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Page 5 of 6
Nuclei: The “Foreman” Of Muscle Growth
It is also important to note the difference in effect of various AAS at non-skeletal muscle tissue. Satellite cells are stem-cell like in that they allow for the growth of muscle tissue. Rather than increasing cell number though, satellite cells enter existing skeletal muscle cells and add to the number of nuclei. This makes little sense at first, as one would think the addition of more muscle cells would be of greater benefit than cells with more than one nucleus, especially since nearly every other cell in the body has only one nucleus (the DNA center). However, it has been shown that skeletal muscle size is directly related to the number of nuclei present in a cell; more so, the nuclei function best if they are located in the center of the cell.23 When satellite cells add nuclei to the skeletal muscle cell, the potential for growth is increased. Confusing as this is, consider each nucleus a foreman who can only manage 10 laborers; if a company wants to increase production, it cannot simply add more laborers but must also add foremen. Thus, for every additional foreman, the company can grow by 10 more laborers. Without adding foremen, the additional laborers would not know what jobs to perform and the company would not grow.
Satellite cells exist between muscle fibers, but do not migrate into muscle cells without being prompted by mechanical and hormonal signals, such as weight training and AAS. Satellite cells come from a pool of even more primitive cell types, referred to as pluripotent stem cells. This long term describes cells that can become more than one type of cell. In this specific case, these pluripotent stem cells can become skeletal muscle or fat cells. To no one’s surprise, when exposed to threshold concentrations of testosterone or certain other AAS, pluripotent stem cells begin the process of becoming myogenic (meaning progressing toward becoming skeletal muscle) as opposed to adipogenic (or becoming fat cells). Thus, in an environment of higher androgen:estrogen presence, changes in the stem cell pool would promote muscle growth and reduce the predisposition toward gaining fat.24
Many people find it difficult to understand the relevance of AR (androgen receptor) binding, as AAS with a higher AR-affinity (meaning how tightly they connect with the androgen receptor) are not necessarily more potent at promoting anabolic or androgenic effects. DHT has a higher AR-affinity than testosterone, but is less effective at promoting muscle growth; 19-nortestosterone has a higher affinity than testosterone, but is less effective in generating androgen-based changes in the prostate. In part, this may be due to the co-regulators mentioned earlier. Very few of these co-regulators have been identified and none are well understood. In each type of tissue (prostate, skeletal muscle, skin, heart, etc.), there are different co-regulators, accounting for many of the differences seen among various tissue types.25 The co-regulators attach onto the AAS-AR complex and help or hinder the complex attaching onto and activating the androgen-sensitive genes in the DNA.26 To attach onto the AAS-AR complex, the co-regulators look for a specific shift in the shape of the molecule, anticipating the openings that would be present if testosterone or DHT combined with the AR. When a synthetic AAS attaches, the AAS-AR may not shift completely, failing to generate the necessary opening for the co-regulators.
In the absence of a complete AAS-AR-co-regulator complex, the genes may not be stimulated to the same degree, if at all. As a number of genes are turned on by testosterone-AR, the possibility exists that changes may be seen in certain genes being activated while others proceed as if the AAS is a completely natural hormone. As stated, this is an area just beginning to be understood and will undoubtedly provide future advancements in this area.
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Research and Review 
