When Should You Do Conditioning?

By Jordan Feigenbaum MS, CSCS, HFS, USAW Club Coach, Starting Strength Staff

If you haven’t seen this article yet give it a read, as it should set the tone for this blog post. Just as an aside to those who disagree with this blog post or Mark’s article, save the ad hominem attacks and please present your analysis within the context of both anecdotal evidence and scientific evidence. If you’re going to use the latter, please make sure you read the entire study and look at the data before you make claims, as it will save everyone a lot of time and you some future embarrassment if you, ya know, missed something.

At any rate, I recently got hit with this statement and was asked for a response:

Quick question for you-my friend goes to Gold’s and one of the trainers there said it is “better to do cardio before weights”. I would love to get your opinion on the matter.

So instead of calling into question the validity of a trainer’s opinion who works at a Gold’s gym, which would be an ad hominem attack that doesn’t really address this statement, I thought I’d do this in a blog post about conditioning in general. I’m saving the heavily annotated discussion of this topic for my book and thus, this will merely be a reflection of what I believe the current science says and my experience in working with people as a coach.

To begin, we need to talk about what the goals of a training program, in general, actually are for an individual. In other words, WHY IS A PERSON TRAINING? If there is no clear-cut goal, I’d make the semantic argument that the person is just exercising for no particular reason, which is fine too. On the other hand, if a person does have a specific goal, yet is not taking specific steps to achieve this goal then the person’s training is, by definition, suboptimal. In short, we need to clarify what is the goal of the person we’re answering this question [When should I do conditioning?] in order to provide an accurate answer. Additionally, we need to get a clearer picture of what exactly the person is doing training or exercise wise depending on their current level of commitment to their goal. As you can see, there are lots of unknowns here that we can’t possibly answer and thus, the discussion needs to shift to be more general. So what we’ll do is go over the important considerations to determine optimal conditioning timing, frequency, etc. with respect to three general goals:

  1. Health
  2. Weight Loss
  3. Performance

Here’s the first question: How much conditioning* training is optimal? (cue explosions for dramatic affect)

* conditioning can be considered analogous to cardio (low intensity steady state-LISS, High intensity interval training (HIIT), circuits, etc.)

I’d make the argument that within the context of an individual who is following an intelligent training program that’s centered around planned progressive overload of the big lifts, e.g. the squat, bench, deadlift, press, power clean, and chin/pullup, that the optimal conditioning volume (total frequency and duration of conditioning efforts) should be the smallest amount needed to produce the desired goal. Let’s look at this from the health perspective first.

We know that training increases oxygen delivery to tissues, causes adaptations at both the tissue (macro) and cellular (micro) level, and alters hemodynamic properties (hemoglobin, blood viscosity, etc.) that all result in increased capacity to do work and sustain activity. The real question we should be asking from this perspective, however, is what sort of training most optimally reduces major negative health outcomes…ya know, like death, cancer, cardiovascular incidents, etc. Well, as it turns out the literature suggests that the stronger someone is, i.e. the more force they can produce with their muscles to move an external object, the lower the morbidity and mortality rates when compared to both sedentary populations and those who were more “aerobically developed” from doing typical conditioning/cardio training and, more interestingly perhaps, the same rates of morbidity and mortality as those who were the strongest and the most aerobically developed. As it turns out, there’s more than a nugget of truth on ol’ Rip’s adage:

Stronger people are harder to kill than weaker people, and more useful in general”-Mark Rippetoe

Does this mean I’m saying people who are training/exercising for health purposes shouldn’t do any sort of conditioning? No, that’s not what I’m saying. I’m implying that you get a pretty decent stress from weight training to drive conditioning adaptations that have an observably profound effect on clinical outcomes. If you desire additional capacity for another purpose, i.e. you want to be able to run further/faster or have more “wind” when doing a particular activity (e.g. pick-up basketball), then doing some supplemental conditioning work will be useful in achieving these goals. However, let’s not be confused with what the literature is saying about how this will affect health.

This being said, if someone is not training in an intelligently implemented manner with a focus on the only incrementally loadable, systemically stressing modality there is, e.g. barbells, then he or she will need to do more conditioning work in order to supplement the lack of actual training stimulus he or she is getting from the gym. High intensity interval training (HIIT) is the obvious choice, as the adaptations and metabolic responses to this style of conditioning tend to mirror that of resistance training, whereas low intensity steady state cardio pales in comparison (though there is a purpose for this style training that we’ll discuss alter).

HIIT causes the skeletal muscles to move to relatively high velocities and contract with high forces compared to LISS. Because the demand for energy is so high during HIIT, it is appropriately referred to as anaerobic or glycolytic training, as the rate of energy production is so high that aerobic (with oxygen) energy producing pathways can’t keep up. When done appropriately, HIIT increases basal metabolic rate (BMR) significantly over many hours post exercise (more calories burned in total), increases mitochondria biogenesis (makes new energy producing and calorie burning power plants in the cell to increase BMR chronically), increases skeletal muscle’s uptake of nutrients (instead of fat), does not cause muscle catabolism (like LISS), and results in even more pronounced cardiorespiratory conditioning adaptations in the heart, lungs, and vascular tissues. HIIT works so well, clinicians are using it in COPD, MI, and Obese patient populations instead of LISS. Just sayin’…..

In sum, I don’t think there’s a good reason to do tons of conditioning work if you’re just interested in health UNLESS you need the extra conditioning work to produce other desirable changes, e.g. performance increases or fat loss.

So, how much conditioning is optimal for increasing performance? The answer (duh), is IT DEPENDS ON YOUR SPORT. If you’re a marathoner you’re obviously going to have a higher total conditioning volume than a weightlifter. Similarly, the types of conditioning are going to be different. Marathoners need steady state “tempo” work in order to develop efficiency in running, which is more strength and strength-endurance limited than it is limited by someone’s lungs/heart. In other words, you don’t stop running because you’re out of breath, you stop running because your legs are tired. This is a strength deficit, through and through, which is ameliorated by actually training to get strong AND doing longer runs to acclimate the body to become more efficient at running and therefore require less energy. If you’re a weightlifter, the only reason you’re doing conditioning is to improve your ability to lift weights, i.e. put pounds on the bar or improve recovery enough to increase training frequency (by being better conditioned) to aid in putting weight on the bar.

So the optimal amount of conditioning for a marathoner and a weightlifter are different, but the answer is still the same as what we covered in the health section, i.e the smallest amount needed to produce the desired goal. This will, of course, be different for everyone.

I bet you already know the answer to how much conditioning is optimal for weight loss (and you’d be correct): the smallest amount needed to produce the desired goal. Basically, we want to get the most out of the least so we have somewhere to go when we get stuck. Anyone who’s ever gotten really lean knows about getting stuck, which requires manipulation of conditioning efforts (usually adding more), training, and food intake (usually small reductions in carbs and fat). Unfortunately, people get greedy with results and think MORE IS BETTER, and cut out a bunch of energy (calories) and add a bunch of conditioning. Truth is, more isn’t better; BETTER IS BETTER.

By removing a bunch of calories when it’s not needed or, equivalently, adding a bunch of conditioning when it’s not needed you miss out on getting the best return on investment (ROI) possible and are, for no reason, reducing the amount of food you’re eating and increasing the amount of activity you’re doing. What do you think the body is going to do? It’s gonna say “Screw you guys I’m going home!”

Look, two things are happening here.

Thing 1: With calorie restriction, which is needed to lose weight, your metabolism slows down.

Thing 2: If your conditioning is mostly LISS, your metabolism slows down, i.e. you become more efficient at creating energy (no, this is not good). The current thinking on this mechanism has to do with reduced expression of uncoupling proteins in the mitochondria, which normally make the mitochondrial less efficient at creating energy (ATP).

So, imagine all the typical cardio bunnies starving themselves and doing hours of cardio on the elliptical; low intensity mind you because how are you supposed to read Elle magazine when you’re doing HIIT? Their metabolisms are slowing down from both ends and then boom, a big blowout weekend (or week) and what happens? Lots of fat deposition because their metabolisms are so depressed it’s the only thing that can happen. Yes Virginia, their BMR will increase transiently due to the “refeed” of a hypercaloric couple of days, but lots of adipose tissue will also get stored.

So, in short….how much conditioning should you do? The smallest amount needed to produce the desired goal.

The next question is rather obvious, what is the purpose of conditioning?

From a health perspective, there’s really not a lot of purpose for pure conditioning modalities unless it’s either facilitating another related (e.g. fat loss) or unrelated goal (e.g. more conditioning for sport) OR the person isn’t training and therefore needs something to supplement them.

From a performance standpoint, the purpose of conditioning is to drive the adaptations specific to that sport. Returning to the marathoner vs. weightlifter, the marathoner is obviously going to spend more time doing steady state stuff and their interval work will have different work to rest ratios (1:1-1:3 will be the bulk of it) versus the weightlifter not doing hardly any steady state stuff and sticking to interval work with 1:5-1:20 work to rest ratios. The only exception to the “drive the adaptations specific to that sport” mantra is if the sport is a weight class sport and thus the conditioning’s purpose may also include fat loss/weight manipulation

From a weight loss perspective, the purpose of conditioning is fat loss pure and simple. HIIT trumps LISS in this regard, as even though a longer LISS session certainly burns more calories during the activity, the HIIT burns more calories in total than the LISS by increasing resting metabolism over the course of hours-days post workout. People will say “Well you burn a higher percentage of fat doing LISS than HIIT”, which is true. On the other hand, I don’t really care about the percentage of fat I burn, I care about the total number of fat I burn, which is much greater in HIIT since the total energy expenditure is much higher. Kind of a dumb argument if you ask me.

The final question, which is the original motivation for even writing this things is: When should you optimally do conditioning?

Now, there’s really no reason to discuss the health perspective on this since the only reason to do conditioning for health is in order to increase performance or improve fat loss so we’ll stick with those.

Performance-wise, this all depends what kind of athlete you are. If you’re in a sport that’s conditioning focused then there will likely be plenty of times you’re going to be doing conditioning only during practice or programmed sessions. I could make the argument that if there are skills you need to practice that these should be incorporated first before the conditioning work, as it is highly fatiguing and might interfere with practicing optimal technique of the skill. This is the same for strength/power training, i.e. it should come first for virtually any athlete who’s going to train multiple modalities in the same day even if he or she is going to split them up into multiple training sessions in the course of the day (i.e. 2 or 3-a days). Will doing a heavy squat session first or in the AM negatively impact the ability to do a long tempo run second or in the PM? Of course, duh. However, the squat session is going to have less of an effect on the run as the run would have on the squat. Moreover, the runner is going to get a more useful stimulus from the squats than the run provided the context we’re discussing is the off season or GPP/accumulation phases. On the other hand, I could make the argument that during more specific training phases or in-season cycles, the runner should run first and then do a lighter, more attenuated squat session later to try and preserve strength during the season. Applying this same rationale to a weightlifter and the answer becomes crystal clear, conditioning comes after the weights 100% of the time with respect to developing performance.

When talking optimal conditioning timing concerning weight loss, the answer is really even clearer in my opinion. Optimally, you’d do conditioning (HIIT mostly) on your OFF days, i.e. days you’re not training with weights. See, resistance training provides a super potent stimulus to the body to increase metabolism, burn calories for hours post workout, partition nutrients favorably, and otherwise adapt to the stress imparted upon it. Adding conditioning workouts to a resistance training session, therefore, is not optimal in that you’re already getting a big time stimulus from training anyway and there’s MORE benefit to be had by doing it on your off days where you where previously receiving no stimulus (or a waning stimulus from the previous day’s training). Remember, the goal here is to signal as much possible increase in BMR, favorable nutrient partitioning, and net calorie burn as possible.

Understandably, many people do not have a flexible enough schedule to do this and so the crux of the matter becomes this: Should I do cardio before or after weights? Answer (you probably already know this): AFTER!!!!

Resistance training provides a more potent stimulus than conditioning, period. Why? Because resistance training is heavier, has longer ranges of motion, and overall imparts more stress on the human organism (or at least it should). If you did conditioning before training, you’re fatiguing motor units, depleting the muscles of energy, and overall reducing possible intensity, volume, etc. that could possible be attained in the session as a whole. Now, weight training first will certainly attenuate the amount of intensity or effort a person can put into conditioning but this is not as severe as the opposite since, ya know, conditioning is easier than burying a heavy squat.

My stock recommendation for those who have to get in and out of the gym in an hour and can’t train more than 3-4x a week is as follows: Spend 45 minutes doing progressively heavier barbell training and 15 minutes doing HIIT everytime. Period.



Top 10 Mistakes People Following Starting Strength Make

By Jordan Feigenbaum MS, Starting Strength Staff, CSCS, HFS, USAW Club Coach


1) Not reading the book

Seriously, most people who are doing “Starting Strength Novice Progression” have never even read the book. They got the “routine”, replete with rows in place of power cleans, of the Internet and are 100% unprepared for what this program requires. Further, because they have not read the book and thus, are lacking in understanding the rationale- the WHY- behind the program, they do a bunch of inappropriate things as seen in the other 9 items below. Bompa, Issurin, and Zatsiorisky all agree that explaining to an athlete the “why” behind the “what” is important for compliance. If you want to do Starting Strength Novice Progression, you need to read the book. Period.

2) Starting too heavy.

This is usually a result of a failure to read the book, however there are still some people that will start too heavy because the heavier you start the faster you’ll get strong, right? Wrong. What we’re aiming to do is use the smallest effective dose to stimulate the maximum potential response. In lifting terms, we want you starting with a weight that begins to challenge your ability. This can be gauged, roughly, by when the speed of the bar slows down or the technique suffers slightly. If the former happens, then you’ve just done a set of 5 reps that is heavy enough to drive the adaptations we want, i.e. strength, neuromuscular coordination, hypertrophy, etc. If the latter happens, however, we need to back the weight down just a tad in order to preserve proper form (see below).

3) Having poor technique.

This mostly stems from people not doing Step 1, i.e. reading the book, OR not watching all the videos, reading all the articles, etc. on the site, YouTube channel, or various other mediums. Bottom line is, if you’re technique is not good you’re going to see less than optimal results through any training program, period. When compounded by the fact that this program aims to get you as strong as possible in the shortest amount of time, things start to escalate quickly. It would behoove any person to see a Starting Strength Coach within their first week of training just to hammer this all out. If that’s not possible, post a form check on the Q/A the coaches so graciously run.

4) Eating like a bird.

I was thinking about putting this as number one, but alas, I thought the other things were actually more important and, specifically, doing number 1 would take care of this number. Look, if you’re a 16-23 year old male and <165 lbs, you need to gain a significant amount of body weight, like yesterday, in order to be facilitate the fastest rate of strength and muscle size acquisition. This is done through food, like LOTS of it. I’ve already written extensively about this topic in this article, so I suggest checking that out. Look, here’s the simple fact:

You have one chance in your life to put on muscle at an almost unnatural rate. This moment in time also coincides with the ability to gain a tremendous amount of strength, if you’ll only eat to facilitate this process. For 3 months forget about your abs so you can build the ice chest to put the 6-pack in.

The older, heavier, or more female you get away from this “ideal Starting Strength candidate” the less extra food you need to drive these processes. Again, see the article linked above “To Be a Beast” for more discussion on this topic.

5) Not resting long enough between sets.

After 3 minutes, approximately 80% of your muscle’s ATP has been replenished, at 5 minutes, approximately 95% is back in the game, and at 8 minutes ~ 100% is there. Don’t try to hit PR’s, which happen everyday on this program, with 80% of your muscles’ energy available.

6) Adding in too much bullshit.

Remember that we’re using the minimum effective dose to get the maximum response here. Adding in a bunch of extra stuff dilutes the “effective dose” AND spreads the body’s available resources for adaptation to the “dose” too thin for optimal results for a novice trainee. Of course, as you become more “trained” and thus, can tolerate more volume, frequency, and intensity, you’ll be able to add more exercises, sets, reps, etc. 

If, on the other hand, you add too much tomfoolery TOO SOON in your training career, you run a very serious risk of attenuating (diminishing) your adaptive responses to training, thus blunting your progress.

The take home, keep it simple Santa (K.I.S.S.- I don’t like calling people stupid, normally). The big five, squat, bench press, press, deadlift, powerclean plus chins, curls, and back extensions will work beautifully for your dedicated novice progression. Read the book to see implementation, or this excellent article on Fitocracy by Michael Wolf.

7) Resetting a million times.

Sometimes you just have to call a spade a spade and realize it’s time to move on. Whether it’s due to not enough food, not enough recovery, or poor technique, etc. you just need to either get some help or move on. If you’re not progressing every training session, you’re no longer on the Novice Progression anyway, so don’t be married to it if it’s not working for you (and you’re doing all the necessary things to make it work).

That being said, having a training program that revolves around the big 5 and some HIIT (if necessary) is the best base template you could hope for, with rep ranges, total volume, and frequency all reflecting an individual’s needs and goals. Put simply, you could do a lot worse than to keep resetting over and over again, but do you really want to stay weak? Figure out the limiting reagent and nip it in the bud. Grow. Progress. Profit.

8) Missing workouts (and not adjusting accordingly).

Simple enough, right? If you miss a workout on this program you are, by default, failing to provide a stimulus for your body to adapt to. This adaptation response is what is used to drive the next training day’s progress. Thus, if you miss a day you shouldn’t be expecting to “go up” in weight the next training day, although in the beginning this is more feasible. Moreover, novices tend to de-train more quickly than advanced trainees, as they’ve had less cumulative exposure to the lifts, progression, etc. and thus, it’s not unusual to see some of these detraining or deconditioning effects if a person misses a workout.

So, what do you do if you miss a workout? Simply repeat the last workout you did and start from there. If you miss a series of workouts and are a true novice, you’ll just start all over again. I really shouldn’t have to say this, but how about just not missing workouts?

9) Reading too much bullshit.

Bro 1: “Hey man, did you see that new exercise on MonsterMuscleGainer.com today?”

Bro 2: “Nah, bro. What was it?”

Bro 1: “It’s like this weird lunge thing with kettlebells. All the Russians used to use it and that’s why their legs are so jacked. I heard Klokov invented it!”

Bro 2: “Dude, this is awesome. We don’t have to do squats today then. Let’s do like 40 minutes of mobility, to make sure we activate all our muscles during training, then do Klokov lunges with kettlebells.”

Bro 1: “Yea, squats are so old-school. MonsterMuscleGainer.com said these were better for hypertrophy anyway. I don’t care about being strong, I just want to LOOK strong.”

Sadly, this sort of crap happens everyday in gyms (CrossFit and black-iron gyms are not exempt from this either) across the country. People mistake “new” or “proprietary” with “better” and try to reinvent the wheel. Look boys and girls, barbells are the most efficient way to load the human musculoskeletal system and stress the body. Because it’s the most efficient*  way to stress the body, it’s the most efficient at causing the body to adapt and these adaptations are more robust than any other silly shit your “guru” is pushing.

*ef·fi·cien·cy: noun, plural ef·fi·cien·cies.

1. the state or quality of being efficient; competency in performance.
2. accomplishment of or ability to accomplish a job with a minimum expenditure of time and effort: The squat is increasing Christy’s exercise efficiency by working all the muscles of her legs and trunk instead of wasting hours doing isolation/activation bullshit.
3. the ratio of the work done or energy developed by a machine, engine, etc., to the energy supplied to it, usually expressed as a percentage.

10) Being a p*ssy.

Any program that’s designed to add weight to the bar 3x a week is going to be hard, make no bones about it. If you want it to be easy or, more commonly, easier week to week you need an attitude check.

“It never get’s easier, you just go faster”- Greg LeMond

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.

Screen shot 2013-06-12 at 6.07.19 PMSmooth 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.

Gonadal-AxismennewestNormally, 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.


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 ApcMin/+ 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...

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:

Screen shot 2013-06-02 at 12.02.08 PMor 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.

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? 🙂

paleo_smallSo 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.


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.