Muscle Observation Report

It can be said that voluntary movement plays a critical role in most vertebrates’ ability to survive. Inside the bodies of vertebrates consist of three muscle types: skeletal, cardiac and smooth (Widmaier et al., 2015, 257). Out of those three, skeletal muscles are primarily responsible for the generation of movement and force (Hopkins, 2006). For humans, skeletal muscles comprise 40% of their entire muscle mass, thus signifying its importance (Hopkins, 2006). However, the ability to generate muscle contractions leading to movement is not an isolated event in the body. Skeletal muscles interact and receive messages from the central nervous system before eliciting any activity (Widmaier et al., 2015, 257). Skeletal muscles are connected

What makes skeletal muscles unique from cardiac and smooth muscles is that they are voluntary, meaning it requires the central nervous system to send nerve impulses to the motor endplates in order to generate a movement (Hopkins, 2006). A plausible and efficient method of how the nervous system works with skeletal muscles is through muscle innervation. Here, a single motor neuron innervates multiple muscle fibers. The site of communication between neurons and muscle fibers is located in the neuromuscular junction. In formality, the process in how these two components communicate is known as the excitation-contraction coupling. The start of this process is when an action potential arrives at the presynaptic terminal (the end of the axon), causing calcium voltage gated channels to open. Leading to an influx of calcium inside the terminal to bind and fuse with the acetylcholine vesicle plasma membranes. Acetylcholine diffuses to the presynaptic cleft until they bind to the Nicotine Acetylcholine Receptors of the motor end plate, leading to a sodium influx inside the muscle fiber. Consequently, a depolarization occurs across the transverse tubules where the ryanodine receptors are activated. Here, the sarcoplasmic reticulum releases calcium into the cytoplasm where the ions will bind to troponin. As a result, this induces a conformational change to the tropomyosin blocking the site where