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.