The normal process that muscles go about strengthening is a much more complicated process than I had anticipated.  The major cell type resent in skeletal fibers is the multinucleated myotube, a long cylindrical cell that does the contracting.  These myotubes arise from precursor cells, mononucleated myoblasts, by means of their fusion with each other and with pre-existing myotubes.  Myoblasts (precursor cells), in turn, are formed by differentiation of a particular stem cell found in muscle tissue, called a satellite cell.  Muscle satellite cells are multipotent stem cells that exhibit myogenic, osteogenic, and adipogenic differentiation.[1] 

            The multiplication and differentiation of satellite cells into myoblasts is regulated by several specific protein growth factors (Primarily insulin-like growth factor 1 [IGF-1] and hepatocyte [liver cells] growth factor [HGF].  I will focus on the most used one, IGF-1).  Hormones such as growth hormone, testosterone, and estrogen also influence this process.  Growth hormone secreted by the pituitary acts in the liver to stimulate synthesis of IGF-1 and its subsequent release into the circulation. 

In muscle tissue, IGF-1 binds to specific receptors on the surface of satellite cells to stimulate their multiplication, producing both differentiations of satellite cells into myoblasts as well as more satellite cells.

Importantly, a slightly different form of IGF-1 (muscle IGF-1 or mIGF-1) is also produced locally in muscle tissue in response to stretching the muscles during exercise.  This form is thought to act the same way as circulating IGF-1 does in stimulating satellite cell manipulation and differentiation.  However, because mIGF-1 is slightly different in chemical structure from IGF-1 produced in the liver, mIGF-1 apparently does not enter the circulation, so its effects can be restricted to promoting growth and repair of muscle tissue locally.  Exercise (muscle stretch) increases the production of a specific locally active form of insulin-like growth factor (mIGF-1), a major mediator of muscle stem cell growth and differentiation.  As a consequence of IGF-induced stimulation muscle stem (satellite) cells multiple, differentiate and fuse.  The end result is that the number of muscle fibers increases.  

            Now, how would this work through genetic enhancement? 

            Experiments currently being conducted in animals such as mice are bringing about thoughts of the extension of these experiments to humans.  For humans, they hold out the promise of treated various diseases of muscle tissue, for sarcopenia and the weakness of old age, as well as the general enhancement of muscle strength and fitness in all people.  Biotechnological research and development have introduced the possibility for increasing natural muscle enhancement both on a genetic and pharmacological level.  The DNA sequences for mIGF-1 in not only animals but also humans have been determined and the genes themselves have been cloned.  Now, IGF-1 genes can be inserted into cells through viral vectors to determine the effect of enhanced IGF-1 or mIGF-1 production on muscle size and strength.

            There exists another route towards the same end that exploits the ability at embryonic stages of life, to create transgenic animals in which a foreign gene is expressed throughout the creature’s entire life.  Another case of this was done with mice, still involving the injection of rat mIGF-1 genes, just now into early stage mouse embryos.  After it was injected, it became fused with mouse chromosomal DNA.  The resulting transgenic mice actually produced, themselves, a substantial amount of rat mIGF-1 along with their normal mouse IGF-1 and mIGF-1.  The development of these mice through the embryonic stages was normal.  However, as soon as ten days after birth, the new mice had enlarged skeletal muscles.  As these mice aged, this muscle enlargement continued.  Whereas in normal mice, muscle strength reached its peak at about 6 months, the transgenic mice remained at peak muscle until about 20 months. 

            Based on the current scientific understanding of genetic enhancement, three current methods are believed to be possible.  The first involved the introduced of muscle-enhancing gene directly into one’s muscles.  However, to so, this would require the development of recombinant viral vectors containing the human IGF-1 gene that would be controlled so that the gene would limit its expression to the area around the injection.  The second method uses the introduction of mIGF-1 genes into human embryos (very similar to the previous example with mouse embryos).  The last possibility uses a combination of stem cells and genetic engineering.  First, the human muscle stem (satellite) cells need to be isolated and expanded in vitro, a human IGF-1 gene could be introduced into those cells and then the cells would be transplanted back into muscles. 

            Of course, none of these techniques have so far been used in humans.  There are both upsides and downsides to all three techniques.  From FDA approval, to the cost of the experimentation and development of the techniques in humans and the unforeseeable problems that may occur when trying to implement these on a large population of people, this experiments lie in the not-so-soon future for humans.  Clinical trials on humans for treatment of muscular dystrophy using mIGF-1 may even start within the next few years.  Development is near, and people need to be aware about what exactly their own genetic enhancement entails.  High school coaches have already begun to express interest for their players to undergo the techniques used in mice.  The temptation for this to be done is too great for us to remain ignorant about it; any product that has the entire human race as its consumer focus is almost impossible to resist developing.