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Thread: Muscle Fiber Hyperplasia in Bodybuilding and Weightlifting. Growth In Muscle Mass

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    Default Muscle Fiber Hyperplasia in Bodybuilding and Weightlifting. Growth In Muscle Mass



    Muscle Fiber Hyperplasia in Bodybuilding and Weightlifting
    By Wesley James


    The dictionary defines hyperplasia as from the latin plasia meaning growth: A nontumorous increase in the number of cells in an organ or tissue with consequent enlargement of the affected part. Corns, calluses and goiters are all examples of hyperplasia. For our purposes, it refers to the growth of new muscle cells and their development into new muscle fibers. To be more exact, we are discussing myofibril hyperplasia. The existence of such a phenomenon, if it does exist, could have dramatic repercussions in bodybuilding. It is the intention of this article to review the current state of knowledge on this subject and to put it into perspective.

    The currently accepted theory of muscle growth is the hypertrophy model. This model holds that we are born with a proscribed number of muscle fibers, which is genetically determined by the twenty-fourth week of fetal development. Muscle growth, this model holds, occurs when repeated stress, such as weight training, causes the fibers to thicken as an adaptive reaction. More precisely, fibers demonstrate a compensatory cross-sectional area increase. The important point here is that most researchers believe that while muscle fibers thicken their number remains constant.

    If the hypertrophy model is correct and, more critically, complete as has long been believed, the implication for the bodybuilder is that the potential to become Mr. Olympia is set long before birth. The industry doesn't want you to think about this to much because if you accept your genetics as a limitation you're less likely to spend money on products that ignore that reality, simple economics. The industry also doesn't want you to look too seriously at hyperplasia because there are no products they can sell you that will produce or even encourage it. The general denial of the prevalence of steroid use reflects the same predicate: If you can't sell it, deny its significance. Some of you may remember how long the magazines of the period denied that steroids had any beneficial effect for bodybuilders. At the same time, magazines want to run photos of steroid enhanced athletes and supplement and equipment sellers want endorsements from these individuals to have credibility. In short, hyperplasia is bad for business, so you haven't read much about it. The more that bodybuilders become aware that muscles with short bellies, as an example, stymie their aspirations the fewer products they will buy. No one wants to accept that their natural shape is less than aesthetically impressive. Nevertheless, shorter muscles have fewer fibers and thus a smaller maximum cross-sectional area. Such unfortunates are, if hypertrophy is the whole story, in fact, genetically doomed to relatively small and less graceful looking muscles. Nature doesn't care about bodybuilders' aesthetics. Short muscles work quite well. Hyperplasia would change the prognosis for such individuals in spite of nature's original intention. Thus, the industry is wrong. If muscle cells are able to split and form new fibers, previous genetic limits might no longer apply. Let's see where we stand.

    William Gonyea was not mad, a sadist nor an animal hater. He did not harbor a diabolical plan to create Arnold Schwartzefeline. Still, Dr. Gonyea made his cats lift weights. In fact, in 1978, using a Skinnerian behavior modification technique known as "operant conditioning", Dr. Gonyea transformed ordinary cats into devoted weightlifters. Gonyea attached weights to his cats' paws then required them to press levers to obtain food. To do so, they had to lift their weighted paws. To simulate progressive resistance training, he gradually increased the amount of weight attached to the cats' limbs. Gonyea was investigating hyperplasia. He was well aware of the debate among scientists as to whether myofibril hyperplasia exists. By attaching weights to his cats paws Dr. Gonyea was attempting to produce hyperplasia. Ultimately, he did. He reported a 19.3-20.5% increase in the number of muscle fibers in his test cats. Some scientists dispute the method Gonyea used to determine the number of new fibers. Others consider the experiment invalid because cats have as many as eleven different types of muscle fibers while humans have no more than five. (They are more often considered to have only two or three.) These researchers argue that Gonyea's work adds nothing to our store of knowledge about human hyperplasia. While superficially true, we have known since at least 1902 that myofibril hyperplasia can occur in humans. At least in those afflicted with Muscular Dystrophy (Erb, 1891) and in pregnant women's abdominal muscles (Durante, 1902). One can reason that if Gonyea produced hyperplasia in healthy cats, and we know that humans are capable of producing hyperplasia (even if only in abnormal states), it is probable that myofibril hyperplasia can be made to occurs in humans. We have no ethical way of proving hyperplasia in vivo because the repeated removal of cells from the same subject on a recurring basis would be invasive and destructive of that individuals healthy muscle function. We are left to prove myofibril hyperplasia indirectly.

    Scientists Tesch and Larsson, in a 1982 study, used an interesting indirect approach. They reported persuasive evidence. Their subjects consisted of three groups: competitive bodybuilders, powerlifters and ordinary, untrained physical education students. Performing minimally invasive fine-needle biopsies on all three groups, their surprising finding was that the world-class bodybuilders showed smaller muscle fibers than the powerlifters. Even more surprising, the bodybuilders muscle fibers were no thicker than the physical education students' who were not weight-trainers. There study was repeated in 1986, to confirm the finding, with the same result. Their conclusion was that the increased muscle size of the bodybuilders was likely the result of fiber-splitting (hyperplasia) rather than hypertrophy. This calls into serious question the almost universally accepted hypertrophy model. One can reason further (even if they didn't). Powerlifters train with fewer reps and heavier weights, In other words, more intensely then bodybuilders; even, as in this case, where the average training experience of the competitive bodybuilders was 10 years. One could reasonably assert that high-intensity training leads to hypertrophy while lower intensity high-load training leads to hyperplasia. Here's how the new model might look.

    Within each muscle fiber there are three different types of sarcomere (muscle cells). They define a fiber as Slow-Twitch or Fast-Twitch. The current trend in physiology is to refer to these as Type I, Type IIa and Type IIb, hence three types. They can best be remembered as running muscle, lifting muscle and jumping muscle respectively. (Type IIb cells may be those most affected by plyometric style training.) Under the hypertrophy theory, the first adaptation the body makes when faced with sustained excess demand is to convert (known as isoform switching) Type IIb cells to Type IIa. (It is not thought possible for the body to convert Type I cells to Type II.) This is one reason why strength increases precede girth increases. This transformation takes about two weeks. If excess demand still persists, the body must turn to another technique, the production of new Type IIb cells. This is the first truly hypertrophic process and a source of long-term strength increase. Since muscle cells themselves are mitotic (don't divide) the new Type IIb cells come from extra-myofibril satellite cells which, unlike muscle cells, do divide. This formation process takes about six weeks. For this reason, in trained bodybuilders, there will be few Type IIb cells at any given time. The mitosis of satellite cells to Type IIb cells and the isoform switch from Type IIb to Type IIa is contemporaneous and continuous. After a period, perhaps as long as two years, the fibers may reach a critical level of thickness. With still continued demand there is further need to adapt. At that point, perhaps only at that point, new fibers begin to form. It is likely the mechanism is for satellite cells to transform into spindle shaped cells called myoblasts. These cells might then differentiate into cells called myotubes. From these myotubes, myofibrils or muscle fibers would form. This is the same process that occurs in utero during fetal development. If this is an accurate depiction of the cycle, the current hypertrophy model could coexist with this newer hyperplasia model. This is not, however, the only possible scenario. Studies performed on elite athletes provide clues to a different pattern. Biopsies done on swimmers' muscles found that their most intensely trained muscles, their shoulders, appeared to have undergone muscle-splitting. Another study looked at cyclists. They rode 4 days a week, 30 minutes per session, for 6 weeks. Biopsies taken from their frontal thighs were observed to show distinct evidence of fiber splitting. This evidence suggests that sustained but lower intensity demand, perhaps regardless of ultimate duration, may encourage hyperplasia. If this is true, different forms of anaerobic exercise may produce different results. This theory seems to be supported by empirical gym wisdom. Let us see if we can find other evidence to support this theory.

    Bodybuilders who use large amounts of anabolic steroids sometimes become afflicted by a disorder called rhabdomyolysis where muscle tissue is destroyed by over-stimulation of the steroid receptors. In these individuals, some new muscle fibers are seen to develop to replace the destroyed ones but with no net increase in size or strength. One might, therefore, suggest that over-stimulation of the steroid receptors combined with the high-rep, high-set, low intensity training (common in steroid using bodybuilders) encourages this pathology or that the steroid overload produces the damage and the training style the compensatory fiber growth. Either explanation is possible and supported by the general evidence. The two major causes of hyperplasia of other types is irritation (such as corns and calluses) and hormonal over-stimulation (such as goiters). If the new fiber production is training related it supports the theory that high-rep, high-set, relatively low intensity exercise encourages myofibril hyperplasia. If it is symptomatic of rhabdomyolysis, we can dismiss the correlation. My investigation of the literature shows no significant research on this subject though rhabdomyolysis does occur in non-athletes.

    There is an additional cause of myofibril hyperplasia that we may look to for data. If training is started while the trainee is still in the growing stage, for example teenagers, hyperplasia is more likely to occur. This is because of the characteristically high HgH levels present during these maturation years. Some research theorizes that HgH combined with high-intensity exercise is capable of stimulating hyperplasia, at least in teenagers. Before you run out to obtain HgH you should be aware that this effect appears to apply only to immature individuals. Ironically, these are the very people that are most harmed by use of exogenous growth hormone. In teenagers it is likely to produce a sometimes grotesque disorder known as acromegaly. The only significant conclusion that can be drawn from this is that one of the hormones produced in the growth cycle plays a role in producing hyperplasia. It should be understood that in spite of all the bodybuilding press to the contrary, HgH does not produce hypertrophy. It isn't even anabolic. If it were, every teenager would have large muscles. HgH is a very effective fat burner and during the re-building process that takes place during sleep it burns fat to provide the energy for repair. HgH is also anti-catabolic while it is present in the system. This anti-catabolic function is, however, primarily prophylactic. The presence of HgH suppresses Cortisol release. In sum, HgH is lipolytic and anti-catabolic but not anabolic under normal conditions.


    Stimulating Hyperplasia

    Let us assume that hyperplasia does exist and can be produced in healthy individuals. Is there any way of encouraging this ostensibly beneficial condition? The answer must be a qualified, yes. A practice, developed with other intentions and strongly advocated by such authorities as Fred Koch, has come to be known as Periodization. It can be applied here. It relates to the idea of having a long term view of what you're trying to accomplish with your training and planning the phases you'll go through to get there. In this case, if you have short, shallow-bellied muscles, you would want to emphasize a pro-hyperplastic phase to create new, additional muscle fibers. A pro-hypertrophic phase would follow to increase the cross-sectional thickness of the fibers, both old and new. If, however, you began with long but less than dense muscles, you might want to stress a pro-hypertrophic phase first. At a later date, you might selectively choose to add additional fibers to those muscles you judge would benefit, then loop through the cycle again. Finally, if and when you got to the point where you were happy with the balance of your muscles, you could use a balanced phase. This would merely maintain what you'd already created. Here's how such programs might be structured.


    The Hypertrophic Phase

    Arthur Jones, Ellington Darden, Mike Mentzer and, more recently, Wayne Wescott, and Dorian Yates, among others have vigorously argued that high intensity training (HIT) is the approach of choice. Their collective opinion and the preponderance of evidence suggests that this type of one set, five to eight (or eight to twelve) reps, Point of Failure training produces optimal hypertrophy. On this point there is little doubt. I have considerable experience with this type of training dating back over twenty years. So do most physical therapists. It is highly effective. At the same time, I would hasten to add that the advocates of this system have, perhaps more than its critics, been its worst enemy. Repeatedly, Mentzer, Yates and the others have lead the rallying cry, "More intensity, more intensity!" It appears they have failed to realize that once a muscle fails, truly fails, any plea for more intensity is meaningless and futile. Here's a simplified explanation of why. Imagine you had only 100 fibers in one of your muscles and each fiber could lift one pound one time. You could then lift 10 lbs. 10 times. At that point you would have exhausted every fiber completely. If, however, you were lifting 15 lbs., you'd get through the first 6 reps but fail on the seventh because it would take 15 fibers to lift the weight again but you'd have only 10 fibers left available. Those 10 fibers might never have contracted in spite of the muscle reaching failure. Still, no appeal for more intensity, no matter how fervent, would change this fact nor give you another rep. Certainly, the body is more complex. There are many more fibers, not all fibers have the same power output, fibers fire more than once during a single contraction and fibers don't deplete uniformly after a given number of contractions. Regardless, and no matter how well one knows ones body, the chances of completely depleting all fibers, even momentarily, is almost non-existent. Ultimately, the Golgi Tendon Organ prevents it So, you see, the cry for ever more intensity is ludicrous. It is essential that you work till failure; that is a given. There may even be value in continuing a set past failure via an immediate reduction in weight (a Break-Down) or with some assistance from a partner or a free hand (a Forced-Rep). Taking a muscle to negative failure may also be of value. Each of these techniques brings the muscle closer to the theoretical "Point of Complete Depletion" (PCD) but failure is another matter. Failure occurs when the body is incapable of performing another unassisted rep at the initial weight. It is for all practical intents and purposes, as hard as you need to work to achieve exceptional results.

    All of the above having been said and in spite of the potential benefit, one might reasonably argue against pushing the muscle past failure to advanced depletion. It may be counterproductive to hypertrophy since hypertrophy is a balancing act between anabolism (the build up of muscle tissue produced by increased protein synthesis) and catabolism (the breakdown of muscle tissue resulting from the inhibition of protein re-synthesis). It also differs from "ketosis" a pathogenic state that signals that the body is cannibalizing its own tissue to supply energy needs, a common mistake in pre-contest training. Fortunately, there is nothing mystical about this balance or the training style. Determining whether you're doing it right is easy. Train with all the weight you can handle for five to eight reps. (I prefer training beginners with eight to twelve reps for the first three months. This is safer and allows the trainee to build up the necessary capillary support network to feed blood and remove waste product from the area.) When you can perform eight strict reps, its time to increase the weight. If the new weight doesn't allow you to perform five reps, use the Rest-Pause technique to get five reps and reduce the weight a bit the next workout. If you find you can perform more than eight reps with the weight, make the ninth rep a Super-Slo rep to force failure after the ninth or, at worst, on the tenth rep. The most important gauge of whether you're doing it right is progress. If you can't perform more reps or handle more weight every workout than you did the previous workout, you're probably training too often. Without question, every workout should be better than the previous one. When you're truly working to failure, in every set of every workout, you get stronger every workout. If you're not, there are three possible explanations. Either you're not working to failure, you're working past failure too often or you're not providing enough time, rest or nutrients for recuperation. Correct the problem and progress is assured. This is how you train to produce hypertrophy. It is tested and proven.

    The second approach, designed to create hyperplasia, is more controversial. Three to eight sets, twelve to fifteen reps, 20 or more sets per body part is advocated here. This popular style of training will likely produce hyperplasia as suggested by the research. Like hypertrophy training, hyperplastic training should produce benefit with every workout but measuring that progress is a considerably more difficult proposition. Theory suggests that the growth of new fibers takes about 96 hours. These new fibers when first created are immature and don't contribute much in the way of additional strength. They should, however, contribute in some small way to the size of the muscle. They should also increase the body's ability to use protein. Unfortunately, neither of these is readily measurable. This makes it difficult to determine whether you're working correctly. The best advice I can offer is that the look of your muscles should change. Over time your muscles should begin to become more striated. You won't, however, see those striations if you're carrying excess body fat (above 15%). When your body fat percentage is low enough the change should be fairly apparent on an almost daily basis.

    While it's inconvenient to measure, there are bio-markers indicating the synthesis of new tissue. If you need concrete proof there is a way to obtain it. Immature tissue is particularly hungry for synthesizing material, primarily glutamine. Using commercially available urine test strips while counting all your daily protein intake, both dietary and supplemental, you would see your excreted urea nitrogen levels drop as utilization increases. This is not a guarantee that new tissue is being formed because other factors can affect nitrogen levels; it is, however, strongly suggestive. particularly when compared against a baseline level. The largest component of muscle tissue, other than water, is protein (up to 90%). New tissue formation surely increase the bodies ability to use protein. All other factors being constant, a body growing protein-hungry new tissue will use more protein. This will result in greater protein utilization, driving excreted nitrogen levels down.

    Finally, however subjectively, your muscles should become visibly less dense, but measurably more "pumpable". As new tissue forms, the fascia surrounding the muscle expands to provide space for the new tissue. At the same time, the body does not wish to sacrifice capillary structures or sarcoplasm. If the fascia expands but the sarcoplasm level remains more or less constant, even with the addition of new tissue, the overall bundle will be less dense in its un-pumped state. This should be particularly noticeable in the hours after the workout pump has subsided but before protein synthesis has met demand. A chart of your nitrogen levels would be at or near the lowest point at this time. That understood, the relatively loose fascia makes for a very pumpable muscle. In theory, very accurate measurements of the upper arm, upper and lower legs would reveal a quantifiable increase over baseline pumped and un-pumped sizes. The actual size difference is not important. It is the percentage of change that's indicative. Such guidelines will have to suffice until better methods of confirming can be developed.

    The goal of this training style is not to continually increase intensity as it is in the hypertrophic phase. Rather, it is to continually increase the total load handled. In the hypertrophic phase, intensity is determined by load and duration. The greater the amount of weight lifted within a fixed period of time the higher the intensity. In this, the hyperplastic phase, duration is much less a factor, though it can not be eliminated from consideration completely. If the work load is too low relative to the duration, the work becomes aerobic rather than anaerobic. Moreover, the duration should not be too great, regardless of load, or it threatens to become too taxing on the body's recuperative ability. The limits of this factor are not well understood. Serge Nubret and some of his protege's have, for years, used a style of training based almost solely on duration rather than load, with apparently excellent result. Generally, the way to proceed in this phase is to begin with three sets of twelve to fifteen reps. When the fifteenth rep of the last set doesn't coincide with failure it's time to add another set. When the last rep of the last of five sets doesn't coincide with failure, it's time to increase the weight and reduce the number of sets back to three. For purposes of this training style, "failure" can be expanded slightly in definition. Failure may, in this case, occur due to capillary insufficiency. This prevents newly produced ATP from reaching local cell sites. Without fuel the cells can not contract. As a general rule, hyperplastic training should be conducted at a faster pace, with less rest between sets. The last set should be performed at an even faster pace then the previous ones. While performing at a faster pace, form should never be sacrificed. Further, during hyperplastic training, the negative aspect of the rep should not be emphasized. Neither should the weight be allowed to drop at the completion of each rep. The weight should be controlled but not resisted. There is significant evidence that it is the negative, eccentric, phase of contraction that produces the micro-cellular damage that is the forerunner to hypertrophy. Since our goal here is hyperplasia rather than hypertrophy, it is undesirable to increase the recuperative burden on the system.

    You should never loose sight of the ultimate goal, to add new tissue. This requires balancing the hyperplastic effect of the training against the strong tendency of the body toward catabolism. Cortisol is the body's bio-chemical agent for catabolism. Training, particularly heavy training, raises Cortisol levels. When Cortisol levels rise, new tissue is favored over old tissue. This raises the potential for a net loss of muscle tissue. This is clearly counterproductive. It is in this area that Anabolic steroids have most helped bodybuilders. steroids bind the muscle's Cortisol receptors reducing the ability of Cortisol to work its catabolic destruction. Were it not for the terrible toll steroid use takes on the body, even in small doses, they could be useful during the hyperplastic phase. Anabolic steroids are laboratory produced mimics of Testosterone, usually with one part of the molecule altered. These alterations make the new compound slower to release and/or more stable passing through the digestive tract. It is Testosterone that is responsible for the larger muscles of men over women. It is possible that Insulin management can provide some protection against the effect of Cortisol. Insulin has an important role in deterring the effect that Cortisol has on muscle tissue. If research is successful in this area, in the near future, the injunction against high-intensity and/or negative training may be removed. Till then, this caveat remains.


    The Maintenance Phase

    The third style of training I will cover in some detail because it is so rarely discussed. It may be called mixed or balanced phase training. It should be pointed out that current advocates of similar training styles don't regard it as a purely maintenance approach. Neither does Dr. Scott Connelly who has endorsed a somewhat similar approach. Nevertheless, for our purposes, balanced training will be used for maintenance. If any growth is produced, it will be the result of over emphasis of one or other style of training. The goal of this phase will be to prevent any form of tissue loss. We don't want muscle fibers to become thinner nor do we want catabolism to reclaim any of the more recently added fibers. This is best accomplished by duplicating, but not exceeding, the load that produced the tissue in the first place. As we've discussed, there are three resistive elements that are responsible for the creation of new tissue. All three must be balanced to maintain that tissue. Two workouts per week should be sufficient for most individuals. During alternate sessions you'll be performing either high-intensity or high-load workouts. The trainee should perform twelve reps, three sets. Failure should be reached on the twelfth rep of the third set. If failure occurs earlier you need to increase trainee frequency. If failure is not reached by the twelfth rep of the third set, you should reduce training frequency. In this way you will hone in on the weight and workout frequency necessary to maintain what you've built in the way of new fibers. To re-emphasize, this form of training is not intended to produce new fibers nor maintain the thickness of your already existing ones. Its only purpose is to forestall the body's tendency to catabolize unused tissue. The thickness of the fibers will be maintained by the high-intensity component of your training. Roughly one session per week you will perform one set, five reps, to failure. If failure occurs before rep five, Rest-Pause your way to eight reps. If you fail to perform five reps without Rest-Pause two workouts in succession, reduce the time between workouts by one day. Should the opposite condition occur, you don't fail after five reps, make the sixth rep a Super-Slo negative. You should fail on the seventh rep. Here again, if you exceed five reps in two consecutive workouts reduce your workout frequency.

    Eventually, you will determine the frequency for both the high-intensity and the high-load components of your training. Once you have found them they should remain fairly consistent for years at a time. With age, hormone, strength and recuperative abilities will change. These will require compensatory changes in your workouts. Otherwise, no change should be required. Finally, at core, bodybuilding, as distinguished from weight training, is an aesthetic pursuit. Your eyes may tell you that a change is necessary. More often then not it is diet and lifestyle that need changing. Your measurements should change very little once you've settled into the maintenance phase. Should you find your measurements and/or bodyweight increasing (particularly your waistline), the problem is probably your dietary fat intake. This can creep upward deceptively quickly. If your daily calorie intake is 2500 calories, one slice of cheese, a mere three grams of fat, can skew the percentage of fat by more than one percentage point. On a recurrent basis that can add a half inch of fat to your waistline rather quickly. Keep your daily fat intake below 15% and your total calories within 25% of your maintenance calorie level and you should be fine. Your daily calorie intake, depending on your metabolic rate, should be between ten and fifteen calories per pound of bodyweight. Add 20 to 30 minutes of 75%-max-heart-rate cardiovascular stimulation two to three times a week and 10 minutes of Yoga and you could die at 105 with a gorgeous body, vital to the end.

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    WHAT IS HYPERPLASIA?

    Hypertrophy refers to an increase in the size of the cell while hyperplasia refers to an increase in the number of cells or fibers. A single muscle cell is usually called a fiber.

    HOW DO MUSCLE FIBERS ADAPT TO DIFFERENT TYPES OF EXERCISE?

    If you look at a good marathon runner's physique and compared him/her to a bodybuilder it becomes obvious that training specificity has a profound effect. We know that aerobic training results in an increase in mitochondrial volume/density, oxidative enzymes, and capillary density (27). Also, in some elite endurance athletes the trained muscle fibers may actually be smaller than those of a completely untrained person. Bodybuilders and other strength-power athletes, on the other hand, have much larger muscles (14,40). That's their primary adaptation, their muscles get bigger! All the cellular machinery related to aerobic metabolism (i.e., mitochondria, oxidative enzymes, etc.) is not necessary for maximal gains in muscle force producing power, just more contractile protein. We know that this muscle mass increase is due primarily to fiber hypertrophy; that is the growth of individual fibers, but are their situations where muscles also respond by increasing fiber number?

    EVIDENCE FOR HYPERPLASIA

    Scientists have come up with all sorts of methods to study muscle growth in laboratory animals. You might wonder what relevance this has to humans. Keep in mind that some of the procedures which scientists perform on animals simply cannot be done on humans due to ethical and logistical reasons. So the more convincing data supporting hyperplasia emerges from animal studies. Some human studies have also suggested the occurence of muscle fiber hyperplasia. I'll address those studies later.

    DOES STRETCH INDUCE FIBER HYPERPLASIA?

    This animal model was first used by Sola et al. (38) in 1973. In essence, you put a weight on one wing of a bird (usually a chicken or quail) and leave the other wing alone. By putting a weight on one wing (usually equal to 10% of the bird's weight), a weight-induced stretch is imposed on the back muscles. The muscle which is usually examined is the anterior latissimus dorsi or ALD (unlike humans, birds have an anterior and posterior latissimus dorsi). Besides the expected observation that the individual fibers grew under this stress, Sola et al. found that this method of overload resulted in a 16% increase in ALD muscle fiber number. Since the work of Sola, numerous investigators have used this model (1,2,4-8,10,19,26,28,32,43,44). For example, Alway et al. (1) showed that 30 days of chronic stretch (i.e., 30 days with the weight on with NO REST) resulted in a 172% increase in ALD muscle mass and a 52-75% increase in muscle fiber number! Imagine if humans could grow that fast!

    More recently, I performed a study using the same stretch model. In addition, I used a progressive overload scheme whereby the bird was initally loaded with a weight equal to 10% of the its weight followed by increments of 15%, 20%, 25%, and 35% of its weight (5). Each weight increment was interspersed with a 2 day rest. The total number of stretch days was 28. Using this approach produced the greatest gains in muscle mass EVER recorded in an animal or human model of tension-induced overload, up to a 334% increase in muscle mass with up to a 90% increase in fiber number (5,8)! That is pretty impressive training responsiveness for our feathered descendants of dinosaurs.

    But you might ask yourself, what does hanging a weight on a bird have to do with humans who lift weights? So who cares if birds can increase muscle mass by over 300% and fiber number by 90%. Well, you've got a good point. Certainly, nobody out there (that I know of), hangs weights on their arms for 30 days straight or even 30 minutes for that matter. Maybe you should try it and see what happens. This could be a different albeit painful way to "train." But actually the physiologically interesting point is that if presented with an appropriate stimulus, a muscle can produce more fibers! What is an appropriate stimulus? I think it is one that involves subjecting muscle fibers to high tension overload (enough to induce injury) followed by a regenerative period.

    WHAT ABOUT EXERCISE?

    The stretch induced method is a rather artificial stimulus compared to normal muscle activity. What about "normal" muscular exercise? Several scientists have used either rats or cats performing "strength training" to study the role of muscle fiber hyperplasia in muscular growth (9,13,17,18,20-22,25,33,34,39,41,42). Dr. William Gonyea of UT Southwestern Medical Center in Dallas was the first to demonstrate exercised-induced muscle fiber hyperplasia using weight-lifting cats as the model (20,21,22). Cats were trained to perform a wrist flexion exercise with one forelimb against resistance in order to receive a food reward. The non-trained forelimb thus served as a control for comparison.

    Resistance was increased as the training period progressed. He found that in addition to hypertrophy, the forearm muscle (flexor carpi radialis) of these cats increased fiber number from 9-20%. After examining the training variables that predicted muscle hypertrophy the best, scientists from Dr. Gonyea's laboratory found that lifting speed had the highest correlation to changes in muscle mass (i.e., cats which lifted the weight in a slow and deliberate manner made greater muscle mass gains than cats that lifted ballistically) (33).

    Rats have also been used to study muscle growth (25,39,47). In a model developed by Japanese researchers (39), rats performed a squat exercise in response to an electrical stimulation. They found that fiber number in the plantaris muscle (a plantar flexor muscle on the posterior side of the leg) increased by 14%. Moreover, an interesting observation has been made in hypertrophied muscle which suggests the occurrence of muscle fiber hyperplasia (13, 17, 28, 47). Individual small fibers have been seen frequently in enlarged muscle. Initially, some researchers believed this to be a sign of muscle fiber atrophy. However, it doesn't make any sense for muscle fibers to atrophy while the muscle as a whole hypertrophies. Instead, it seems more sensible to attribute this phenomenon to de novo formation of muscle fibers (i.e., these are newly made fibers). I believe this is another piece of evidence, albeit indirect, which supports the occurrence of muscle fiber hyperplasia.

    EXERCISE-INDUCED GROWTH IN HUMANS

    The main problem with human studies to determine if muscle fiber hyperplasia contributes to muscle hypertrophy is the inability to make direct counts of human muscle fibers. Just the mere chore of counting hundreds of thousands of muscle fibers is enough to make one forget hopes of graduating! For instance, one study determined that the tibialis anterior muscle (on the front of the leg) contains approximately 160,000 fibers! Imagine counting 160,000 fibers (37), for just one muscle! The biceps brachii muscle likely contains 3 or 4 times that number!

    So how do human studies come up with evidence for hyperplasia? Well, it's arrived at in an indirect fashion. For instance, one study showed that elite bodybuilders and powerlifters had arm circumferences 27% greater than normal sedentary controls yet the size (i.e., cross-sectional area) of athlete's muscle fibers (in the triceps brachii muscle) were not different than the control group (47). Nygaard and Neilsen (35) did a cross-sectional study in which they found that swimmers had smaller Type I and IIa fibers in the deltoid muscle when compared to controls despite the fact that the overall size of the deltoid muscle was greater. Larsson and Tesch (29) found that bodybuilders possessed thigh circumference measurements 19% greater than controls yet the average size of their muscle fibers were not different from the controls.

    Furthermore, Alway et al. (3) compared the biceps brachii muscle in elite male and female bodybuilders. These investigators showed that the cross-sectional area of the biceps muscle was correlated to both fiber area and number. Other studies, on the other hand, have demonstrated that bodybuilders have larger fibers instead of a greater number of fibers when compared to a control population (23,30,36). Some scientists have suggested that the reason many bodybuilders or other athletes have muscle fibers which are the same size (or smaller) versus untrained controls is due to a greater genetic endowment of muscle fibers. That is, they were born with more fibers.

    If that was true, then the intense training over years and decades performed by elite bodybuilders has produced at best average size fibers. That means, some bodybuilders were born with a bunch of below average size fibers and training enlarged them to average size. I don't know about you, but I'd find that explanation rather tenuous. It would seem more plausible (and scientifically defensible) that the larger muscle mass seen in bodybuilders is due primarily to muscle fiber hypertrophy but also to fiber hyperplasia. So the question that needs to be asked is not whether muscle fiber hyperplasia occurs, but rather under what conditions does it occur. I believe the the scientific evidence shows clearly in animals, and indirectly in humans, that fiber number can increase. Does it occur in every situation where a muscle is enlarging? No. But can it contribute to muscle mass increases? Yes.

    HOW DOES MUCLE FIBER HYPERPLASIA OCCUR?

    There are two primary mechanism in which new fibers can be formed. First, large fibers can split into two or more smaller fibers (i.e., fiber splitting) (6,25,39). Second satellite cells can be activated (11,16,17,43,44).

    Satellite cells are myogenic stem cells which are involved in skeletal muscle regeneration. When you injure, stretch, or severely exercise a muscle fiber, satellite cells are activated (16,43,44). Satellite cells proliferate (i.e., undergo mitosis or cell division) and give rise to new myoblastic cells (i.e., immature muscle cells). These new myoblastic cells can either fuse with an existing muscle fiber causing that fiber to get bigger (i.e., hypertrophy) or these myoblastic cells can fuse with each other to form a new fiber (i.e., hyperplasia).

    ROLE OF MUSCLE FIBER DAMAGE

    There is now convincing evidence which has shown the importance of eccentric contractions in producing muscle hypertrophy (15,24,45,46). It is known that eccentric contractions produces greater injury than concentric or isometric contractions. We also know that if you can induce muscle fiber injury, satellite cells are activated. Both animal and human studies point to the superiority of eccentric contractions in increasing muscle mass (24,45,46). However, in the real world, we don't do pure eccentric, concentric, or isometric contractions. We do a combination of all three. So the main thing to keep in mind when performing an exercise is to allow a controlled descent of the weight being lifted.

    And on occasion, one could have his/her training partner load more weight than can be lifted concentrically and spot him/her while he/she performs a pure eccentric contraction. This will really put your muscle fibers under a great deal of tension causing microtears and severe delayed-onset muscle soreness. But you need that damage to induce growth. Thus, the repeated process of injuring your fibers (via weight training) followed by a recuperation or regeneration may result in an overcompensation of protein synthesis resulting in a net anabolic effect (12,31).

    HAS THE DEBATE BEEN SETTLED?

    In my scientific opinion, this issue has already been settled. Muscle fiber hyperplasia can contribute to whole muscle hypertrophy. There is human as well as rat, cat, and bird data which support this proposition (1-3,5-8,13,17,20-22,25,29,35,37,47), a veritable wild kingdom of evidence. Does muscle fiber hyperplasia occur under all circumstances? No. There are several studies which show no change in fiber number despite significant increases in muscle mass (4,18,19,23,26,30,36,41).

    Is it possible that certain muscles can increase fiber number more so than others? Maybe. Can any Joe Schmoe off the street who lifts weights to get in better shape increase the number of fibers for instance in their biceps? Probably not. What about the elite bodybuilder who at 5'8" tall is ripped at a body weight of 250 lbs.? Are his large muscles purely the result of muscle fiber hypertrophy? I think it would be extremely naive to think that the massive size attained by elite bodybuilders is due solely to fiber hypertrophy! There is nothing mystical about forming new muscle fibers.

    Despite the contention that fiber number is constant once you're born (18,19), we now have an abundance of evidence which shows that muscle fiber number can increase. Besides, there is nothing magical at birth which says that now that you're out of the womb, you can no longer make more muscle fibers! A mechanism exists for muscle fiber hyperplasia and there is plenty of reason to believe that it occurs. Of course, the issue is not whether fiber number increases after every training program, stress, or perturbation is imposed upon an animal (or human). The issue is again, under which circumstances is it most likely to occur.

    For humans, it is my speculation that the average person who lifts weights and increases their muscle mass moderately probably does not induce fiber hyperplasia in their exercised muscle(s). However, the elite bodybuilder who attains the massive muscular development now seen may be the more likely candidate for exercise-induce muscle fiber hyperplasia. If you are interested in a comprehensive scientific treatise on this subject, read a scientific review article that I wrote a few years ago (7).

    KEY TERMS

    anabolic - in reference to muscle, a net increase in muscle protein
    catabolic - in reference to muscle, a net decrease in muscle protein
    concentric - shortening of a muscle during contraction
    eccentric - lengthening of a muscle during contraction
    hyperplasia - increase in cell number
    hypertrophy - increase in cell size
    isometric - no change in muscle length during a contraction
    mitochondria - is an organelle ("little organ") found within cells and is involved in generating ATP via aerobic processes
    muscle fiber - also known as a myofiber; is the multinucleated cell of skeletal muscle
    myoblast - an immature muscle cell containing a single nucleus
    myogenesis - the development of new muscle tissue, esp. its embryonic development
    satellite cell - are the cells responsible in part for the repair of injured fibers, the addition of myonuclei to growing fibers, and for

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