Double Muscling Research Paper

Double muscling is a phenotype that is known to enhance the muscle mass of an individual. The Myostatin (MSTN) gene (Bellinge et al. 2005) causes the double muscling phenotype. When an individual possesses the MSTN gene, they will experience a larger amount of muscle mass (Bellinge et al. 2005), however, an individual must be homozygous for MSTN to show the phenotype (Bellinge et al. 2005). This means that they must possess two MSTN genes in order to be double muscled (Bellinge et al. 2005). Double muscling occurs because muscle fibre composition is no longer controlled (Bellinge et al. 2005). The MSTN gene is triggered by a Frameshift mutation that results in the deletion of some nucleotide bases in the gene (Bellinge et al. 2005). The MSTN gene has been
researched for treatment use on mice, and may benefit humans in the future. The MSTN gene has considerable potential to be used a physical therapy strategy for both mice and humans. This MSTN gene has the potential to help people struggling with muscle loss to regain muscle (Lee 2004). The MSTN gene facilitates the growth and maintenance of muscles in these individuals (Lee 2004). The addition of MSTN to people experiencing muscle loss would allow these individuals to redeem lost muscle (Lee 2004). The MSTN gene would regenerate muscle fibres (Bellinge et al. 2005) and improve the muscle capability (Lee 2004). This allows the muscles to develop properly. This type of treatment may also be applicable to those experiencing obesity and/or type II diabetes (Lee 2004). The addition of MSTN into the system of an obese person would prevent body fat from collecting, therefore, gaining more muscle (Lee 2004). If this treatment is successful, then the MSTN gene could be fully introduced to humans as a form of treatment. The MSTN gene is also effective in treating injured mice (Joulia-Ekaza and Cabello 2007).
A new technique has been developed where the MSTN is injected into an injured mouse using a needle (Joulia-Ekaza and Cabello 2007). This technique has only been tested on laboratory mice (Joulia-Ekaza and Cabello 2007). The injured mice were proven to have restored skeletal muscles sooner than their wild-type counterparts who did not receive the MSTN treatment (Joulia-Ekaza and Cabello 2007). When the mice are injected with the MSTN gene, their muscle function tends to increase (Joulia-Ekaza and Cabello 2006). The MSTN treated mice also experienced a large increase in structural cells within a given area of the body (Joulia-Ekaza and Cabello 2007). It is important to recognize that these treated mice do have improved muscle function and they still maintain a normal muscled phenotype (Joulia-Ekaza and Cabello 2006). This is significant because the MSTN treatment does not affect the physical body image of a mouse, which may encourage future human patients to receive treatment with the MSTN gene. This MSTN treatment is underway, but does not yet have an exact role in the field of treatment and physical
therapy. In conclusion, the MSTN gene has considerable potential to be used as a physical therapy strategy (Lee 2004). The MSTN gene is fairly successful in treating laboratory mice (Joulia-Ekaza and Cabello 2007), and therefore could be a successful treatment option for chronic muscle loss, obesity, and type II diabetes in humans. Although the exact treatment role of the MSTN gene has not yet been established (Joulia-Ekaza and Cabello 2007), the double muscling gene has large potential in the future.