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Although different in proportion and muscle articulation, both the classical and contemporary pictures testify to the importance of muscles in images of male strength and power. Large muscles were also supposed to help males attract females, a point that is still emphasized by males working out in gyms. Interestingly, female body-builders reportedly initially pursued the same path illustrated by the picture of Arnold Schwarzenegger.

The result was female body-building champions with smaller but similarly individually developed and articulated skeletal muscles. Genetic treatments are not the only biotechnological approach to increasing muscle size and strength. Anabolic steroids are among the most widely used chemical compounds that are used in combination with weight lifting to increase muscle size and strength. As information about their effects has diffused throughout American society, they are coming to be used more and more by professional and amateur athletes. Use of some of them is banned by anti-doping organizations.

Many including the ones listed above , are listed as available for sale on the Internet. The major cell type present in skeletal muscle fibers is the multinucleated myotube. These fibers arise from the fusion of mononucleated myoblast cells with each other and with pre-existing myotubes.

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Myoblasts, in turn, are formed by differentiation of a particular stem cell found in muscle tissue, called a satellite cell. 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 growth factor HGF and also influenced by hormones such as growth hormone, testosterone and estrogen. Secretion of growth hormone by the pituitary acts on the liver to stimulate synthesis and release of IGF-1, which is released into the circulation Figure 3. In muscle tissue, IGF-1 binds to specific receptors on the surface of satellite cells to stimulate cell multiplication, producing more satellite cells, and differentiation of satellite cells into myoblasts see Figure 4.

Importantly, a slightly different form of IGF-1 mIGF-1 is also produced locally in muscle tissue in response to stretching the muscles exercise. This form is thought to act the same way as circulating IGF-1 does in stimulating satellite cell multiplication 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.

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It is a common human experience that muscle size and strength can be increased by exercise. The number of muscle fibers increases as a consequence of exercise-induced stimulation of the multiplication and differentiation of muscle stem cells. Exercise both transiently damages muscles and causes them to increase in size and strength. While exercise was previously the only way to do this, biotechnological research and.

Figure 4. Schematic diagram of some important processes in skeletal muscle fiber growth and repair. Gene expression vectors have been developed that permit the regulated production of IGF-1 proteins both the liver and muscle forms for investigation.

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With aging, we become more sedentary and use our muscles less. With aging the production of growth hormone and circulating IGF-1 also decreases. There is thus less IGF-1 available to keep the muscles large, and they become smaller and weaker. In addition, aged muscle cells are apparently less responsive to the action of IGF-1 and mIGF-1 6 so that the impact of even vigorous exercise on muscle size and strength diminishes with age.

Gene identified that produces benefits of steroids, without the detrimental side effects

Figure 5 graphically illustrates the appearance of leg muscles as they become smaller and weaker with age sarcopenia. As we age, several things change that predispose to the development of sarcopenia.

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The loss of alpha-motor neuron input to muscle that occurs with age 7 is believed to be a critical factor 8. Nerve cell-muscle cell connections are critical to maintaining muscle mass and strength. A loss of muscle size and strength in a significant problem for older persons. While not painful or directly debilitating, sarcopenia is associated with an increased tendency to fall and break bones.

Such falls and broken bones are major causes of morbidity among the elderly. Figure 5 — Illustrating progressive age-related loss of muscle tissue sarcopenia iii. Selective stimulation of skeletal muscle growth in experimental animals. Recombinant viruses created from genetically engineered human Adenovirus-associated Virus AAV have proved to be efficient delivery systems of foreign genes into muscle cells. As AAV is a small virus, only small foreign genes can be used effectively with this virus.

In experiments described by Barton-Davis and coworkers 9 , AAV recombinant viruses containing a rat IGF-1 gene were injected into the anterior compartment of the rear legs of mice containing the extensor digitorum longus EDL muscle. Assuming such future treatments were shown to be safe and effective, producing sufficient recombinant AAV to treat millions of dystrophic and aging humans would remain a substantial logistical challenge. However, there may be ways around this logistical problem involving the production and transplantation of human muscle stem cells engineered to produce more IGF-1 see below.

The ability to create transgenic mice, in which an appropriately regulated foreign gene is expressed throughout embryonic and adult life, offers another way to assess the biological role s of the transgene product. Musaro et al10 introduced a rat mIGF-1 transgene into early stage mouse embryos, where it became integrated with mouse chromosomal DNA. In these transgenic mice, the rat mIGF-1 transgene was connected to gene expression regulatory elements that restricted production of the rat mIGF-1 protein to muscle tissues containing primarily fast twitch fibers.

Embryonic development of these transgenic mice proceeded normally. However, as early as 10 days after birth, enlargement of skeletal muscles where rat mIGF-1 protein was being produced was observed in the transgenic animals compared to the non-transgenic control mice. Moreover, the skeletal muscle enlargement persisted as the transgenic mice aged.

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Muscle size and strength were maximal around six months in unmodified wild type mice and decreased as expected by 20 months of age. In contrast, at 20 months the size and strength of skeletal muscle in the rat mIGF-1 transgenic mice remained at essentially the same as at six months. In previous studies of this type, the IGF-1 transgene was not connected to gene expression regulatory elements that restricted production of mIGF-1 to muscle tissue.

This led to overproduction of IGF-1 in the circulation, and eventually to pathological enlargement of the heart muscle. The growing understanding of muscle physiology at the molecular level coupled with sophisticated genetic engineering has made it possible to enlarge skeletal muscles selectively, without damaging heart muscles in the process.

These and other experimental results stimulate thought about possible extensions of these approaches to humans. Similar procedures might be useful treatments for various diseases of muscle tissue, and well as a possible use in older persons to counteract sarcopenia. Could these biotechnological approaches be applied to human muscles?

Could the mIGF-1 gene procedures that increase skeletal muscle size and strength in young and old experimental animals be adapted for use in humans? Based on our current understanding, at least three different approaches could be considered. First, one might develop recombinant AAV-based virus vectors containing the human mIGF-1 gene under the control of appropriate regulatory elements that would limit its expression to muscle cells near the site of injection. Alternatively, one might introduce an appropriately regulated mIGF-1 gene into human embryos, as was done in the experiments with mice.

Finally, a combined approach might be developed in which one first isolated human muscle stem satellite cells and expanded them in vitro, next introduced an appropriately regulated human mIGF-1 gene into those cells in vitro, and finally transplanted the genetically modified satellite cells back into the muscles of the person being treated.

The first approach would be similar to other human gene therapy projects. The appropriately regulated human mIGF-1 gene would be combined with a vector capable of efficient delivery to muscle cells, perhaps AAV. This material could be produced in large volumes, carefully characterized by tests in experimental animals, stored frozen and used as needed.

While the logistics of producing the large amounts of recombinant AAV that would be required for treatment of thousands or millions of patients are daunting, in principle this would be possible. The advantages of this approach are 1 that it would develop and use a single, well-characterized biological agent; 2 that treatment could be started very slowly by introducing the recombinant mIGF-1 gene-containing AAV into one muscle at a time and evaluating its effects; 3 that treatment could be stopped immediately if untoward side effects developed.

Disadvantages include 1 the possibility that a large number of injections would be necessary to treat each of the large number of human skeletal muscles; 2 the possibility that this would not be an effective treatment for humans who had antibodies to AAV as a consequence of a previous infection. I swear, under penalty of perjury, that the information in the notification is accurate and that I am the copyright owner or am authorized to act on behalf of the owner of an exclusive right that is allegedly infringed.

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Chemically Engineered Steroid and Muscle

Push beyond your genetic potential using steroids to build massive muscle. If you grew up as a skinny geek like i did then you understand why some people decide to use steroids to push beyond the limits that nature left them with. Or perhaps your just getting to "that age" when your testosterone levels are dropping leaving you are feeling depressed, weak, and would like to feel like your in your 20's again. Perhaps your not sure of you where to start.

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Wondering if you should start on Testosterone E to supplement your bodies natural testosterone production, or use HCG to fool your body into producing its own? Maybe you have been working out for years, but don't seem to be making the kind of gains that you would like.