What is the sliding filament theory and how is tropomyosin involved?

The sliding filament theory is the process of how a muscle contracts. Muscles are made up of many smaller units called myofibrils each containing thousands of contracting units called sarcomeres. These sarcomeres contain myosin (thick) filaments and actin (thin) filaments. On the actin filament are proteins called Troponin and Tropomyosin. When Calcium is released from the sarcoplasmic reticulum, it binds to these proteins and causes them to change shape. This causes tropomyosin to move out of the myosin binding site on the actin filament. This means that the globular head of the myosin filament is free to bind to the actin filament. As it does so, through the use of ATP, it bends and moves the actin filament closer to the centre of the sarcomere, hence causing the myofibril to shorter and the muscle to contract. It then releases itself and binds to another actin filament closest to the sarcomere’s centre and will repeat this process of binding and releasing until the muscle is fully contracted.

Tropomyosin is really important in muscles but it does not come alone as attached to tropomyosin is troponin. Both of these are attached to actin (the is the thin microfilament in muscles). When troponin is attached to tropomyosin it blocks the siding of actin over myosin so no muscle contraction can happen. However, when troponin is removed from tropomyosin this means tropomyosin can attach to myosin (forming an actin-myosin crossbridge) and allowing myosin to be slid over actin (like a rowing movement).

This answer is to make sure that your understanding is solid however together we would ensure that the model answer involves all the necessary exam technique.

For muscle contraction, there are actin and myosin filaments. Calcium binds to troponin and changes the shape of one of muscle filament bands. This causes tropomyosin to move and expose myosin binding sites on actin filaments. The actin and myosin filaments form a bridge and slide over each other which causes the muscle fibres to shorten and hence contract.

The sliding filament theory is a model of how muscle contraction takes place at a molecular level in skeletal muscle fibres.

There are two types of filaments involved: actin (thin filament) and myosin (thick filament). The actin filament is tightly wrapped in a thinner filament called tropomyosin and also spherical proteins called troponin. The troponin is what tightly binds tropomyosin to the actin filament.

Calcium ions released from the sarcoplasmic reticulum target the troponin proteins and bind to them causing a change in shape. This ultimately loosens the tropomyosin filament thus the actin is less tightly wrapped. In addition to this, myosin binding sites on the actin filament are now exposed.

The sliding filament theory describes the action myosin makes as it "slides" past the actin filament to mediate muscle contraction. The myosin heads bind to the now exposed myosin binding sites on the actin and undergo a series of chemical reactions resulting in the myosin being pulled up each consecutive myosin binding site (much like a rowing team going up a river). Finally, ATP is required to shift the myosin heads back to their starting position to bind to the next myosin binding site.

The sliding filament theory details how the muscle contracts and relaxes. At first a calcium ion will attach to a troponin molecule- this in turn causes the tropomyosin to expose myosin binding sites on actin. This joining causes ADP and phosphate to be released from the head of the myosin. This moves the head forwards over the actin. ATP is formed from the ADP- this energy is used to detach the head from the actin. The ATP is returned back to ADP and Pi via hydrolysis conducted by the enzyme: ATPase found on the head. This in turn allows the myosin head to return to its original position.

Tropomyosin is a molecule that in resting position- blocks the myosin binding sites so that the head cannot bind.

Muscle fibers contain units known as Actin and Myosin. Actin is associated with Tropomyosin and Troponin's C,I, and T, together these structures form the thin filament. Myosin forms the thick filament and consists of Myosin heads which have an ATPase function. During the sliding filament model of muscle contraction, calcium efflux from the smooth endoplasmic reticulum occurs. These calcium ions bind to Troponin C, which causes a conformational change in the shape of the Troponin complex and also displaces Tropomyosin which covers the Myosin binding site on Actin proteins - allowing the formation of a cross bridge. Myosin ATPase hydrolyses ATP which yields the energy required for a power stroke to occur in which the thin and thick filaments slide past one another leading to muscle contraction.

The sliding filament theory describes how muscles contract by the sliding of actin and myosin filaments within the muscle fibre or sarcomere. Myosin heads attach to an actin filament, bend to pull the actin filaments closer together, then release, reattach, and pull again. So, it is a cycle of repetitive events that causes actin and myosin filaments to slide over each other.

Tropomyosin is a protein that regulates muscle contraction and relaxation. In a resting sarcomere, tropomyosin blocks the binding of myosin heads to filamentous actin, therefore there is no sliding mechanism or contraction of the muscle.

To enable muscle contraction once again, calcium ions are released enabling tropomyosin to change conformation and uncover the myosin-binding site on an actin molecule.

Sliding filament theory outline the process by which muscles contract.

An impulse reaches the muscle fibre - the electrical impulse is transmitted through the sarcoplasm with the help of the T tubules in the sarcolemma.

The electrical impulse causes voltage gated Ca2+ channels to open in the sarcoplasmic reticulum therefore allowing Ca2+ ions to diffuse into sarcoplasm.

Ca 2+ binds to troponin which then moves the tropomyosin filament hence exposing the binding site for the myosin head to bind to form a cross bridge.

The myosin head flexes and pulls the actin filament along and create tension. ADP present on myosin head is released.

ATP replaces the ADP causing conformational change in shape of myosin head therefor it is no longer complementary to myosin binding site on actin filament hence myosin head detaches.

ATP converted to ADP and Pi and releases energy for the myosin head to unflex and revert back to original position for the process to repeat again.

The tropomyosin is a protein which binds to the myosin binding site on the actin filament - prevents the binding of myosin head at rest so that muscles only contract when stimulated.

Hope that helps

The sliding filament model helps us to visualise what happens when striated skeletal muscles contract and relax. For muscle contraction the two wo types of muscle protein fibres slide over each other; tropin and actin. This sliding is dependent on the formation of cross bridges between actin and myosin. For muscle relaxtion a third protein, Tropomyosin blocks myosin heads, preventing interaction of tropin and actin and therefore blocking muscle contraction.

The sliding filament theory describes the mechanism that allows muscles to contract. According to this theory, myosin (a motor protein) binds to actin. The myosin then alters its configuration, resulting in a "stroke" that pulls on the actin filament and causes it to slide across the myosin filament. Calcium is required by two proteins, troponin and tropomyosin, that regulate muscle contraction by blocking the binding of myosin to filamentous actin. In a resting sarcomere, tropomyosin blocks the binding of myosin to actin.