Skeletal Muscle Contraction - Essay Example

Physiology Student Name/ No: Institution: Date: Essay Question 2: Give an overview of the processes that lead to skeletal muscle contraction (40%).Discuss how these processes are disturbed by muscular dystrophies and with reference to one type of dystrophy explain the mechanism in detail. (60%) Skeletal muscle contraction occurs because of a stimulation in the form of an impulse from a motor neuron. To correctly understand the mechanism of skeletal muscle contraction, evaluation of the nervous response that is necessary for triggering the production of calcium which is the first step towards enabling muscle contraction is required. It’s also very critical to understand the role of calcium in basically turning the skeletal muscle “on” and to comprehend all the steps that are necessary for the muscle to relax after undergoing contraction (MacIntosh, Gardiner and McComas, 2006). Contraction occurs when there is an interaction of myosin, actin, and filaments. Skeletal muscles only contract in sliding filament model (a theory that explains the process under which muscles contract to be able to produce force, the cross bridges that result due to binding end up sliding towards each other eventually creating a contraction). To begin with, an action potential from CNS reaches the motor neuron. This results in action potential down at the axon. The action potential is later on transmitted to the motor neuron, and as a result, it causes an ion influx of calcium through channels that are calcium dependent (MacIntosh, Gardiner, and McComas, 2006). The myosin heads which are present in the skeletal muscle are firmly anchored to the thick filament backbone. Because the myosin heads in the two halves of a thick filament have opposite polarities, acting filaments slide towards the middle of the thick filament while the thick filament remains immobile. Myosin heads hydrolyze ATP during the process of muscle contraction in the skeletal muscle, then become reoriented and re-arranged enabling them to be energized. The contraction cycle continues as long as ATP is released, the Ca2+ level is within the required amounts, and the sarcoplasm remains constant at high concentrations (Gehlert & Suhr, 2015). Later on, the myosin heads bind together with the actin which eventually leads to the formation of cross bridges. The third step in the cycle of skeletal muscle contraction involves the myosin heads rotating towards one of the centers’ of the sarcomere which can also be referred to as a power stroke. The ATP will be changing throughout the entire process after having been converted to ADP. In the final stage of the cycle that eventually lead to muscle contraction, as myosin heads once again bind with ATP, the cross bridges detach from the actin (Herzog, 2000). The entire cycle is continuously repeated several times in each second, as long as the [Ca2+] remain high enough and ATP levels or rather reserves are sufficient. Each power stroke that is present in the muscle will shorten the sarcomere by about 1% because the entire sarcomeres contract together as a unit; the whole muscle will thus shorten at the same given rate. In the skeletal muscle, the action potential will have a very short duration, and if just one action potential arrives at the neuromuscular junction, only one will experience the brief muscle contraction in the skeletal type of tissue specifically. Further contraction will occur only if there are additional action potentials that will arrive in rapid succession and intervals at the nerve terminal. In the calf muscle, the latent timeline and difference in time before muscle contraction is 2 ms (rather action potentials spread across sarcolemma). The phase of contraction will be seen when tension reaches its peak as the muscle fibre contracts, and this occurs for about 15 ms after a single stimulation (Herzog, 2000). When a wide range of action potentials are produced in the sarcolemma, the levels of Ca2+ are kept high in the sarcoplasm and in the long run, contraction cycle will take place over and over with time. When the levels of action potentials are low or finished, the sarcoplasmic reticulum quickly begin to take up and use the released Ca2+ (Ding, Ryder, Stull, & Kamm, 2009). Hence, the Ca2+ levels eventually fall. This drop in [Ca2+] lead to Ca2+ being detached from the troponin-C. Troponin-C then changes its conformation, leading to changes in the tropomyosin conformation. This creates the effect that the myosin binding sites on actin filaments become once again covered by the tropomyosin. This ends the contraction process. Relaxation period for any calf muscle twitch is approximately 25 ms. As the tropomyosin recovers the actin sites, the number of active cross-bridges declines at the same time. Thus, the tension generated by the fibre falls back to its resting levels. It should be noted that; a single twitch is very brief that there no time to activate any significant percentage of the present cross-bridges and therefore any single twitch is ineffective in performing any useful work. Good contraction by skeletal muscle occurs when there is the summation of twitches due to the cascade of action potentials (Hortemo, Munkvik, Lunde, & Sejersted, 2013). Once the contraction has stopped, the sarcomere will not automatically return to the original length. There is no active mechanism for the reversal process. External forces thus act on the contracted muscle fibre to stretch the myofibrils and sarcomeres to their initial dimensions. A muscle fibre returns to its original length through a composition of elastic forces, gravity and opposing muscle contractions. After contraction, there is a sequence of events that turn off the contraction process. At the neuromuscular junction, the acetylcholine is broken down with the aid of acetylcholinesterase that later terminates action potential mainly along the muscle fibre. The sarcoplasmic reticulum stops the release of calcium ions and then starts to sequester all the calcium ions that had been initially released. In case there is the shortage of calcium ions, there will be the change in the alignment of troponin and tropomyosin that blocks the action of molecules of myosin heads, and contraction stops eventually (Klauss, 1973). External force, for instance, gravity or an antagonistic muscle pulls the muscle back to its original length. In a resting position, the motor nerve action potential gets to the motor end plate which then initiates the release of acetylcholine, sarcolemma, and membranes that are depolarized (Na+ flux into fibre). The action potential is transmitted through T-tubules to the sarcoplasmic reticulum. Ca++ that is released from sarcoplasmic reticulum terminal cisternae to the sarcoplasm Ca++ that is bound by troponin. Myosin ATP is activated then ATP gets hydrolyzed. Tropomyosin then shifts from the actin binding site. Actin-myosin influence cross bridge formation. There are repetitive breakdown and formation of cross bridges that results to the sliding of filaments and shortening of a sarcomere. Muscular dystrophy is well known to affect processes involved in contraction of skeletal muscle. Dystrophies refers to a composition of diseases that result to weaknesses in the muscle and loss of mass too. This condition can be inherited. The muscles that are weakened by muscular dystrophies are the ones that are necessary for movement, and once they are affected by these diseases, it means that movement will be hindered upon contraction. Mutations are mainly linked to the interference of protein production which is essential and useful for the healthy formation of muscles. Mutations cause muscular dystrophies when they lead to disassembly of fibres and the cytoskeleton. It eventually results in a compromise of the linkage between these two sections of the matrix. Muscular dystrophies occur in different forms, and they can be observed at early stages in young children, especially in boys. There are some reported cases of the complication appearing soon at infancy up to the middle age proceeding later on. Muscular dystrophy is mainly associated with males. The ailments can affect people in different ways. For instance, certain kinds of dystrophies affect people by showing mild symptoms, although they just lead a normal life until the diseases progresses slowly and eventually live on until they die in their 70s and 80s. However, other people can be affected by the ailment in an entirely different way. Their muscles are swiftly and severely attacked becoming weak, and these symptoms make them waste away more quickly. As a result, some people who have been seriously attacked by the disease at their young age end up dying very quickly in their early stages of life. Dystrophies sometimes result in walking disability as well as problems in swallowing and breathing. This complication does not have a formal cure other than therapeutic treatments and medications that are efficient in slowing down the course of the disease. In some forms of muscular dystrophy, body organs such as the heart are affected. They include: myotonic, Duchenne, Becker, limb-girdle, congenital, oculopharyngeal, distal, emery-Dreyfuss and facioscapulohumeral. Myotonic, for instance, is the most common type especially in adults. The name itself refers to a condition myotonia, which means prolonged spasm and stiffening of the muscles after use. It also affects the central nervous system, the eyes, the gastrointestinal tract and the heart. It also affects the hormone-producing glands. People with this condition are not threatened by their daily living conditions, but their life expectancy is lowered, just like people with the other forms of dystrophies (Guzmán, García, & Rodríguez-Cruz, 2012). Myotonic results from a defect in the genes and is inheritable due to X-linked disorders genetic diseases that mothers can transfer to their sons even though they are not affected by the condition themselves. Unlike women, men have both the X chromosome and the Y chromosome which makes them more susceptible to the condition. Duchenne is another type of muscular dystrophy that is very common in children. However, Duchenne is a form of muscular dystrophy that mainly affects the male children. In most cases, it affects children between the ages of 2 to 6. This condition results from the lack of dystrophin. It is the absence of this protein that causes muscular degeneration (Nowak & Davies, 2004). Dystrophin is part of a large complex of protein composition although it is located in the vicinity. When symptoms start showing up in children, their muscles start reducing in size and grow weaker. Although the condition affects people differently, most males affected by this disease at the age of 12 end up using a wheelchair, since the muscles in the legs are too weak for them to move around with ease. Duchenne is also associated with cognitive impairment, including deformation of the arms and legs. The spine also progressively gets deformed which explains the inability to move properly and the problem of co-ordination of the muscles on the limbs and legs. In severe cases of the condition, there is intense breathing with many complications, and cases of heart problems may also be reported. Children with Duchenne don’t get to live long as they pass away in their late teens. Some forms of muscular dystrophies are not inheritable at all but occur due to new genes or mutation (Servais & Aubert, 2014). The good thing is that advances have been made to ensure proper treatment for the various forms of dystrophies. Muscular dystrophies affect a vast number of people across a wide age bracket, and as a result, many fatalities have been linked to dystrophies conditions. These medical advances have ensured that children with muscular dystrophy can grow into their adulthood and live longer than they did before this milestone in medical treatment was achieved. In conclusion, muscle contraction is very essential as it is significant in the movement process of both the limbs and the hands. Muscle contraction enables movement which is very useful for our bodies as it even allows breathing. The contraction process of skeletal muscles enables walking and running. There are subtle changes produced by the skeletal muscles that allow facial expression, movement of the eye such, as blinking, and respiration processes. It also makes it possible to maintain body posture and the stability of the joints. Poses including sitting and standing are aided by skeletal muscle contraction. All these are attributed to the contraction and relaxation processes. It is therefore very important to ensure that activities that hinder this processes, including dystrophies are well prevented. References Read More