The sliding theory of Muscle Contraction
Animals are made of a skeletal system that has various functions, among them stimulating movement in animals. In the process of movement, the muscles attached to the skeletal system are also useful since it is their contraction and relaxation that causes movement. The process of muscle contraction starts with the motor neuron sending a signal, mainly the neurotransmitter, thus causing fiber innervation. As a result, there would be depolarization of the local membrane of the fiber that would further make positively charged sodium ions to get in and trigger an action potential that will then spread to the whole membrane, thus making it depolarized (Shiffman, 2011). The T-tubules will also be with be depolarized in the process. As a result, the sarcoplasmic reticulum will be triggered to produce the stored calcium ions, which then initiate the process of contraction that is maintained by adenosine triphosphate. The muscle is bound to contract to the shortest possible anatomical limit if troponin has been bonded by calcium ions that have remained in the sarcoplasm. Troponin is responsible for un-shielding active binding sites. Besides, adenosine triphosphate should be in place to facilitate cross-bridge cycling and ensuring that myosin is pulling actin strands.
During the process of muscle contraction, the neuromuscular junction plays a significant role in creating contact between muscle fiber and a motor neuron. The motor neuron is mainly charged with facilitating movement through impulse delivery. It is at the myoneural junction that then the motor neuron can easily transit a signal to the muscles that will then trigger muscle contraction (Shiffman, 2011). Each motor neuron is connected to muscle fiber and has its cell body at the central nervous system and have axons and axon terminals at the further end that then penetrate the perimysium of the muscle. The synaptic end bulb refers to the tip of the axon near the muscles that has enlarged in size and mainly constitutes the nervous system components at the myoneural junction (Shiffman, 2011). The motor endplate, on the other hand, is the muscular component of the muscle fiber. The synaptic cleft, on the other hand, is useful in ensuring that action potential coming from the nervous system at the neuromuscular junction is transverse mainly by ensuring the electrical signals that are turned chemical so that they can easily pass by the synaptic cleft. The mitochondria are the essential organelles found within the muscle cells in numbers to ensure the production of metabolic energy for muscle contraction (Shiffman, 2011). Besides, the endoplasmic reticulum also acts to assist the mitochondria in maintaining homeostasis and filtering molecules to enhance the function of the mitochondria.
The sliding filament theory is a submission that seeks to explain the process of muscle contraction by mainly analyzing the behavior of the actin filaments, sarcomere, and the myosin filaments. Using high-resolution microscopy, it was established that during the process of contraction, a part of the sarcomeres remain constant while the other reduced in length. The muscle is made up of striations of essential muscle elements that are referred to as sarcomeres, which are mainly arranged in a stacked pattern in muscle tissues (Shiffman, 2011). The sarcomeres are made up of proteins that can change in length, thus causing a change in muscle length. The sarcomeres contain actin and myosin filaments whose interaction causes a change in length of the sarcomeres and further the muscle, thus the sliding filament theory (Squire, 2016). The theory explains that during a process of muscle contraction, thick myosin filaments remain centrally constant and do not change in length while the actin filaments thin in nature changed shortened in length together with the sarcomere. The movement of the actin filaments is always referred to as a power stroke. A cross-bridge which is necessary for the process is formed when the myosin-binding site is exposed by the tropomyosin on an actin filament (Squire, 2016). As a result, the sliding filament theory was described as the sliding effect between the actin and myosin filaments with further causes muscle contraction. The theory explains that sarcomeres change in length together with the actin filaments since the actin filaments are connected to the lateral ends of the sarcomeres; thus, the change in length of the actin filaments would also cause a resultant change within the sarcomeres.
The process of muscle relaxation begins with the action of the motor neuron not releasing its chemical signal to the neuromuscular junction. The process will eventually also lead to a relaxation of the skeletal system. As a result, the muscle fibers will automatically repolarize, thus inhibiting the production of calcium ions by the sarcoplasmic reticulum. Further, the actin-binding sites that are mainly found on the thin filaments within the sarcomere will have to re-shield (Squire, 2016). As a result, the thick and the thin filaments would have it impossible to form cross-bridges, thus loss
Shiffman, C. (2011). Electrical impedance changes during muscle contraction. Muscle & Nerve, n/a-n/a. https://doi.org/10.1002/mus.22148
Squire, J. (2016). Muscle contraction: Sliding filament history, sarcomere dynamics and the two Huxleys. Global Cardiology Science And Practice, 2016(2). https://doi.org/10.21542/gcsp.2016.11
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