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The two sources of cytosolic Ca2+ in smooth muscle cells are extracellular Ca2+, which penetrates through calcium channels, and Ca2+ ions released by the sarcoplasmic reticulum. The increase in cytosolic Ca2+ results in a stronger binding of Ca2+ to calmodulin, which binds and then activates the myosin light chain kinase. The calcium-calmodulin-myosine light-chain kinase complex phosphorylates myosin on the 20 kilodalton (kDa) light chains of myosin on the amino acid residue serine 19, initiates contraction and activates myosin ATPase. Unlike skeletal muscle cells, smooth muscle cells lack troponin, although they contain the thin filament protein tropomyosin and other notable proteins – caldesmon and calponin. Thus, smooth muscle contractions are triggered by the phosphorylation of ca2+ activated myosin and not by the binding of Ca2+ to the troponin complex, which regulates myosin binding sites to act as in skeletal and cardiac muscles. Passive stretching. This type of muscle contraction occurs when your muscle is passively elongated. For example, bend over to touch your toes. There is no extra weight that your thigh muscle needs to hold or lift by exerting strength, but it still stretches from movement. When an event changes the permeability of the membrane for Na+ ions, they enter the cell.

It changes the tension. This is an electrical event called action potential that can be used as a cellular signal. Communication between nerves and muscles is via neurotransmitters. The action potentials of neurons cause the release of neurotransmitters from the synaptic terminal into the synaptic cleft, where they can then diffuse through the synaptic cleft and bind to a receptor molecule on the motor end plate. The end plate of the motor has connecting folds – folds in the sarcolemma that create a large area for the neurotransmitter to bind to the receptors. Receptors are actually sodium channels that open to allow Na+ to pass into the cell when they receive a neurotransmitter signal. Figure 5. When (a) a sarcomere (b) contracts, the Z lines move closer together and the I band becomes smaller. The A-band remains the same width and at full contraction the thin filaments overlap.

Eccentric contractions usually occur as a braking force as opposed to a concentric contraction to protect the joints from damage. With virtually all routine movements, eccentric contractions help keep movements smooth, but can also slow down quick movements such as a punch or throw. Part of the training for fast movements such as throwing in baseball is to reduce eccentric braking so that greater strength can be developed throughout the movement. Myofibrils are made up of smaller structures called myofilaments. There are two main types of filaments: thick filaments and thin filaments; Each has different compositions and locations. Thick filaments occur only in the A-band of a myofibril. Thin filaments attach to a protein in the Z disk called alpha-actinin and occur along the entire length of band I and partially in the A band. The area where the thick and thin filaments overlap has a dense appearance because there is little space between the filaments. Thin filaments do not extend into the A-bands, leaving a central area of the A-band containing only thick filaments. This central area of the A-band appears slightly brighter than the rest of the A-band and is called the H-band (Figure 4).

The center of the H zone has a vertical line called the M line, where accessory proteins hold the thick filaments together. The Z disk and the M line hold the myofilaments in place to maintain the structural arrangement and stratification of the myofibrillus. Myofibrils are connected by intermediate filaments or desmin that adhere to the Z disk. The main component of thin filaments is actin protein. Two other components of the thin filament are tropomyosin and troponin. Actin has binding sites for binding to myosin. Tropomyosin strands block binding sites and prevent actin-myosin interactions when muscles are at rest. Troponin consists of three spherical subunits.

A subunit binds to tropomyosin, a subunit binds to actin, and a subunit binds to Ca2+ ions. The strength of skeletal muscle contractions can be roughly divided into contractions, summation and tetanus. A contraction is a unique cycle of contraction and relaxation generated by an action potential in the muscle fiber itself. [26] The time between a stimulus to the motor nerve and the subsequent contraction of the innervated muscle is called the latency period, which typically lasts about 10 ms and is caused by the time it takes to distribute the nerve action potential, the chemical transmission time at the neuromuscular junction, and then the subsequent steps of the excitation-contraction coupling. [27] A multi-step molecular process in muscle fiber begins when acetylcholine binds to receptors in the muscle fiber membrane. Proteins in muscle fibers are organized into long chains that can interact with each other and reorganize to shorten and relax. When acetylcholine reaches the receptors on the membranes of muscle fibers, the membrane channels open, and the process of contraction of a relaxed muscle fiber begins: heart muscle tissue is found only in the heart, and heart contractions pump blood through the body and maintain blood pressure. Like skeletal muscle, heart muscle is scratched, but unlike skeletal muscle, heart muscle cannot be consciously controlled and is called an involuntary muscle. It has one nucleus per cell, is branched and is characterized by the presence of intercalated discs. Coupling, depolarization conduction and Ca2+ release processes occur in the excitation and contraction of skeletal and cardiac (E-C) muscles.

Although the proteins involved are similar, they differ in structure and regulation. .