Myostatin Protein Analysis

Muscle atrophy is the loss of skeletal muscle mass and function that occurs when there is a long period of inactivity of the muscles or defects in motor neuron's (Reilly, Beau 2015). Defects in the motor neurons that stimulate the muscle cause the muscle mass to decrease as proteins that initiate contractions of muscle dissipate. Stimulus is not transferred to the weakened muscle fibers effectively, reducing the contractile force possible for generation from the stimulus. Muscle mass increases upon recovery, as restimulation of the muscle enlarges fiber size, thus a greater contractile force can be generated from the stimulus.

When a muscle contracts, myosin heads in thick filaments bind to actin in thin filaments and pulls the thin filament, shortening the length of the muscle fiber. However, without Ca++ when troponin binds to actin, the tropomyosin moves into a position that

Actin and Myosin proteins serve the primary role of producing muscle contraction. Myosin molecules will create pressure in the skeletal muscle, where ATP hydrolysis causes Myosin to bind to Actin. A conformational change of the molecule then result in Myosin being

Under normal conditions, satellite cells are inactive, but become activated when there’s a serious injury, and when muscles lose their nerve supply. Satellite cells repair muscle fibres, but when they become old, they disrupt signals and skeletal muscle cannot be prepared and regenerated effectively. This results in muscle fibre degeneration, an increase in connective tissue between single muscle cells, and weakens the single muscle cell and neuromuscular junction connection (Tsitkanou, Della Gatta, Russell,

. Skeletal muscle make up 50% of total body protein, a compelling loss of skeletal muscle mass deteriorates metabolism, immunocompetence and strength. (Muller et al.) Muscle mass is age dependent, after the age of 50 it is expected that

The article Why Muscles Don’t Break: New Research Offers Possibilities for MD Therapies explains in-depth the functions of the muscles in the human body. Throughout the article the author, Joana Fernandes, presents the extensive amount of research that she has performed regarding this insightful topic. She cites a study published in the Proceedings of the National Academy of Sciences, called “α-Actinin/titin interaction: A Dynamic and Mechanically Stable Cluster of Bonds in the Muscle Z-disk”. Essentially, the study explains that the reason muscles don’t break is due to the two binding proteins called a-actinin and titin. Fernandes utilizes evidence from the study to formulate her article and describe how these two proteins work together in unison to withstand a force of up to five piconewtons, “The experiment showed the bond between these two proteins is able to withstand a force of five piconewtons, a small force comparable to nearly one billionth the weight of a bar of chocolate” (Fernandes). As the article progresses, Fernandes analyzes how such small forces hold a muscle together for a lifetime and explains to the reader that this is possible because there is seven times more strands of a-actinin than titin.

More and more people each year die of an age related disease. One of these diseases is as simple as aging. But what people don’t realize is that no matter what diet they have, exercise is extremely essential for developing healthy muscles as the years go by. The amount of skeletal muscle fibers that people have as kids, and/or young adults can degenerate as people age and lack/decrease in exercise/weight training. The healthy human muscle has the ability to flex and contract and is not very easy to break opposed to an unhealthy human muscle with low muscle fiber levels.

consequently the stopping of the synthesis of the ATP, thus a decrease in the contractile

The skeletal muscles of vertebrates are responsible for all voluntary movements, as well as many involuntary actions. They are made up of many bundles of skeletal muscle cells, called muscle fibers. Within the muscle fibers are bundles of the proteins actin and myosin, which control contraction; these bundles are known as myofibrils. Within a myofibril, repeating units of overlapping actin and myosin filaments make up the sarcomeres. Actin filaments with the sarcomeres are wrapped with tropomyosin, another protein, which has troponin protein molecules attached to it. At end points of the myosin filaments are globular heads which are capable of binding to sites on the actin and moving the actin. The movement of actin by the myosin is referred to as the power stroke. The sarcomeres shorten during contraction (Sedava et al, 2014).

A strong belief in most gyms is that you have to lift heavy weights to build muscle. However, according to a study by Nicholas Burd, “lifting heavy weights may not be the most effective way to build muscle. Muscle growth, sometimes known as hypertrophy, is the development of mass, density, shape, and function of muscle cells. This adaptation allows the muscle to meet exercise, function induced stress. Muscle cells are sort of like a bunch of sticks bundled up for firewood. Myofibrils are cylindrical bundles of filaments composed of sarcomeres. Sarcomeres are the fundamental unit of muscle contraction and are composed of myosin and actin. After you work out, your body repairs or replaces damaged muscle fibers through a cellular process where it fuses muscle fibers together to form new muscle protein strands or myofibrils. These repaired myofibrils increase in thickness and number to create muscle hypertrophy (Kwon and Kravitz). Muscle growth occurs whenever the rate of muscle protein synthesis is greater than the rate of muscle protein breakdown. This adaption, however, does not happen while you actually lift the weights. Instead, it occurs while you rest. So how do you actually add muscle to your muscle cells? This is where satellite cells come in

Protein synthesis takes time and the few hours of muscle cell hyper-expansion doesn't sufficiently exploit this powerful

What is muscle atrophy? Muscle atrophy is the “decrease in size or wasting away of a body parts, tissue, or muscle.” Why is muscle atrophy important? For example if you break your ulna bone and have it in a caste for a few months, than your muscles on the bone that you broke would be considerably diminished to the muscle on your other arm. This raises the questions of “What happens to astronauts muscles in space? And how are we handling muscle atrophy in space?”

Skeletal muscle is the major reservoir of the body proteins and represents 50% of the total body weight. Their function is to provide the body movement, strength, respiration, balance, posture and to regulate the temperature (Lenk et al., 2010).

Satellite cells are cells that can develop into skeletal muscle cells and have been shown to re-enter the cell cycle from G0 to initiate growth of muscle fibers (Lee, 2004). In comparing wild type mice to mutant mice for the myostatin gene it has been shown that there are a larger number of satellite cells in mice that mutant (Lee, 2004). This demonstrates that when the satellite cells leave G0 phase and enter the cell cycle, myoblast begin to develop into muscle fiber cells increasing the muscle mass (Lee, 2004). The growth of satellite cells is beneficial to the body for growth and repair of the muscle cells (Lee, 2004) but not necessary otherwise. In order to ensure normal function of the myostatin gene it is essential to have the cell cycle regulating the myoblasts to stay in a state of quiescent, the G0 phase (Lee, 2004) so they are not being expressed or

“The removal of the gene for myostatin causes differentiation in the muscle.” The muscles would likely become very big and strong pulling on surrounding tendons and bones that might cause tears or fractures. Gene doping is very dangerous and can ruin athletes careers, but they still decide to use because it helps them in a tremendous way. It enhances their ability to perform certain things, but it will catch up with them one day when they get caught and banned from the association they’re with.