Muscle Contraction Essay

As result, the bonding causes the sodium and potassium gates to open. As result, end plate potential is formed and excites areas of muscle tissue. Action potential is created and the muscle moves or contracts.

How is contraction ended? Ach is released and binds to receptors on the motor end plate, then an action potential is produced which releases Ca+. The Ca+ binds to troponin, then myosin binds to actin to form crossbridges. The myosin pulls the actin then releases from actin and ADP is bound to the myosin.

For muscle to contract, actin and myosin filaments need to slide past each other, causing the sarcomere to shorten in length . Each myosin filament has a protruding bulbous head, which can bind with the binding sites on the

The power stroke is responsible for the contraction of the muscle and force generation. ATP binding to the myosin head detaches the myosin head from the actin filament and allows the cycle to repeat. The coordinated contraction and relaxation of many muscles in an antagonistic fashion is the basis for the kinematics of any movement.

Rationale, Significance and Hypothesis. An extrinsic factor, which exerts a dominant influence on skeletal muscle fiber phenotype, is the nervous system. Buller et al. (1960) elegantly demonstrated the plastic nature of skeletal muscle fibers in response to changes in innervation type. Later, Lφmo and Westgaard (Lφmo and Westgaard, 1974; Westgaard and Lφmo, 1988) demonstrated that depolarization of muscle with specific patterns and frequencies of electrical activity are sufficient to cause changes in mature muscle fiber phenotypes. However, how myofibrillar gene expression and structural organization is affected by the frequency of impulses during activity, the amount of activity over time, or other characteristics of patterned activity is essentially unknown. To answer these questions will require the isolation and study of subsets of muscle-specific proteins in relation to different electrical activation patterns in vivo, an issue that cannot be easily addressed in preparations currently used in the study of muscle development and maintenance. However, using novel in vivo approaches can, in part, circumvent this difficulty.

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

Facilitation occurs when postsynaptic potentials evoked by a stimulus are increased when that stimulus closely follows a pervious stimulus. Five stimulus pulses were given at decreasing interpulse intervals. The data for this experimenet displays that when the interpulse interval changes from 10msec to 8 msec, the number of pulses needed to reach the maximum MAP increases rather than the expexted outcome. This is most likely due to movement of the muscle in the chamber, causing the recordings to be reading different areas of the muscle. Different neuromuscular junctions in the muscle require different amounts of Ach in order for muscle action potentials to reach threshold.

If calcium ions levels become too low, insufficient ATP is available or if the action potentials are not passed into the muscle cells, the tropomyosin complex will return to its position covering the active site and the contraction of the muscle cell will no longer

There is cross bridge form with exposed active sites and binding of heads of myosin. This allows contraction of the muscle. In relaxation the neurotransmitter acetylcholine is broken down and calcium ions are recaptured by the sarcoplasmic reticulum preventing the cross bridge formation hence relaxation of muscles occurs. The process involved allows movement. In the nervous system, when one wants to move, the motor cortex in the brain transmits electrical signal through the local nerves and spinal cord. The skeletal muscle is then able to contract and shortened allowing moving. In the process of movement, a feedback signal is send through the nerves to the cerebellum to enhance good coordination of movement. (Fredrick Martini et al,

1.a) Contractile protein molecules that are seen in skeletal muscle fibres are actin (thin filaments) and myosin (thick filaments). Together, they produce the force of muscle contractions by forming cross bridges, and moving via a power stroke. The regulatory proteins that are seen within a skeletal muscle are troponin and tropomyosin. These proteins play a role in starting or stopping muscle contractions. When a muscle fibre is relaxed, there are no contractions because actin is unable to bind with the cross bridge. This is because tropomyosin covers the myosin binding sites on the actin proteins. In addition, troponin is not bound to calcium when a muscle fibre is relaxed, thus keeping the tropomyosin in its blocking position. When calcium enters the muscle fibres, it binds with troponin. This binding causes the tropomyosin to move away

1. Myosin is inactive and folded when smooth muscle is relaxed. The muscle is able to contract when the myosin becomes unfolded. Phosphorylating the myosin regulatory light chain activates the muscle contraction in vertebrates. This phosphorylation is dependent on calcium concentrations. A conformational change occurs when the calcium concentration rises and binds to CAM.This complex is then able to bind to and activate the myosin light chain kinase. This kinase is able to activate the light chain and cause the myosin to contract. Muscles are relaxed when calcium concentrations are low because the light chain is dephosphorylated.

A muscle fiber is a thin, elongated cylinder with rounded ends. Beneath its cell membrane, they cytoplasm contains many small, oval nuclei and mitochondria. This contains threadlike myofibrils, which are parallel to each other.

form of myosin ATP and are not very good at delivering calcium to the muscle

The action potential arrives at the axon terminal. Calcium channels open allowing calcium ions to enter the axon terminal. Acetylcholine is released into the synaptic cleft and calcium ions are pumped out of the axon terminal. Acetylcholine binds to receptor sites on the motor end plate. An action potential is generated which propagates and travels down t-tubulues. The action potential causes the release of calcium ions. Calcium ions trigger a contraction of the muscle cell.