Some Steroid Gains Are Permanent
Are Steroids Just a Temporary Fix?
By William Llewellyn
The old adage “steroids are a temporary fix” may in fact be wrong. Former users may notice training advantages long after the drugs have been ended, perhaps indefinitely.
A study published by the National Academy of Sciences is sure to raise eyebrows in the steroid world and anti-doping establishment alike. At first glance, the title may seem quite academic: “Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining.”1The paper, however, discuss an extremely important mechanism involved in muscle growth and athletic performance. More to the point, it provides further evidence that some of the benefits of anabolic steroid use may be permanent. This may change many things, especially for those trying to level the playing field and remove the potential influence of anabolic steroids. I’d like to discuss this paper, and what its potential implications may be for former steroid users.
Muscles and Nuclei
To better understand the findings, I’d like to rewind a little bit and go over some of the very basic mechanics of muscle growth. In adulthood, muscles tend to expand by an increase in the size of muscle cells, not necessarily their number. This process is called muscle hypertrophy. Alternately, when the process involves an actual increase in the number of muscle cells (as in early physical development), the process is called hyperplasia. Muscle cells have an enormous capacity for hypertrophy. Even if they cannot dramatically increase in number, they can become many times larger than their basal states under the influence of exercise, simply via this expansion. This explains why individuals often have remarkable physical transformations with regular training, even well into adulthood.
Hypertrophy involves the synthesis of new contractile proteins, which gives the muscle fibers their strength and texture. These proteins are assembled within the muscle cells from component amino acids drawn in from the surrounding environment. The more contractile proteins that are synthesized, the bigger and stronger the muscle fibers become.
There are other factors controlling muscle expansion, however. One of the most important is the ratio of cell nuclei (muscle cells contain more than one nucleus) to the cell volume. The nuclei are responsible for controlling many cell functions including protein synthesis, but each can only manage a certain maximum cytoplasmic area. The cell cannot grow beyond what its nuclei can regulate. Part of the hypertrophic process, therefore, also involves an increase in the cell nuclei content. These additional nuclei are obtained from neighboring satellite cells, which fuse with damaged muscle fibers and donate their nuclei during the repair/growth process.
Nuclear Permanence
Muscle protein always exists in a state of flux. It is constantly being synthesized and broken down, and many factors can quickly shift the balance to one side or the other. The protein gained is, likewise, usually regarded as a temporary aspect of training and steroid use. It can be easily lost later on. As we can see, however, the process of hypertrophy also involves an increase in one of the most important functional components of the muscle cells, the cell nuclei. It is what happens to these nuclei after training is discontinued, and what this means for the individual, which rests at the heart of this discussion.
The researchers in the cited investigation examined the effects of alternating bouts of resistance/overload training and muscle disuse (denervation) in mice to see what would happen with both the muscle size and cell nuclei content. As predicted, the muscle fiber size increased quickly (approximately 35 percent) with 14 days of overload. The fiber size decreased almost as quickly during disuse, however. The nuclei content, on the other hand, responded very differently. Cell nuclei density did predictably increase (37 percent) with training. Both old and newly acquired nuclei, however, remained within the cell throughout the period of atrophy. In fact, the increased cell nuclei content persisted throughout the experiments, which accounted for a large portion of the animals’ life span. The study suggests that unlike protein content, increased cell nuclei may represent a permanent or near-permanent aspect of hypertrophy.
Benefits/Muscle Memory
According to the findings, an individual with prior training experience is expected to have more muscle cell nuclei than someone will less experience. What does this actually mean, though? As it turns out, there are benefits to having more nuclei beyond a mere expansion of the total manageable cell volume. One advantage, noted in the same study, is a reduced sensitivity to detraining. Cells with more nuclei appear to be more resistant to catabolic processes (protein breakdown). These animals were able to maintain a larger muscle fiber size during disuse, compared to those with lower nuclei content. This suggests that for a given amount of time off, an individual with greater training experience and nuclei density may lose less muscle tissue and performance, compared to a less experienced competitor.
Another advantage may be a greater responsiveness to training, overall. People have long talked about the existence of “muscle memory.” This concept explains that it is easier to regain muscle you have lost than it is to gain it the first time. These new findings suggest that muscle memory is indeed a real phenomenon, and it may be the cell nuclei that are responsible.
The mechanism of muscle memory is fairly straightforward. The individual with prior experience approaches training with a higher concentration of muscle cell nuclei. As the anabolic processes are again stimulated, more nuclei are available to synthesize proteins (each contributing individually). The additional step of drawing in more nuclei is also not necessary. Thus, muscle tissue should be accrued at a faster pace than before, and peak conditioning achieved in less time. Logic suggests that higher nuclei density should also provide some ongoing benefits with the regulation of protein synthesis.
Steroid Memory
Anabolic steroids are known to increases the number of nuclei in muscle cells beyond what’s noticed with training alone.2 The implications for steroid users at once become very clear. If these nuclei are to persist after the drugs are discontinued, then the muscle cells of a past steroid user should have a permanent functional advantage, just as someone with prior training experience has an advantage over someone without such experience. They may have an easier time making physical gains, and maintaining performance improvements, than an individual who has never used steroids. This steroid-memory effect has always seemed logical, and readers may recognize that I’ve even proposed the nuclear permanence angle before. These studies help us better substantiate this theory.
The above findings have a couple of practical implications. For one, the idea of permanent improvements may be very damaging for the anti-doping movement, which at present cannot identify or exclude former steroid users from competing. The ideal of a “level playing field” seems even further away now than it did before. Nuclear permanence also means that the old adage “steroids are a temporary fix” may in fact be wrong. While extreme (beyond normal) physical development indeed will always be difficult to maintain without drugs, former users may notice training advantages long after the drugs have been ended, perhaps indefinitely.
William Llewellyn is widely regarded as one of the world’s foremost authorities on the use of performance-enhancing substances. He is the author of the bestselling anabolic steroid reference guide ANABOLICS and CEO of Molecular Nutrition. William is an accomplished researcher/developer in the field of anabolic substances, and is also a longtime advocate for harm reduction and legislative change. He built the website anabolic.org, an extensive online database of information on anabolic steroids and other performance-enhancing drugs.
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References:
1. Proc Natl Acad Sci USA, 2010 Aug 24; 107(34):15111-6. E-pub, 2010 Aug 16.
2. Anders Eriksson, UMEÅ University Medical Dissertations. New series No 1032, ISBN: 91-7264-101-0.
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