Muscle Fiber Hyperplasia in Bodybuilding and Weightlifting
ByJamesWesley
http://www.pipeline.com/~wjames/MuscleMaker/
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.