- 1. Part I - What Happens to the Body During Resistance Training
- 1.1. So does nutrient timing (especially peri-workout) matter?
- 1.2. Improving body composition
- 1.3. Optimizing muscle hypertrophy
- 1.4. Optimizing fat burning
- 1.5. One or the other: The AMPk-mTOR see-saw
- 2. Part II: Breaking Down the Macronutrients: Proteins, Carbohydrates and Fats
- 2.1. Protein Source—Does it matter?
- 2.2. Protein Quantity—Is there a limit?
- 2.3. Carbohydrates and the role of insulin
- 2.4. Carbohydrate sources and glycemic load
- 2.5. Dietary fats
- 2.6. Saturated fat sources
- 2.7. Unsaturated fat sources
- 3. Part III: Optimizing Your Peri-Workout Nutrition Plan
- 3.1. Prepare. Perform. Replenish.
- 3.2. Phase I: Prepare
- 3.3. Phase II: Perform
- 3.4. Phase III: Replenish
- 4. Final Thoughts
- Why nutrition is not a one-size-fits-all topic
- What happens to the body during resistance training.
- How to optimize body composition via the use of intra-workout nutrition.
- About intra-workout protein quality and quantity, and if they matter.
- How carbohydrates and fats impact the muscle building and fat loss process.
- The steps you can take to optimize your peri-workout nutrition.
This guide serves as an adjunct to the Peri-Workout Supplementation Guide.
Nutrition is not a one-size-fits-all topic.
With so many different nutritional theories out there, many people find themselves with the cumbersome task of deciphering facts from fiction; it’s not a black and white topic like many people make it out to be. The conundrum with giving precise nutrition advice to a broad demographic is that it’s a field that requires personalization and often trial and error to find what is optimal (and practical) for the individual in question. A plethora of intrinsic (e.g. metabolic rate, endocrine functions, immune response, etc.) and extrinsic (e.g. caloric intake, activity level, etc.) characteristics contribute to how we tolerate and utilize certain nutrients.
Moreover, it would be foolish to disregard the goal(s) and form(s) of physical activity that the individual in question is nourishing their body for. Obviously a young, 230lb male bodybuilder looking to add mountains of muscle to his frame will have different nutrient requirements than a 40-year old, 130lb soccer mom prepping for a marathon. It may seem intuitive, but this just reinforces the point that variables must be considered when optimizing one’s diet.
That being said, the variables previously mentioned are what make nutrition a field of great diversity and ongoing research, as many approaches are plausible. Some people get great results by limiting their carbohydrate intake, while others can flourish on a higher-carbohydrate intake while keeping fat intake a bit lower. Some individuals may follow an “intermittent fasting” type of eating pattern and achieve great results, and some may eat every 2-3 hours (read: like a “bro”) and do just as well. There is more than one way to skin a cat; we are an adaptive species and our nutritional habits are no exception.
Before we move on, another point to consider is that people tend to migrate towards the extremes in the world of exercise and nutrition. If someone reads a study that barbell curls are more efficient than dumbbell curls for bicep stimulation, it often gets interpreted as, “Dumbbell curls are a useless biceps exercise.” This all-or-none way of thinking just imposes limitations and restrictions on you. The goal should be to find what’s optimal, but more importantly, what’s practical for each individual. Even if a certain extreme protocol is optimal, more often then not, it’s impractical. At the end of the day if one can’t apply a protocol to their life (whether it’s optimal or not) then it’s a moot point.
Part I - What Happens to the Body During Resistance Training
Prior to discussing the nutritional side of things, its prudent to have a fundamental understanding of what happens physiologically to our bodies during bouts of resistance/weight training. This can be tricky to summarize since there is a vast array of research showing that different training variables (i.e. volume, intensity, frequency, etc) elicit different physiological responses. (2) As noted earlier, someone training for pure strength purposes (such as a powerlifter) will likely have a different approach to training than a physique competitor looking to build more muscle (this will be further addressed later in the guide to keep this portion as a general overview of our body’s physiological response to weight training).
For this instance, we will approach this in a manner that assumes the trainee is performing moderate volume (e.g. 2-3 sets of 6-12 reps per exercise), moderate intensity (e.g. a weight that challenges the individual but does not incur failure on the last rep) weight training 3-4 times per week. This is a type of programming that would serve to build muscle and strength (no pun intended) and be sort of a middle-of-the-road approach in terms of activating different muscle fibers. (3)
So lets take this program and apply it to John (or Jane) Doe and see what happens physiologically in response to these bouts of weight training. When this individual performs their exercises, they are exerting a contractile force with the necessary muscle(s) during each repetition; to develop this contractile force the muscle cells use energy (in the form of ATP) and eventually reach a point of fatigue where no more repetitions can be performed (i.e. muscular failure). Bear in mind that this is a (very) truncated summary of what happens during anaerobic exercise such as intense weight training (elaboration on the specific mechanisms behind muscle contraction and subsequent breakdown would only convolute the issue).
After exhausting a muscle sufficiently through anaerobic pathways, the cells will actually be damaged and acquire a generous build up of metabolites in the surrounding tissue. This leads to an inflammatory-repair response, known as delayed-onset muscle soreness (DOMS), in the interim after training has occurred. (3) Thus, resistance training is the stimulus Mr./Ms. Doe provides to his/her muscle tissue that results in a milieu of physiological responses.
The specific physiological benefits this individual will derive in response to weight training are numerous, such as enhanced cardiorespiratory functioning, positive adaptations of the endocrine system, and favorable changes in muscle tissue morphology. (4,5) Some of these benefits are acute, such as vasodilation of skeletal muscle and improved insulin sensitivity, while others are rather latent and become more pronounced once weight training is a habitual activity. (6,7) Keep in mind that these acute adaptations are what comprise the purported post-workout “anabolic window of opportunity”.
The main thing to take home in this case is that intense weight training acts as a stimulus for muscle tissue; the muscle tissue is subsequently damaged and elicits a medley of physiological responses. This is why the notion some gym-goers have that muscle growth (hypertrophy) occurs during the act of weight training is nonsense; we repair (i.e. grow) muscle tissue during the recovery period hours/days after training has taken place (assuming proper nourishment is provided).
So does nutrient timing (especially peri-workout) matter?
For those unfamiliar with the term peri-workout, it is a designation for the pre,during,and post-workout timeframe. As alluded to previously, this is thought to be a critical timeframe for athletes and trainees due to the cascade of favorable metabolic and hormonal responses to exercise, a simple example being up-regulation of glucose transport proteins (i.e. GLUTs) in muscle tissue. (1) Intuitively, we would want to take advantage of every opportunity we have with regards to the peri-workout timeframe, especially if this timeframe really is the “window of opportunity” for anabolic purposes (unless, of course, you’re not one for reaping the most of what you sow). Another way to pose this scenario is that if you can get more bang for your buck (hypothetically), why would you choose the less rewarding option? I don’t know, martyrdom maybe?
Not surprisingly, the nutrient-timing question seems to creep its way into everyone’s head the minute they think about nutrition. My initial response is always the same—yes, it does matter, but the more proper question is just how much does it matter? When we take a step back and look at the overall hierarchy of proper nutrition, the specific time you eat your nutrients is surprisingly low on the list (at least in the literature). It appears that the more important factor is total macronutrient/energy intake. But we still need to define what the nutrient-timing question pertains to more clearly to provide a better answer.
Thus, lets dichotomize the question, one part directed towards body composition and one to athletic performance. Even if studies don’t show a significant change in body composition based solely on differing feeding patterns, we cannot discount the fact that some people just perform better in the gym or in athletic events when nourished a certain way (or fasted, should they choose to go that route). Before we dive into this further, keep in mind we are after what’s optimal and practical. The research/science provides us with general clues as to what is optimal, while personal experience and adaptation are what make it practical.
Improving body composition
Ideally speaking, in order to reap maximum benefits for body composition purposes, we would want to follow a peri-workout nutrient protocol that optimizes two things—fat burning and muscle hypertrophy. Unfortunately, these two goals are theoretically mutually exclusive (i.e. you can’t do both concurrently). This is probably the greatest conundrum physique competitors have brooded over ever since they set foot in the gym; alas, without the use of pharmacological doses of PEDs (and even then), it is an exercise in futility to try and concurrently optimize both muscle hypertrophy and fatty acid oxidation (unless you intend to overcome thermodynamic laws, which I invite you to refute). However, this does not mean you can’t improve your body composition at any given time.
One thing most people seem to fly right over when they set a new physique/fitness goal is the fact that bodyweight alone is not a sufficient measurement tool for progress. There are few scenarios where someone’s goal should be to solely lose or gain weight just for the sake of seeing a quantitative change on the scale. I’d rather see individuals become familiar with the idea of always aiming to improve their body composition.
If this is a new concept to you, improving your body composition simply entails increasing your ratio of muscle to fat tissue, respectively (i.e. lowering your body fat percentage). So if we take Brutus Biceps from the earlier example and add 5lbs of muscle to his frame while only adding, say, 2lbs of fat, we have just improved his body composition. Likewise, if Brutus was able to shed off 5lbs of fat and only lose 1lb of muscle mass he again would have improved his body composition. So to reiterate, we either want to maximize muscle hypertophy (while limiting fat gain) or maximize fat burning (while limiting muscle catabolism/loss). Hopefully these examples make the concept of body composition more tangible.
Optimizing muscle hypertrophy
Before we discuss how to optimize nutrient intake/timing peri-workout, we need to understand what comprises a state of muscle anabolism/hypertophication. Essentially, it breaks down to what is called the net protein turnover ratio, which is a quantitative measurement of muscle protein synthesis (MPS) versus muscle protein breakdown (MPB). A net turnover ratio of where MPS>MPB is indicative of muscular hypertrophy (e.g. a state of anabolism) and vice versa. A medley of factors can cause this ratio to fluctuate, such as exercise, nutrient intake, disease/immune conditions, gene expression, pharmaceutical agents, over-the-counter supplements, etc.
So in order to optimize muscle hypertrophy, we ideally want to maintain a high rate of MPS and a low rate of MPB (thus the muscle protein turnover ratio is in favor of anabolism). Seems like a simple task, but muscle protein synthesis is tightly regulated via a protein encoded by the FRAP1 gene in humans called the mammalian target of rapamycin (mTOR). (8) This protein acts as the backbone to mTOR protein complexes (such as mTORC1 and mTORC2) that activate protein synthesis when suitable cell conditions are met (and ultimately result in cellular growth and proliferation). (9) Granted the entire regulation of protein synthesis pathways is highly complex (and beyond the scope of this guide), it’s still useful to have this rudimentary understanding of how muscle cells actually grow.
The activity of mTOR protein complexes are controlled by the cell’s energetic state, circulating growth factors and hormones (especially insulin), nutrient availability, and oxidative stress. So our goal is to bolster these signals in a manner that is conducive to upregulating MPS.
Optimizing fat burning
Indeed, the mechanisms needed to maximize fat loss are more or less directly antagonistic to those mechanisms involved in muscle hypertrophy (and vice versa). Fat burning appears to be largely influenced by the enzyme adenosine monophosphate-activated protein kinase (AMPk), a trimeric protein expressed in many tissues in the body.
As you likely know, ATP is the energy currency of the cell and the breakdown of ATP forms ADP and free energy. Science jargon aside, AMPk is switched on when the cell is in a state of energy deprivation (e.g. the ATP:ADP ratio drops). This occurs during times of nutrient (specifically glucose) deprivation, exercise, ischemia, and /or use of certain chemicals/drugs. Intuitively then, things such as eating and excessive glycogen levels inhibit AMPk activity (since the ATP:ADP ratio is elevated).
Why is this of concern you ask? Well, simply put, AMPk increases lipolysis, enhances fatty acid oxidation, improves glucose uptake in muscle tissue, and inhibits lipogenesis. (18) Essentially, it is the “metabolic switch” for burning fat.
One or the other: The AMPk-mTOR see-saw
Herein lays the conundrum we talked about earlier, whereby we can’t concurrently maximize muscle hypertrophy and fatty acid oxidation since they are operated by antagonistic mechanisms. Unfortunately, while AMPk is great for turning on fat burning, it is also an inhibitor of mTOR (and thus, muscle protein synthesis). (19) Furthermore, mTOR reciprocates by inhibiting AMPk, so when MPS is activated fat burning is inhibited.
If you think about it pragmatically, this makes sense since cellular energy levels can only be sufficient or depleted, with respect to the ATP:ADP ratio, at any given moment. Granted this is a simplistic overview of these metabolic pathways, it still provides an idea of why you can’t have your cake and it eat it too, so to speak, when it comes to fat burning and muscle building.
This is not to say you can’t switch back and forth between these two conditions, and in fact that’s what certain things like yo-yo dieting, intermittent fasting and refeeding protocols are founded upon. Theoretically, it would be wise to give each of these pathways (AMPk/mTOR) sufficient stimulation/activation when trying to improve body composition, even if it’s only intermittently. Thus we use the see-saw analogy.
Part II: Breaking Down the Macronutrients: Proteins, Carbohydrates and Fats
Protein Source—Does it matter?
For now, we are mainly concerned with what we can do from a nutritional standpoint to promote the necessary signals for muscle protein synthesis to occur. Since amino acids are the building blocks of proteins, the amino acid levels in the cell act as regulators of mTOR protein complexes. (10) Even in a positive energy state, if the cell does not have the necessary amino acid stores than protein synthesis will remain inhibited (its analogous to building a brick house without first stockpiling any bricks…Probably not going to result in much).
A study completed by Norton et al. found that the inherent leucine content of various protein sources (egg, wheat, soy, and whey) resulted in differing postprandial (i.e. after feeding) plasma leucine levels and stimulation of MPS; only the whey and egg groups exhibited stimulation of MPS beyond that of food-deprived control groups. (11) Naturally then, we want to ingest a sufficient dose of amino acids, and more importantly, amino acids that activate mTOR protein complexes (such as leucine). (12)
Thus far, research has shown that so long as the protein source contains the necessary leucine content (and other essential amino acids) then there is little difference in MPS between sources (e.g. milk, animal protein, egg protein, etc). (13,14) So the take-home message here is that protein source is indeed important, but only in the sense that the source contains sufficient leucine and essential amino acids. Again, the difference in MPS rates between protein sources in insignificant if the leucine/EAA content/quantity is enough to maximize the MPS response; we will discuss this quantity below.
Protein Quantity—Is there a limit?
There seems to be a theory in bodybuilding lore that the body can only digest “x” amount of protein in a given bolus (for some reason this amount conveniently runs around 50g and applies to the entirety of our species). Well, for lack of a better term, this theory is unsubstantiated. The body can handle a significantly large amount of any macronutrient in a given feeding, but the question we should be concerned about is how much of that dose results in a sustained rate of MPS? Furthermore, is there a ceiling/cap to postprandial MPS?
The past several years of research have elucidated upon this topic substantially. One such example being the finding that co-ingestion of leucine with whey protein did not result in a significant difference between whole-body protein turnover in individuals who drank solely whey protein. (15) Granted the caveat of this study is that it was concerned with whole-body protein turnover, not just skeletal muscle protein turnover (for body composition purposes, we obviously aren’t looking for hypertrophy of say, liver or gut tissue).
Furthermore, a different study found that peak activation (but not duration) of MPS was proportional to the leucine content of a complete meal (i.e. one containing fats, carbohydrates, and proteins). (16) However, it’s been found that a way to extend the duration of MPS is by supplementing with leucine (and/or carbohydrates) between feedings (so long as feedings are spaced far enough apart to allow MPS to return to baseline levels, generally 4-6 hours after a sufficient meal is ingested). (17)
It appears that a conservative estimate, based on the data, is that 30+ grams of a leucine-rich protein source (such as most animal proteins and whey protein) is plenty to sufficiently elevate MPS for a good 3-4 hours. (31) Again, this is just a baseline minimum for active individuals but is by no means a strict rule.
Carbohydrates and the role of insulin
Many people tend to migrate to the extremes when it comes to carbohydrate intake, being either “high-carb” or “no-carb” advocates. Moreover, there seems to be a lot of misconceptions about what exactly insulin does and how it impacts fat loss and muscle hypertrophy.
First off, even if you’re a “no-carb” dieter, you’re still going to be secreting insulin; amino acids are insulinogenic to a degree. Also, chronic low-carb dieting doesn’t appear to offer any metabolic advantages over moderate-carb diets (21), and most studies have only shown benefits when very-low carb diets are used in the short-term. (22)
Secondly, insulin is indeed a “storage” hormone, but this is also why it is highly anabolic. People seem to have this dreadful fear of insulin like even the minutest amount of insulin is going to turn them into the Pillsbury Doughboy. Do not fear insulin! It’s actually your ally if you’re looking to optimize muscle hypertrophy. Numerous studies have verified that the MPS response to a nominal dose of amino acids can be enhanced by the presence of sufficient carbohydrate intake (and thus an increased insulin response).(20,23)
However, this is where we need to be careful and avoid hyperboles. The key is to feed a “sufficient” dose of carbohydrates to promote a nominal insulin response, not too binge on a bunch of simple carbohydrates in a vain effort to jack up insulin as high as possible. Insulin, in the physiological range, does not enhance the MPS response to meals in a linear fashion like many people believe. (24) Pharmacological doses of insulin do in fact enhance the response above that of a physiological response, but that isn’t relevant in this instance since it requires the use of exogenous insulin and is impractical for the majority of gym-rats.
The take home message here is that carbohydrates (and insulin) are your ally when seeking to optimize the MPS to a complete meal, but don’t overdo it and take in a superfluous amount of carbohydrates since the synergistic effect of insulin (in physiological range) is not linear. You want to take in a moderate amount of carbohydrates to efficiently stimulate insulin secretion (the specific amount at each meal will depend on a variety of factors, but there isn’t any need to really disproportionately load all your carbs at one meal, even post-workout).
Carbohydrate sources and glycemic load
For the majority of individuals who are eating complete meals (i.e. they contain fats, proteins, and carbohydrates) the source of their carbohydrates is secondary to their total carb intake. The one exception to this would be individuals who allocate an excessive amount of pure sugar (dextrose) to one feeding in order to “spike” insulin, which we just discussed above.
There is no need to (and ultimately little extra benefit, if any) to using pure high-glycemic index (GI) carbohydrates to ramp up insulin levels. This does not mean you need to avoid all simple sugars and high-GI carbs, but it just reiterates the point that spiking insulin levels (in the physiological range) doesn’t augment MPS any more than a more moderate rise in insulin seen with lower-GI carbs such as oats, sweet potatoes, and other complex carbohydrates. (24)
Another point to keep in mind is that glycemic index (and ultimately, the glycemic load) of carbohydrates are altered when co-ingested with other food sources. For example, eating a complete meal with a high-GI carb (like jelly beans) will lower the glycemic load of those carbs since fats and fibers slow digestion.
As with most things in the world of nutrition, practice moderation; try and balance your carb intake between sources and don’t eat a diet exclusively based around sugary, high-GI carbs. Sure, it’s fine to have some sugar/high-GI carbs, just be sensible about it.
Fats are unique in that they’re energy dense (9 calories per gram) and tend to provide a good amount of satiety. They’re essential for cellular integrity and play a variety of roles with regards to cellular mechanisms; thus, fats should not be under-eaten, especially in active individuals.
Saturated fat sources
Fatty acids are composed of chains of hydrocarbons, and when all the carbons are saturated with hydrogen atoms they are referred to as saturated fats. Saturated fats are generally demonized by the media and people looking to shed body-fat, but they have their role in a healthy diet much like any other nutrient.
For example, coconut oil is almost purely saturated fat, but it’s composed mostly of medium-chain triglycerides which are a form of fat that is readily used for energy rather than being stored. Moreover, saturated fats appear to be correlated with sex hormone (androgen) production in males. (25)
Yet again, the key to remember (like with the aforementioned insulin conundrum) is that just because a nominal dose of something confers benefit doesn’t necessarily mean a large amount is even better. In fact, chronically-high saturated fat intake is linked to insulin resistance and increases the risk of a variety of metabolic impairments. (26,28)
Depending on your total fat intake and your goals, your saturated fat intake may fluctuate accordingly. A conservative approximation for the majority of active individuals would be to take in at least %25 of their total fat intake from saturated fatty acids. You don’t want an imbalance of unsaturated fats (which are discussed below) to saturated fats in your diet, nor is it really practical.
Unsaturated fat sources
In contrast to saturated fatty acids, unsaturated fatty acids contain one (monounsaturated) or more (polyunsaturated) carbon-carbon double bond (thus the carbons are not saturated with hydrogen atoms). Monounsaturated fatty acids are primarily found in nuts and vegetable oils. The ever-so-popular omega-3 fatty acids are all polyunsaturated and found primarily in fresh fish.
Numerous metabolic disorders have been linked to a deficiency of omega-3 fatty acids (27), so naturally we want to ingest a sufficient amount of these specific fatty acids. The general consensus is that supplementation with 3.5g omega-3 fatty acids (with a DHA:EPA ratio of 2:1) is enough to ameliorate one’s health, but active individuals may require more. (29)
Due to the overall heart and metabolic health benefits of unsaturated fatty acids, it is recommended to ingest the majority of your fat intake from mono/polyunsaturated sources. (30)
Part III: Optimizing Your Peri-Workout Nutrition Plan
Prepare. Perform. Replenish.
There are three pertinent objectives to consider when constructing a peri-workout nutritional plan: preparing the body for training, fueling the body during training, and replenishing the body after all is said and done. Granted these objectives seem pretty straightforward, there are still multiple theories for what is the optimal approach in each instance. Naturally, growth/repair of muscle tissue relies heavily on proper nourishment.
As noted earlier, it is difficult to provide specific nutritional advice to a broad audience since every individual will have variables that can alter what is best for their performance and physique. Research and anecdotal evidence give us general direction and clues, and personal tweaks provide the final touches. It’s important to remember that we’re seeking to optimize the aforementioned three objectives (prepare, perform, replenish) as they pertain to the individual in question. Thus, the optimal peri-workout nutritional regimen will be relative to the individual and their specific needs/training goals.
The good news is that despite the inherent individuality aspect of nutrition, there are still some general protocols that apply to most any individual looking to improve their efforts in the gym. This guide will break down the basic principles of peri-workout nutrition and assess what the research says is optimal. After establishing these fundamental points, this guide will provide further fine-tuning of peri-workout nutrition based on the aforementioned individual factors that come into play. With this in mind we can now direct our attention to peri-workout nutrition protocols.
Phase I: Prepare
If you prefer to train fasted, there is no reason you can’t do so and still achieve great results. Whether or not fasted training offers any significant metabolic advantages over non-fasted (fed state) training is still highly debatable, but the anecdotes I’ve seen from people who follow such a regimen are certainly promising. Obviously fasted training entails that you abstain from food during the pre-workout phase so you can move onto the latter sections of this guide if you please.
Intuitively, many people believe that carbohydrates should be loaded up on prior to and during training since our body readily oxidizes glucose for energy production (via glycolysis). This is what the conventional endurance athlete day-before “carb-loading” routine is based upon as the athlete is looking to fill muscle glycogen stores prior to their event/exercise. If you look at the primary ingredient in the popular sports beverage Gatorade, you will notice it is dextrose (or another form of simple sugar); they throw some electrolytes in the mix and voila, there is your energy in a bottle (metaphorically speaking).
Scientifically/theoretically speaking, loading up on carbohydrates prior to endurance events is a sound proposition, but this protocol is skewed when we throw other goals in the mix, such as maximizing muscle hypertrophy (as well as minimizing muscle catabolism), stimulating lipolysis, and performance enhancement. And last time I checked, most bodybuilders/physique competitors are looking to get as shredded and muscular as possible, not be the next Steve Prefontaine.
The pre-workout (or pre-game) period is ultimately the time to get mentally prepared for the impending workout (or competition), I’d advise individuals to take in foods that digest easy and don’t leave them feeling sluggish. As noted earlier, how you perform after eating a certain meal is just as, if not more, important than the physiological effect of that meal.
Look at it this way, if you’re are not able to perform very well in the gym (or in your athletic competition) because you felt the need to cram down a bunch of food in hopes of propelling muscle growth (or athletic performance), you are actually doing more harm than if you would just eat a nominal meal and have a great training session (or competition).
A “nominal meal” will vary from one individual to another, and it’s just a term I like to use to denote a period of feeding that sufficiently stimulates MPS (which theoretically should be the goal of every feeding period). Given this, the pre-workout phase should emphasize foods that the trainee/athlete tolerates well so their performance is maximized while providing an elevation of MPS. Thus, the main guideline here would be to ensure you eat a 20-30+ gram serving of leucine-rich protein (as noted earlier in the Protein section) and then fill in your carbs and fats according to your preference.
Phase II: Perform
During your training session (or athletic event) you may feel the need to ingest some nutrients to help keep your body “anabolic” and or “anti-catabolic”, but the reality is that if you ate an adequate meal prior to training (1-3 hours before) you don’t absolutely need intra-workout nourishment.
That being said, some endurance athletes (and other athletes) may benefit from a simple-carbohydrate solution (e.g. Gatorade) to replenish their glycogen stores. Moreover, exercise promotes catabolism of EAAs (and specifically BCAAs) so everyday gym-goers and trainees could stand to benefit from ingesting some EAAs/BCAAs during their training, especially if they are training fasted or if it’s been a significant amount of time (roughly 4-6 hours) since the pre-workout meal was ingested. (32) A combination of carbohydrate and EAAs/BCAAs or whey protein would also be a viable option, but not a necessity unless the training session is lengthy.
Phase III: Replenish
The post-training “anabolic window” theory seems to send most trainees into a scurry as soon as they set down there last weight to find the nearest protein shake. As discussed in the adjunct Peri-workout Supplement Guide, the post-workout “anabolic window of opportunity” is not as acute as many people seem to believe, nor is it really all that advantageous in the short-term physiologically.
This is not to say you don’t need to eat after you train. This industry seems to breed extremists, so I don’t want you to get the idea that training intensely for 2 hours and then fasting for a day afterwards is somehow beneficial for muscle growth, because it’s not. Just be practical and use your head, try and eat your next meal after training when it fits your schedule. If that happens 1 to 2 hours after training you’re fine, and no, you won’t suddenly disintegrate into a pile of bone meal just because you don’t chug a whey protein shake 15 nanoseconds after you complete your final rep.
As far as the need to “spike” insulin levels in this period, as discussed in the carbohydrate section that is not a necessity nor does it really provide much extra benefit. Unless you plan on using exogenous insulin (for non-medicinal purposes) than you needn’t worry about taking in a large bolus of dextrose or other fast-digesting carbohydrate.
If you don’t have time to eat a solid meal within a few hours after training, then just pack a protein shake and some on-the-go carbs/fats. Another option would be to sip on some EAAs/BCAAs after training until you have time to eat a complete meal. This would be highly advisable for individuals that choose to train fasted and can’t eat for several hours post training.
Some readers may be a bit disgruntled having read through the guide and not finding any typical quantitative recommendations on the perfect pre-workout ratio of carbohydrates:proteins:fats or what have you. If you still don’t understand why I omitted such blanket statements from this guide it’s because there is no preset universally perfect diet. The permutations of proper nutrition protocols are infinite so I wouldn’t even know where to start with example plans.
My goal with this guide was to impart to the reader the basic knowledge of how the body responds physiologically to training and eating, so with you’ve (hopefully) learned you can use that knowledge and apply it to your own life/routine. The possibilities are really limitless and you ultimately will determine what is optimal and practical for your own lifestyle and diet.
1. 1. Ivy JL. Role of exercise training in the prevention and treatment of insulin resistance and non-insulin-dependent diabetes mellitus. Sports Med. 1997 Nov;24(5):321-36. Review. PubMed PMID: 9368278.
2. Seynnes, Olivier, et al. "Physiological and functional responses to low-moderate versus high-intensity progressive resistance training in frail elders." The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 59.5 (2004): M503-M509.
3. Roth, Stephen. "Why does lactic acid build up in muscles? And why does it cause soreness?: Scientific American." Science News, Articles and Information | Scientific American. N.p., n.d. Web. 22 May 2013. <http://www.scientificamerican.com/article.cfm?id=why-does-lactic-acid-buil>.
4. Fleck, Stephen J., and William J. Kraerner. "Resistance Training: Physiological Responses and Adaptations (Part 2 of 4)." Physician and sportsmedicine 16.4 (1988): 108-12.
5. Hagerman, Fredrick C., et al. "Effects of high-intensity resistance training on untrained older men. I. Strength, cardiovascular, and metabolic responses." The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 55.7 (2000): B336-B346.
6. Wallberg-Henriksson H, Rincon J, Zierath JR. Exercise in the management of non-insulin-dependent diabetes mellitus.Sports Med. 1998 Jan;25(1):25-35. Review. Erratum in: Sports Med 1998 Feb;25(2):130. PubMed PMID: 9458525.
7. Stone, Michael H., et al. "Health-and performance-related potential of resistance training." Sports Medicine 11.4 (1991): 210-231.
8. Tokunaga C, Yoshino K, Yonezawa K (2004). "mTOR integrates amino acid- and energy-sensing pathways". Biochem Biophys Res Commun 313 (2): 443–6. doi:10.1016/j.bbrc.2003.07.019. PMID 14684182.
9. Wullschleger S, Loewith R, Hall MN (February 2006). "TOR signaling in growth and metabolism". Cell 124 (3): 471–84. doi:10.1016/j.cell.2006.01.016. PMID 16469695.
10. Jewell JL, Russell RC, Guan KL (March 2013). "Amino acid signalling upstream of mTOR". Nat. Rev. Mol. Cell Biol. 14 (3): 133–9. doi:10.1038/nrm3522. PMID 23361334.
11. Norton LE, Wilson GJ, Layman DK, Moulton CJ, Garlick PJ. Leucine content of dietary proteins is a determinant of postprandial skeletal muscle protein synthesis in adult rats. Nutr Metab (Lond). 2012 Jul 20;9(1):67. doi: 10.1186/1743-7075-9-67. PubMed PMID: 22818257; PubMed Central PMCID: PMC3488566.
12. Rennie MJ, Bohé J, Smith K, Wackerhage H, Greenhaff P. Branched-chain amino acids as fuels and anabolic signals in human muscle. J Nutr. 2006 Jan;136(1 Suppl):264S-8S. Review. PubMed PMID: 16365095.
13. Katsanos CS, Kobayashi H, Sheffield-Moore M, Aarsland A, Wolfe RR. A high proportion of leucine is required for optimal stimulation of the rate of muscle protein synthesis by essential amino acids in the elderly. Am J Physiol Endocrinol Metab. 2006 Aug;291(2):E381-7. Epub 2006 Feb 28. PubMed PMID: 16507602.
14. Paddon-Jones D, Sheffield-Moore M, Katsanos CS, Zhang XJ, Wolfe RR. Differential stimulation of muscle protein synthesis in elderly humans following isocaloric ingestion of amino acids or whey protein. Exp Gerontol. 2006 Feb;41(2):215-9. Epub 2005 Nov 23. PubMed PMID: 16310330.
15. Koopman R, Verdijk LB, Beelen M, Gorselink M, Kruseman AN, Wagenmakers AJ, Kuipers H, van Loon LJ. Co-ingestion of leucine with protein does not further augment post-exercise muscle protein synthesis rates in elderly men. Br J Nutr. 2008 Mar;99(3):571-80. Epub 2007 Aug 13. PubMed PMID: 17697406.
16. Norton LE, Layman DK, Bunpo P, Anthony TG, Brana DV, Garlick PJ. The leucine content of a complete meal directs peak activation but not duration of skeletal muscle protein synthesis and mammalian target of rapamycin signaling in rats. J Nutr. 2009 Jun;139(6):1103-9. doi: 10.3945/jn.108.103853. Epub 2009 Apr 29. PubMed PMID: 19403715.
17. Wilson GJ, Layman DK, Moulton CJ, Norton LE, Anthony TG, Proud CG, Rupassara SI, Garlick PJ. Leucine or carbohydrate supplementation reduces AMPK and eEF2 phosphorylation and extends postprandial muscle protein synthesis in rats. Am J Physiol Endocrinol Metab. 2011 Dec;301(6):E1236-42. doi: 10.1152/ajpendo.00242.2011. Epub 2011 Sep 13. PubMed PMID: 21917636.
18. Ruderman NB et. al. Minireview: Malonyl CoA, AMP-activated protein kinase, and adiposity. Endocrinology (2003) 144: 5166-5171.
19. Bolster, DR. AMP-activated protein kinase suppresses protein synthesis in rat skeletal muscle through down-regulated mammalian target of rapomyacin (mTOR) signaling. J Biol Chem (2002) 277: 23977-23980.
20. O'Connor, P. M., Bush, J. A., Suryawan, A., Nguyen, H. V., & Davis, T. A. (2003). Insulin and amino acids independently stimulate skeletal muscle protein synthesis in neonatal pigs. American Journal of Physiology-Endocrinology And Metabolism, 284(1), E110-E119.
21. Johnston, C. S., Tjonn, S. L., Swan, P. D., White, A., Hutchins, H., & Sears, B. (2006). Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets. The American journal of clinical nutrition,83(5), 1055-1061.
22. Noakes, M., Foster, P. R., Keogh, J. B., James, A. P., Mamo, J. C., & Clifton, P. M. (2006). Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated fat diets on body composition and cardiovascular risk. Nutrition & metabolism, 3(1), 7.
23. Kimball, S. R., Jurasinski, C. V., Lawrence, J. C., & Jefferson, L. S. (1997). Insulin stimulates protein synthesis in skeletal muscle by enhancing the association of eIF-4E and eIF-4G. American Journal of Physiology-Cell Physiology, 272(2), C754-C759.
24. Koopman, R., Beelen, M., Stellingwerff, T., Pennings, B., Saris, W. H., Kies, A. K., ... & Van Loon, L. J. (2007). Coingestion of carbohydrate with protein does not further augment postexercise muscle protein synthesis. American Journal of Physiology-Endocrinology And Metabolism, 293(3), E833-E842.
25. Dorgan, J. F., Judd, J. T., Longcope, C., Brown, C., Schatzkin, A., Clevidence, B. A., ... & Taylor, P. R. (1996). Effects of dietary fat and fiber on plasma and urine androgens and estrogens in men: a controlled feeding study. The American journal of clinical nutrition, 64(6), 850-855.
26. Kraegen, E. W., Clark, P. W., Jenkins, A. B., Daley, E. A., Chisholm, D. J., & Storlien, L. H. (1991). Development of muscle insulin resistance after liver insulin resistance in high-fat–fed rats. Diabetes, 40(11), 1397-1403.
27. Bernardi JR, Ferreira CF, Senter G, Krolow R, de Aguiar BW, et al. (2013) Early Life Stress Interacts with the Diet Deficiency of Omega-3 Fatty Acids during the Life Course Increasing the Metabolic Vulnerability in Adult Rats. PLoS ONE 8(4): e62031. doi:10.1371/journal.pone.0062031
28. Gingras, A. A., White, P. J., Chouinard, P. Y., Julien, P., Davis, T. A., Dombrowski, L., ... & Thivierge, M. C. (2007). Long‐chain omega‐3 fatty acids regulate bovine whole‐body protein metabolism by promoting muscle insulin signalling to the Akt–mTOR–S6K1 pathway and insulin sensitivity. The Journal of physiology, 579(1), 269-284.
29. American Journal of Clinical Nutrition"; Healthy Intakes of N--3 and N--6 Fatty Acids: Estimations Considering Worldwide Diversity; Joseph Hibbeln, et al.; June 2006
30. NIH Publication No. 01-3290, U.S. Department of Health and Human Services, National Institutes of Health, National Heart, Lung, and Blood Institute, National Cholesterol Education Program Brochure, High Blood Cholesterol What You Need to Know, May 2001
31. Areta JL, Burke LM, Ross ML, Camera DM, West DW, Broad EM, Jeacocke NA, Moore DR, Stellingwerff T, Phillips SM, Hawley JA, Coffey VG. Timing and distribution of protein ingestion during prolonged recovery from resistance exercise alters myofibrillar protein synthesis. J Physiol. 2013 May 1;591(Pt 9):2319-31. doi: 10.1113/jphysiol.2012.244897. Epub 2013 Mar 4.
32. Shimomura, Y., Murakami, T., Nakai, N., Nagasaki, M., & Harris, R. A. (2004). Exercise promotes BCAA catabolism: effects of BCAA supplementation on skeletal muscle during exercise. The Journal of nutrition, 134(6), 1583S-1587S.