Are bodybuilders just glycogen?

In order to explain how bodybuilders have large, yet seemingly weak muscles, the concept of sarcoplasmic hypertrophy has been thrown around the strength training sites and has appeared in early editions of some strength training texts (1,2). Under this theory, muscle growth (hypertrophy) can occur through three ways: one where the myofibrillar proteins increase in number, allowing the muscle to have additional sarcomeres and contribute to enhanced force production (increased strength). The second, sarcoplasmic hypertrophy, occurs when components of the muscle sarcoplasm increase while the myofibrillar fraction remains constant (or increases to a smaller degree) that improves fatigue resistance of the muscle with minimal effects on maximal strength. The third method involves what would likely be a reasonable combination of both sarcoplasmic and myofibrillar growth, so that muscle force and endurance would both improve. It’s hard to say precisely how this theory developed, but it has been popularized in recent years to explain the anecdotal differences in strength levels between relatively large bodybuilders and their often smaller powerlifting counterparts.

The problem with the theory of sarcoplasmic and myofibrillar hypertrophy is that despite being theorized decades ago (1,2), there isn’t any significant evidence to suggest that either can occur independent of each other. While it’s nice to theorize that bodybuilders and their higher rep training results in a greater metabolic stress resulting in sarcoplasmic hypertrophy, I haven’t seen any compelling evidence that their training results in growth of only sarcoplasm OR that their levels of strength are really that disproportionate to their muscle size. Leaving debate on sarcoplasmic and myofibrillar hypertrophy aside, I’d like to focus instead on the often cited cause of sarcoplasmic hypertrophy – glycogen accumulation within the muscle.

Can glycogen accumulation explain sarcoplasmic hypertrophy?

Glucose that is not immediately used to fuel the body can be stored as glycogen mainly in the liver and muscle. Glycogen within muscle is a readily-available reserve of glucose to be used during brief, intense or exhaustive exercise. Strength training, especially training styles attributed to bodybuilders (high repetitions, low rest training) taxes not only the high energy phosphate system (creatine), but also relies heavily on glycolytic metabolism (use of glucose as fuel).

Not surprisingly, chronic strength training is associated with increased muscle glycogen stores (3). Seeing that glycogen is a hydrated molecule, often attracting 3-4 grams of water per gram of glycogen (4), it makes sense that having more glycogen in the muscle would increase muscle size as a side effect of fluid retention in the muscle. The concept of intracellular fluid promoting a stimulus for growth is not new, and this mechanism is often cited as a potential mechanism for creatine supplementation-induced muscle growth. Human nature often leads us to evidence that supports our ideas while ignoring what will discredit them, and our theory of sarcoplasmic hypertrophy is no different. So while many articles talk about bodybuilders, glycogen and sarcoplasmic hypertrophy, I’ve compiled a short list of reasons why glycogen is NOT the primary contributor to hypertrophy.

1. Articles stating differences between bodybuilders and powerlifters are often mis-cited.

I hate to be the science police, seems we have enough of them on the internet already, but seeing as this is a concept near and dear to my heart it’s worth addressing. You can’t get through a single article on sarcoplasmic hypertrophy without two books and articles being cited. The first two, Supertraining (1) and Science and Practice of Strength Training (2), simply theorized about the concept, without providing direct evidence for the process itself. Obviously there’s nothing wrong with that, many of us do this for a living and it is essential to think and theorize about this stuff, but the problem is that these are often cited by later articles in a way that suggests the concept is proven, when they were nothing more than ideas at the time.

Now the second two citations are a little more interesting. Both are classic, original reseach studies comparing bodybuilders and powerlifters (the types of studies that don’t seem to happen anymore today). They are usually cited to suggest that bodybuilders have more glycogen than powerlifters (5), and provide evidence that hypertrophy is a different process in bodybuilders than in powerlifters or strength-trained controls (6). Unfortunately neither of these studies provides evidence for sarcoplasmic hypertrophy or elevated glycogen in bodybuilders compared with powerlifters.

The first study (5), cited to suggest bodybuilders have increased glycogen and connective tissue compared to powerlifters, fails to address either case. The first problem is that while bodybuilders and powerlifters were a part of the study, they were actually one group compared to sedentary controls at rest and following a period of strength training. At no point were the bodybuilders and powerlifters compared to each other, so it would be impossible to conclude about any comparison between the two, only between the group of lifters (both bodybuilders and powerlifters) against the control group. It was evident that the elite bodybuilders AND powerlifters had increased cytoplasmic volumes, suggesting that sarcoplasmic growth occurs in each, and when the untrained controls were strength trained the volume of sarcoplasm increased relative to the myofibrillar fraction as well. So this study suggests that increased sarcoplasmic volume occurs in a mixed group of bodybuilders and powerlifters and that traditional strength training programs common in research studies increase it as well. Hardly a strong argument for the existence of sarcoplasmic hypertrophy as the SOLE mechanism of hypertrophy in bodybuilders, or glycogen’s contribution to the process.

Now the second study (6), which is often cited in support of sarcoplasmic hypertrophy as the authors conclude that hypertrophy in bodybuilders is different than for powerlifters, is actually a strong argument AGAINST sarcoplasmic hypertrophy. In this particular study, it was found that a group of elite bodybuilders, despite having larger muscle mass, had muscle fibre areas that were the same size as your everyday phys-ed student (controls). In contrast, the powerlifters had much larger fibres than both the untrained students and the elite bodybuilders. The authors suggest that hypertrophy is different in the bodybuilders, and that the increased muscle mass could be the product of hyperplasia, where bodybuilders would have a larger number of muscle fibres than untrained controls, with a similar size per muscle fibre. So while this article is often cited in the context of sarcoplasmic hypertrophy, it actually suggests that  hypertrophy of individual fibres doesn’t seem to happen at all in the bodybuilders (hard to believe), but rather increased muscle size is explained by elevated numbers of muscle fibres (or a genetic predisposition to increased fibre number to start with). While muscle hyperplasia is now often dismissed as a cause of muscle hypertrophy, it’s surprising that this citation seems to be used as evidence in support of sarcoplasmic hypertrophy when it suggests just the opposite!

2. Other activities increase muscle glycogen without turning people into bodybuilders

When was the last time you saw a 230lb ripped marathon runner? I’ve certainly never seen one. Do Ronnie Coleman or Jay Cutler double as an ultra-endurance athlete on the side? I don’t think so. So while strength training certainly increases muscle glycogen (3), it turns out that endurance exercise does too (7-12), and the increases are very similar or often greater than those produced by resistance training.

Unfortunately these changes aren’t associated with any massive shifts in muscle size (13). If elevated glycogen is swelling up the bodybuilders’ muscles why would it neglect our endurance trained counterparts? I’ve heard mother nature can be cruel, but I doubt she would play favourites like that. Obviously other mechanisms related to the exercise stimulus could interact here, but this at least suggests glycogen isn’t the major player in bodybuilders’ muscle development.

3. Exercise that depletes glycogen doesn’t cause instantaneous muscle wasting

One of the reasons glycogen became involved in the hypertrophy business is that higher rep sets with low rest intervals deplete muscle glycogen stores (14-16). As a consequence of training, the muscle adapts and stores greater amounts of glycogen to deal with the repeated demands of training, which leads to an increase in water of the muscle and ultimately increased cell size. If the logic that a 25% increase in glycogen (3) is a sufficient stimulus for hypertrophy following strength training, what would happen if we depleted it? Do we see immediate and severe muscle loss in proportion to the change in glycogen when we perform exhaustive exercise? Sure we can see large loss of total body water, often reflected by reduced bodyweight (4), but the answer is obviously no, our muscle mass doesn’t spontaneously disappear. While other factors could act to keep water trapped within the cell that was originally related to glycogen storage, it is hard to argue that this increases muscle size when reductions of similar or greater magnitude don’t result in a rapid, pronounced loss of muscle size. I doubt we’d see a bodybuilder lift a weight again if it resulted in near-instantaneous muscle loss. So even if glycogen was the main component of hypertrophy in bodybuilders, other structural changes would have to occur within the muscle or muscle mass would constantly fluctuate in proportion to changes in muscle glycogen.

4. Carb-loading doesn’t give you superhuman muscle mass

Wouldn’t it be great if we could simply perform an exhaustive exercise bout, deplete glycogen, then load up on a high-carbohydrate diet and turn ourselves into a ripped mound of muscle? Is carb-loading a recipe for an instant bodybuilder physique? I don’t think so. We’ve known for decades that we can utilize high carbohydrate diets to produce glycogen supercompensation, often raising glycogen levels to double the normal resting values with very little work (17), but I’ve yet to see a study that it turned anyone into a bodybuilder. Given the propensity to use these techniques in sports where bodyweight is an issue, I would suspect that the effect of glycogen, while increasing total body water, isn’t likely producing massive amounts of what is often termed ‘non-functional’ muscle, despite elevating muscle glycogen.

While carb loading was originally reserved for endurance athletes, more and more physique athletes employ these techniques around competitions to manipulate bodyweight and muscularity. While the effects on performance are well documented, the potential for these techniques to influence muscle size and aesthetics are lesser known. One trial indicated that bodybuilders who employed a carb-loading strategy found no discernible change in muscle size (18), suggesting that manipulating carbohydrate and glycogen levels may not have the effect on muscle size as hypothesized under the sarcoplasmic hypertrophy model. This study relied on fairly crude measures (muscle circumferences) so take that study with a grain of salt, and a large body of anecdotal experience suggests that carb manipulations around competitions can have profound effects. While more work needs to be done, it seems that short-term carbohydrate overdosing likely won’t give you bodybuilder sized muscles, regardless of glycogen levels.


So while glycogen is getting all the glory these days, in my mind, it probably isn’t the sole or  substantial contributor to muscle hypertrophy in bodybuilders. I’m not convinced that bodybuilders are simply swollen sacs of water and glycogen, and that they’re as weak as everyone suggests, and formal comparisons seem to agree (19). A trip over to Zac Even-Esh’s blog will remind you that the bodybuilders of days past often dabbled in many sports (bodybuilding, powerlifting, strongman, olympic weightlifting), and there are certainly many examples of more recent bodybuilders who have smashed many a heavy weight during their training.

While there isn’t conclusive evidence ruling out sarcoplasmic hypertrophy, and there are certainly cases where metabolites (creatine) can potentially induce cell swelling (20,21), the preferential occurrence of sarcoplasmic growth in bodybuilders has never been documented. Based on the limited evidence available, it would seem that any degree of muscle hypertrophy following strength training is associated with an elevated cytoplasmic volume, indicating that sarcoplasmic growth is simply a component of overall muscle hypertrophy (5). Given the fluctuations that occur with glycogen in response to activity and diet, fluctuations that exceed those of muscle mass on a daily basis, it’s likely that other factors have to come into play IF sarcoplasmic hypertrophy is the primary explanation behind bodybuilder’s well-developed muscle mass. Either way, I don’t think we are at the phase where we should be doling out training advice on internet forums based on theoretical molecular adaptations.


    Mark d says:

    First of all would like to say i like reading your articles and your non biased and non influenced view upon which you present the articles.
    Firstly i am a personal trainer from australia and im currently working to studying my degree in nutrition, upon the hopes of one day presenting an actual and factual no bullshit account of the truths of muscle building.
    Your article on are body builders just "glycogen", appealed to me quite astoundingly as this is one "idea" or "concept", that im trying to establish the truth of.
    So i really apprichate your view on the subject and would like your thoughts on the following questions if you have the time.
    Ok so the theory that bodybuilders are just puffed up water weight or stored glycogen ect, is something that is intriging me.
    Take for instance the "standard" rep recomendations for the "different" types of muscular growth ect.
    ok so take for instance 1 to 3 reps near but not to failure on a cycling programme focued on above 85 percent max weight will allow for maximum neurological strength gains with little increase in the size or volume of the muscle.
    Now say 3- 8 reps reaching failure ensuring maximum weight to failure low volume would focus more on the " myofibrillar" growth of the actual muscle.
    Now in terms of sacroplasmic growth from everything that i have learnt, read, studied, this would be higher rep ranges to failure more reps more sets = more fatigue which requires different adaptions of the muscles.
    eg. due to this fatigue of reps and sets ect the body adapts to increase its storage capicity of atp, creatine, glycogen, ect in order to handle this "differnt" stress and metabolic requirement that has been handed to it.
    Put bloody simply, its been run into the ground and fatigued, it adapts in order to handle this stress next time better.
    Ok so for instance focuses on increasing strenght reguardless of rep range, ( since increased volume or a better wording increased strength or load over time), is the only proven requirment of building muscle, then if this occurs reguardless of the rep range there will me adaptions int he myfibrillar context. EVEN IF is is a pump and rep typical bodybuilder workout.
    Now we have established that one can increas size without strength, one can increase strength and actual myfibrillar growth and some volume and myfrib growth.
    So the question that i ask to you is you state that there really is no scientific evidence of sacroplasmic growth, take the follwoing for example./
    Take a trained person who has been focusing on max strength in terms of 4 -8 reps to failure 1 or two sets with decent gains in the past year in so called "true" muscle growth, hard dense and compact.
    Now if for a month you switch this person to a pump and rep high stress high fatigue routine focusing on "sacroplasmic",growth you will undoubtedly see a very visible and scale measurable increase in the size, growth and volume of the individuals muscles due to the increase storage of glycogen, creatine ect.
    This will happen, the individual is allready adavnced growthwise and strenght wise so this growth is comming directly from what you have "appeard", to disprove doesnt actually exist.
    Now if this person returns to there normal programme after sometime this "sacroplasmic" growth will receed due to the bodys no further requirment to keep the extra energy storage becaused its no longer being stressed and fatigued in this manner.
    Would love as detailed a reply on your thoughts to this in contrast to what you wrote in your article.
    My belief is that this Growth does actually occur and the increasced cell volume and storage is a definitive thing.
    Like i said prove me wrong and let me know your thoughts in as much detail and refrences as you can
    Thanks very much for your reply mate.
    Mark d

    Dan Ogborn says:

    Hey Mark,
    Thanks for taking the time to read the site and comment, much appreciated. Glad to see some Australians on here, while I’ve lived in Canada most of my life, I was actually born in Perth, WA.

    As per the hypothetical scenario you provided, you’ve assumed that the metabolites are directly responsible for any changes in size that have occurred. I do agree that the switch in training methodologies may have a more profound effect on metabolite concentrations as you stated, however muscle is more complicated than simply metabolites. I don’t think we can assume that just because we’ve altered metabolites that these are directly responsible for any changes in muscle size. I’ve provided examples of when we can have extremely large changes in muscle glycogen with no alterations in muscle size in the post. I wish I could provide you with citations specific to your scenario, but unfortunately for us many scientists aren’t interested in the differences between bodybuilders and powerlifters these days. It can be hard to reconcile our own theories, our practical experiences in the gym, and what the scientific literature actually supports on these ideas without that.

    To look back at the post, I don’t say that sarcoplasmic hypertrophy can’t/doesn’t occur, but rather that it is a theory, it probably isn’t the sole contributor to the size of bodybuilder’s muscles, and that metabolite (glycogen, creatine, ATP) accumulation as a consequence of training can’t explain the increased size of bodybuilder’s muscles.

    In the final paragraph, I reference a paper (5) that suggests that cytoplasmic volume increases disproportionately to the myofibrillar fraction as a consequence of strength training. This paper is often used to suggest that bodybuilders have a greater amount of sarcoplasmic hypertrophy relative to powerlifters; however, this paper never made that comparison directly and therefore is not supportive of preferential sarcoplasmic growth in bodybuilders. The histological methods used to determine cytoplasmic and myofibrillar growth can be somewhat subjective and have fallen out of favor, and this is likely why we don’t see that measurement popping up in later papers. Nevertheless, this paper is one that you’d like to have in your collection to support what you’ve written.

    I have a series of four posts that relate to sarcoplasmic hypertrophy on the site. If you’ve got the time to check them out, you’ll see I offer a neurological explanation for any strength differentials between bodybuilders and powerlifters, and that the belief that bodybuilders are weak is purely subjective. I’m yet to meet a weak one myself. I address this in a post, where I found a peer-reviewed investigation on lean body mass and strength levels in female bodybuilders and powerlifters that found similar strength levels between the groups (See Sarcoplasm, Women & Weights). If the bodybuilders were more sarcoplasm than myofibrillar protein as compared to the powerlifters, they should have been weaker when equated for lean body mass, but were not.

    In my last post on this (Non-functional Nonsense), I argue that even if bodybuilders are primarily sarcoplasm, we need to stop calling it non-functional, as the adaptations are specific to training (as you provided in your example), and are therefore functional.

    So I haven’t shut the door on sarcoplasmic hypertrophy, but while glycogen may contribute, there has to be other factors involved. I don’t think we are at the level where we can start assuming sub-cellular adaptations based on our program design and what we see in the gym, definitely cart before horse.

    Mark d says:

    Awsome response.
    Haha yeah after the long post i made i, acutally realised that you had several other relating posts on the topic that i hadnt read yet, though i have now.
    And yes its completely true, well in my beliefs and knowledge, that there also is no such thing as "non Functional" Growth, or a weak body builder.

    The adaptions that do occur, In terms of the "Volume", of "sacroplasmic", growth is indeed functional for the body is very simply adapting to the demands which are placed upon it by the type of training programme implemented.

    Where you talk about a "weak" body builder, in my opinion there also is no such thing, well in reality there isnt.

    For instance how to do build a muscle???

    Place a stress on it and the muscle will adapt

    How do you continue to build muscle???

    Continue to place more stresss on the muscle forcing it to adapt and grow.

    So in terms of a weak bodybuilder there is no such thing for in terms to reach there current size ( however big the particiallar "weak" individual is), they will have most definatly increased there proportional strengh compared to there untrained past.

    Now when comparing the two different individuals a power lifter and a body builder they are learning and training and adapting to two different sides of the same coin.

    For instance take the power lifter and submitt him to the bodybuilders workout and his performance will most definatly not be up to par as that of the bodybuilder and the reverse is also quite true, simply remembering our body adapts to the stresses we put on it.

    Now the bodybuilder will be quite strong, however if he changed and adapted his training focusing on attaining the skill required to become more neurologically efficient and had time he would also be very close and on par with that of the powerlifter.

    All the this and thats, when its simply a matter of one person training for a different adaption.

    For instance we can all drive a car but that doesnt mean that we can all drive a formula one car and win. on the reverse the formula one car driver is so efficient at what they do yet put them in a double semi trailer truck and get them to reverse and driver around tight traffic and citys and they will indeed struggle.

    Same actions but differnt skills sets and adaptions required for the tasks.

    We could all lean to be a truck driver or formula one driver.

    Now in terms of the sacroplasmic growth there is one downfall where many starting trainees fail, i to have done this. one will enter a gym and train for a few months sets afters sets, bis and chest ect pumping and pumping.

    now there will be myofribillar growth and neurological adaptions because the person is comming from doing nothing. however if this individual fails to focus on "increasing" the load over time they will indeed stop making these adaptions. so this person will have adapted and gains some good "fluff" Growth which will be out of porportion to strenght ratio for the fact they didnt focus on increasing weight and strenght. I fell victim to this for years.

    However the bodybuilder who focuses on gaining strenght and size reguardless of how they train will indeed be very strong in relationship to there size.

    sorry for the rave on but this is indeed what my life is about and where my true passions are.

    In terms of blogging i definatly will be having a website and a book on my experiences and my life and what it takes to achieve the things ive done with me and clients.

    Since i havent achieved everything yet im not promoting an unfinished product ( meaning me), but love learning loved your discussions.

    Do you like lyle mcdonalds work, and that of martain berkhan???

    sorry for the long post i can email directly or keep posting let us know

    and would love a response to this huge post

    Cheers mate


    Dan Ogborn says:

    Hi Mark,
    Don't worry about the long comments, I appreciate your enthusiasm! I like your idea about waiting to release products, I think too many people start websites and try to monetize them before they even had a chance to fully develop or test their own ideas.

    I love distinctions between the different training methodologies of bodybuilders and powerlifters, however one thing that I see left out is that fact that there is significant overlap between the two groups in their training. Both groups require a degree of strength and size, so it doesn't surprise me to see both take time to use compound and single joint exercises, with different %RM depending on the exercise. It's not uncommon to see bodybuilders using heavy compound exercises with low reps, just as you'll see powerlifters using single joint, isolation exercises with higher reps. Just the proportions of each are different. It's often easy to make them out as training completely different for the sake of argument, but I think that while this may facilitate discussion, in practice their training can be more similar than we make it out to be.

    I've seen Lyle's stuff on the web for awhile, and I've seen Martin's name popping up around the web but haven't gotten around to really digesting his site yet. It is on the todo list though.

    Steven says:

    Ok so how is that bodybuilders increase the number of muscle fibers? Muscle fiber hyperplasia . Under what conditions does it occur? I read this article to familiarize but the answer is not clearly there. <LINK REMOVED>

    Dan Ogborn says:

    Hi Steven,
    Thanks for reading and you ask an excellent question. Unfortunately I can’t give you a great answer because we don’t really have evidence that hyperplasia contributes substantially to hypertrophy in human muscle. Scientifically I’m not in a position to give you specific training advice to induce it.

    The article you linked to did have a pretty balanced account of the situation. The bulk of the info comparing fibre number was from the 80s, with mixed results. Counting individual fibres is problematic and there are serious methodological concerns depending on the technique. We can’t rule out that hyperplasia occurs, but the bulk of the literature would suggest that hypertrophy of existing fibres is likely the primary mechanism. That being said, we can’t rule out hyperplasia and resident muscle stem cells could play a role in generating new myofibres, just difficult to observe experimentally. It has also been suggested that fibre splitting, where intense exercise causes fibres to ‘pinch off’ and break can cause an increase in fibre number, however this wouldn’t necessarily contribute to increased muscle size as it is simply the original fibre split in two.

    At the end of the day, we do have plenty of science and practical experience on how to promote muscle growth, regardless of the knowledge of the underlying physiology (hypertrophy vs hyperplasia). Are you chasing increased fibre number specifically?

    Steven says:

    Who wouldn’t want greater fibre numbers? No I am not specifically pursuing greater fibre numbers. Mostly just curious as to if and or how it might be achieved. I spent some time researching it and have come across some suggests without direct evidence that manipulating fascia may be a way. Suggested methods are long term stretches, stretches during a post exercise muscle pump, message of the fascia and or with the use of foam rollers, balls etc; stretching through direct injection of oils to the muscle or even surgically altering the fascia. It’s basically the idea that new muscle fibre is limited by fascia premise. A lot of speculation but no proof.

    Back to the bodybuilding vs pure strength trainers in muscle size analysis. Poking around in articles I came across the practice of occlusion training or Kaatsu training. Basically restricting blood flow to muscle even at low intensity shorter duration exercises have the same or better benefits to high intensity regular workouts for muscle growth (Note. I did not say strength). I also read some articles on how blood flow is all but stopped in hard contractions of muscles. I would speculate (this is broad speculation) then maybe the muscle size of bodybuilders is similar to the muscle growth benefits of occlusion training. Longer durations in a muscle contracted state with restricting blood flow and the resulting effects. What exactly that is, are beyond my expertise but considering many bodybuilders work at higher rep ranges while still at high intensity for longer durations seems to correlate. The Pump!

    Dan Ogborn says:

    Hi Steven, Definitely some good ideas, hard to prove, but great ideas nonetheless. It really comes down to that it's so hard to accurately quantify an increase in fibre number that it's near impossible to determine whether any of these techniques can change it. Never hurts to experiment though, hopefully!

    alpha1 says:

    I’ve visited the extremes in weight training:
    1. started out with the cliched 8-12 rep weekly scheduled bodybuilding split (for quite a long period – years)
    2. did 6×12 style splits based on serge nubret (for about a year)
    3. I tried doing 25 rep and 50 rep workouts too (few months)
    4. did 3×5 style workouts (for about a year) (Reg Park, Rippetoe, Stronglifts etc)

    In case of (1) – traditional style, I made noob gains in strength and muscles. The gains stopped in year or two, and I started over training (= no progression in weights)

    I did (2) – Serge Nubret style, and the whole body got “inflated”. Serge had advised to keep progressing with intensity (via reps, mind control, less rest, more weights etc). Somehow I could not progress with weights on this. End result was that I could not increase the size beyond a certain limit.

    I don’t recall what possesed me to test the 25 and 50 rep regimen. But there was absolutely NO progression. In fact I felt slight shrinkage.

    So finally I tried the (4) – 3×5 training style. In the beginning I felt I was shrinking (ad people also mentioned I am looking less pumped). But soon (few months) with progression in the weights – I felt that I am growing. Also could actually see that when the clothes started fitting tight. (And people started telling that I am looking more beefed up)

    So from this I can conlude few things:
    a) you will grow ONLY when the weight you are lifting progresses
    b) you will grow fastest (or perhaps not at all otherwise) when you can actually push the limits. In my case doing lower reps actually helped me because in Serge’s style you do 12 reps using a 20-25RM weight, and take only 30 sec inter set rest. Fatigue makes it quite difficult to actually push yourself and progress with loads.
    c) doing high rep (till a certain limit perhaps 15 reps) pumps your body and will make you appear larger. But the muscle feels squishy when you press them). It is like adding 5-10% clay on top of the base sculpture.
    d) high volume and high intensity works only for genetic elites and externally aided people.

    So how is this relevant to this article?
    Simple, I don’t know about sarcoplasmic, myofibril hypertrophy and glycogen storage – but what I felt was that doing low reps allowed me to progress and actually build underlying muscles. Doing high reps kind of inflated the already existing muscles (but can do this only till a limit.

    If you can progress in high reps – it will work for you. You will get more muscles as well as keep them inflated.

    Peter Bielinski says:

    Nice! Well said.

    bartjan says:

    Sorry to respond to a almost two year old post (while haven’t read your other posts on this subject) but I thought you might like my thought on this.

    From research done by Dr. Fry et al (The role of resistance exercise intensity on muscle fibre adaptations: http://home3/danogbor/ we see that weightlifters and powerlifters have a large portion of their muscles as type II, while bodybuilders have equal portions of type I and type II.

    So I would think that doing more reps/sets with shorter rest time results in more type I fiber muscle growth. As type I muscle fiber is weaker then type II fiber, this results in a different absolute-strength/muscle-cross-sectional-area ratio.

    I would like to hear (read) your opinion about this.

    Dan Ogborn says:

    Hi Bartjan,

    No problem, I welcome comments on all posts, no matter how old they may be. I’ve covered thoughts relevant to the Fry (2004) paper in my post on the role of intensity in fibre-type specific hypertrophy. Here’s a link to the post on the site, but these concepts are also addressed in a t-nation article and an upcoming peer-reivewed article I wrote with Brad Schoenfeld.

    joe says:

    What do you guys think of using both a bodybuilding style workout and a powerlifting workout in the same workout session. To be more specific: You start the workout off with a bodybuilding-type workout which not only gives you the high rep/high volume but also serves as a great warmup. Then in the middle part of the workout you do your heavy powerlifting low rep/low volume stuff. And finally at the end of the workout you go back to the bodybuilding-type workout which serves as a burnout to “finish off the muscles” plus it serves as a cooldown. And say both the first and last part of the workout combined (the bodybuilding workouts) would be about the same total volume as the middle powerlifting part. Could this type of workout serve as a good healthy medium between powerlifting and bodybuilding workouts. Just a random idea from a random guy who likes to workout. Would love any input – doesn’t have to be very long.

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