we know that alcohol is actually metabolized and absorbed in the stomach and what sorts of things affect this? Blood alcohol levels, i.e. the amount of intact ethanol in the blood after ingestion, changes under certain conditions. When alcohol is ingested orally, lower blood alcohol levels are seen than when alcohol is given intravenously [2]. This is due to the first pass metabolism occurring in both the stomach and liver, as both of these organs have high levels of alcohol dehydrogenase. Because the ethanol is metabolized and degraded into acetylaldehyde, as mentioned above, there is less of it that actually enters the blood stream and thus, less alcohol in the blood. These facts, however, do not tell us the importance of the stomach’s metabolism of ethanol. For that, we must dig deeper.

Aspirin and H-2 blockers (histamine receptor blockers) both decrease σ-ADH activity in the stomach, which results in less ethanol being metabolized to acetylaldehyde. These drugs also increase the rate at which the stomach’s contents are emptied into the small intestine. Both of these factors, i.e. less ADH activity and faster emptying, result in higher blood alcohol levels in humans. Interestingly, Japanese persons have lower σ-ADH activity naturally and thus, first pass metabolism is significantly compromised and blood alcohol levels are higher at a given dose than their non-Japanese counterparts [2].

You might be wondering what other sorts of things influence stomach emptying, you know, in case you wanted to see higher blood alcohol levels get drunk quickly. Fasting accelerates emptying, which results in less exposure of ethanol to the σ-ADH in the stomach and more rapid absorption of ethanol in the small intestine. On the other hand, consuming a high fat meal alongside alcohol significantly delays emptying and absorption of food. In general, the effect of food on alcohol metabolism and absorption, i.e. increasing metabolism and delaying absorption, is primarily due to the slowing down of gastric emptying. Alcohol content also influences rate of absorption, with maximum absorption occurring  with consumption of a drink containing approximately 20-25% alcohol  on an empty stomach. The absorption rate may be less when a 40% alcohol solution is consumed on an empty stomach. The rate may also slow down when high fluid volume/low alcohol content beverages, such as beer, are consumed.

So we know that a varying amount of ethanol is metabolized in the stomach and a small amount is absorbed there as well. What happens to the ethanol that remains untouched and makes it to the small intestine? Ethanol in the small intestine, which is made up of the duodenum, jejunum, and ilieum from proximal to distal, is generally absorbed by diffusion from the inside of the GI tract’s lumen into the cells lining the tract, the enterocytes. Mechanistically, this likely occurs due to the high permeability of cells to pure alcohol/ethanol and it also appears that certain simple sugars (monosaccharides and disaccharides) like glucose, galactose, sucrose, etc. also increase the rate of absorption of ethanol in the small intestine. Carbohydrates are all eventually broken down into glucose, galactose, and fructose and are absorbed via sodium-dependent transport, i.e. sodium is concomitantly transported with the sugars. Carbohydrate absorption likely increases alcohol absorption through electrochemical gradient changes. This means the sugar containing margarita likely gets into your bloodstream faster than pure ethanol. Unfortunately, lactose, the main carbohydrate in milk, does not increase absorption rates [3].

Ethanol moves from the lumen of the GI tract, into the enterocyte, then into the veins supplying the gut, which drain into the liver as the portal circulation.

Once into the enterocyte, ethanol diffuses into the veins suppying the enterocyte and is carried to the liver as part of the hepatic (liver) portal circulation. Once in the liver, ethanol diffuses from the venous blood into the liver cells, aka hepatocytes, where the majority of ethanol metabolism will finally occur. In the liver cell ethanol will encounter another isoform of alcohol dehydrogenase and get oxidized into acetylaldehyde. This enzyme, alcohol dehydrogenase, can become saturated at certain levels of ethanol ingestion and thus, extra ethanol will spillover into other metabolic pathways in order to be eliminated from circulation. While not particularly important to our discussion on the effects of booze on training, for the sake of completeness these other liver pathways include Microsomal Ethanol Oxidized System (MEOS)/Cyp2E1 (functions primarily during high levels of ethanol intake) and catalase (minor). An important take way from this is that ethanol must be metabolized or eliminated from the body, as  it cannot be stored and serves no particular purpose. That should beg the question, why do we even have mechanisms and pathways in our body to eliminate ethanol anyway?

Alcohol dehydrogenase and the downstream pathways used to eliminate ethanol from circulation are believed to originate out of necessity due to the small amount, i.e. 3g or so, of ethanol produced daily by resident bacteria in the intestinal tract via fermentation and other biological processes [4]. Similarly, only a small amount (2-10%) of ethanol is eliminated through the lungs and kidney, so the rest must be metabolized in the liver, stomach, etc. Maybe booze isn’t so Paleo after all? 🙂

So now, after all that rigamarole, we have two things that we’re dealing with that can cause potential downstream effects, ethanol and acetylaldehyde. Acetylaldehyde will eventually get metabolized acetate, which will get metabolized into acetyl-coA and contribute to one of the following pathways depending on what else is going on:

1. Fatty acid synthesis (if insulin is elevated)
2. Cholesterol synthesis (if insulin is elevated)
3. Be used for fuel by the heart and skeletal muscle (and turned into co2 and water)

So, if you’re drinking alongside some carbohydrates or a mixed meal, the end products will be different than if you’re just boozing solo. Ethanol will, at some point, get metabolized as described before although while it’s floating around in the blood stream it will certainly exert some effects that will discuss during the rest of this article.

With all the background information out of the way now, we can get down to the business of actually talking about what drinking does performance and health-wise. To begin with, let’s talk about alcohol’s effect on metabolism, i.e. does it have a negative, positive, or neutral effect on you getting lean?

In general, ethanol carries about 7.1-7.5 kCal per gram. A “drink”, as defined by the 14g/ unit metric, therefore contains about 99kCal per “unit” just from alcohol. Remember how we talked about ethanol not being able to be stored and requiring almost immediate metabolism? Well, it turns out the ethanol becomes the “preferred fuel” of the liver and decreases liver fat oxidation by about 70% and protein oxidation by about 39%. It also almost completely abolishes carbohydrates being use for fuel even after an infusion. Normally, when carbohydrates reach the bloodstream their oxidation (metabolism) increases by about 2.5x. In the presence of ethanol, however, carbohydrate’s oxidation for fuel stays at baseline and storage of carbohydrates as fat increases [4].

Ethanol metabolism also requires a coenzyme, NAD+, that gets reduced to NADH when ethanol is converted to acetylaldehyde by alcohol dehydrogenase. NADH levels tend to rise during metabolism of ethanol and NAD+ levels tend to fall, thus increasing the NADH:NAD+ ratio. This increased ratio does a number of things metabolically, like increasing fat storage synthesis and causing damage to the mitochondria. Remember, mitochondria are the “energy powerhouses” of the cell and are very important [4]. Some training protocols we use, like high intensity interval training and weight training increase “mitogenesis”, i.e. the creation of new mitochondria to burn fuel (carbohydrates and fat). Ethanol and acetylaldehyde exposure to mitochondria decreases mitochondria activity, increases reactive oxygen species creation (which can damage other tissues), and can eventually cause mitochondrial dysfunction and death.Decreased mitochondrial activity can have negative impacts on basal metabolic rate, as it will decrease in response to lower levels of mitochondrial density or functioning.

This isn’t meant to be a scare tactic, as with most things, the poison is in the dose. On the other hand, the level of alcohol intake required to become inebriated far exceeds the levels of ethanol and acetylaldehyde that were used experimentally to demonstrate deleterious changes in mitochondrial activity.

Actual metabolic rate based on measuring oxygen consumption will increases upon ingestion of alcohol, as it also does with food alone [5]. Some people have taken this out of context and said that alcohol will increase metabolic rate to a greater degree than an isocaloric diet sans alcohol. Unfortunately, this has not been shown as of yet.

Another important metabolic issue as it pertains to ethanol, is that ethanol reduces the activity of muscle phosphorylase in human skeletal muscle [6]. Muscle phosphorylase, i.e. glycogen phosphorylase that breaks down muscle glycogen into glucose, is an important enzyme needed for the muscles to use stored carbohydrates as fuel. A disease of this enzyme, McCardle’s Disease, presents with exercise intolerance, early fatigue, and excessive muscle breakdown products (myoglobinuria) that may lead to rhabdomyolosis. In any event, in addition to decreased muscle phosphorylase activity, ethanol exposure also decreases rates of muscle protein synthesis and whole body protein metabolism by 15-30% [6]. The worst part is, these affects are primarily seen in type II fast-twitch fibers that we need for high level anaerobic performance!

To wrap up part 1 of this series, which was admittedly science-heavy (sorry), I’d like to state how I’d start to apply all these things practically. I do not believe it’s necessary to cut out all alcohol in the quest for ultimate performance and especially not for health, as we’ll discuss next time. On the other hand, I think many people are way too liberal with having a “few” drinks per day. That being said, I’m a proponent of counting the calories in liquor as carbohydrates, as they both demand preference for use as the primary metabolic substrate. What I mean by that is if ethanol is present, it will be metabolized first and foremost. Other calories and energy containing things will be stored so as not to compete with alcohol metabolism, in general. Carbohydrates are similar in that way, as they will be preferentially used by most tissues when the diet provides high levels of them. Additionally, both promote fat storage in the short term. Whether or not this leads to long term fat accumulation depends on the rest of the diet, i.e. total calories, macronutrients, etc.

So, yeah, count the alcohol as carbs and if it fits within your macronutrients and fiber goals for the day, it’s probably fine. On the other hand, I really like this soon-to-be-famous axiom:

“If you’re drinking enough to get drunk, you’re drinking enough to mess with your results.”

That’s it for part I. Sorry for the science primer, but it will pay off big time in parts II and III.

-thefitcoach

1) Cortot A, Jobin G, Fucrot F, et al. Gastric emptying and gastrointestinal absorption of al- cohol ingested with a meal. Dig Dis Sci 1986;31:343–8

2) Frezza M, Di Padova C, Pozzato G, et al. High blood alcohol levels in women. The role of decreased gastric alcohol dehydrogenase activity and first-pass metabolism. N Engl J Med 1990;322:95–9

3) Broitman SA, LS Gottlieb, JJ Vitale Augmentation of ethanol absorption by mono- and disaccharides  Gastroenterology 1 June 1976 (volume 70 issue 6 Pages 1101-1107)

4) Lieber Charles S. Metabolism of Alcohol. Clinics in Liver Disease, Volume 2, Issue 4, Pages 673-702

5) Rosenberg Kathryn, Durnin J.V.G.A. The effect of alcohol on resting metabolic rate. British Journal of Nutrition (1978). Vol. 40. 293

6) Urbano-Marquez, A.; Fernandez-Sola, J. Effects of alcohol on skeletal and cardiac muscle. Muscle Nerve 2004, 30, 689-707.