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

The sliding filament theory explains how muscles contract once the nervous system receives signals to do. Muscles are made up of contractile units called sarcomeres with thin actin and thick myosin filaments (with the myosin heads binding to the actin-binding site) which then overlap resulting in the shortening of the filament and hence a contraction.

The actin filaments are closely linked with tropomyosin and troponin which are 2 proteins involved in regulation. Once, Ca2+ enters the cell (due to the nervous system) it binds to troponin which then changes shape causing tropomyosin to move. Tropomyosin normally blocks the binding site on actin so movement causes the binding site to be open and therefore allowing myosin to bind.

The sliding filament theory explain how muscles in the human body contract to produce force.

The steps of this theory are outlined below:

• Muscle Activation: The motor nerve stimulates a motor impulse to pass down a neuron to the neuromuscular junction. It stimulates the sarcoplasmic reticulum to release calcium into muscle cells.

• Muscle Contraction: Calcium floods into the muscle cell and it binds with troponin allowing actin and myosin to bind.  The myosin and actin cross-bridges bind and contract using ATP.

• Recharging: ATP is resynthesized which allows actin and myosin to maintain their strong binding state.

• Relaxation: Relaxation takes place when stimulation of the nerve stops.  Calcium is then pumped back into the sarcoplasmic reticulum which breaks the link between actin and myosin. Myosin and actin return to their unbound state causing the muscle to relax. Alternatively, relaxation (failure) also occurs when ATP is no longer available.

Hope this helps.

The sliding filament theory is a suggested mechanism of contraction of striated muscles, actin and myosin filaments to be precise, which overlap each other resulting in the shortening of the muscle fibre length. Actin (thin) filaments combined with myosin (thick filaments) conduct cellular movements

The sliding filament theory describes how muscles contract. The two main components are myosin (a thick muscle filament which has characteristic heads protruding from it at regular intervals) and actin (a thin myofilament featuring a myosin binding site).

The myosin binding sites on actin are blocked by tropomyosin. When an action potential arrives at the muscle, this triggers calcium release from the sarcoplasmic reticulum. When the calcium binds to tropomyosin, it pulls it aside leaving the myosin binding sites on the actin free and available.

Myosin heads can now bind to the myosin binding sites on the actin. This is called an actin-myosin cross bridge. A molecule of ATP is hydrolysed which triggers bending of the myosin head, which pulls the actin along. The myosin head then detaches using a molecule of ATP, and binds to the actin at a point further along. The process of 'head bending' is repeated and thus the actin is pulled along by myosin and the muscle contracts.

The analogy of rowing is often used to describe the repeated motion of the myosin head binding, like a boat ploughing through water due to the repeated oar action.

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.

The sliding filament theory explains how muscles contract when actin filaments slide over myosin filaments, shortening the sarcomere.

In resting muscle, tropomyosin blocks the binding sites on actin. When a nerve impulse triggers calcium release, the calcium binds to troponin, causing tropomyosin to move and expose the binding sites.

Myosin heads then bind to actin, forming cross-bridges. Using energy from ATP, myosin pulls actin inwards (the power stroke), shortening the muscle. ATP is also needed to detach the myosin head for the next cycle.

When calcium is removed, tropomyosin covers the binding sites again and the muscle relaxes.

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.

To answer this question properly, a short preamble on muscle filaments is quite useful. So, muscle fibres are made up of different muscle filaments. There are thick (myosin) and thin (actin) filaments, both of which have different structures. The key things to note are that myosin filaments have globular heads and actin molecules have myosin binding sites for those heads. Actin molecules come together with tropomyosin and troponin complexes to form an actin filament - we'll get into what those do in a bit. Essentially, tropomyosin + troponin complexes + actin molecule = actin filament.

The sliding filament theory essentially exists as an explanation as to how muscles contract, and it involves the thick and thin filaments we mentioned earlier interacting with each other. Try flexing your bicep right now: notice how the muscle seems to clump up together and tighten in your arm? The sliding filament theory explains how this happens at a molecular level.

There are 3 main steps to this theory. The 1st step is stimulation: an action potential arrives and depolarises surrounding muscle components, namely the sarcolemma and sarcoplasmic reticulum. This causes voltage-gated calcium channels on the SR to open up and release calcium ions into the sarcoplasm. This leads on to the 2nd stage - attachment. The calcium ions bind to the troponin complexes, causing a CONFORMATIONAL CHANGE. This causes tropomyosin to be PULLED, EXPOSING the myosin binding sites on the actin filament (so, in a resting state, the tropomyosin acts to HIDE the myosin binding sites on the actin filament). The myosin then binds to its binding site, forming a cross bridge, and experiences what we call a 'power stroke': the myosin flexes, pulling the actin along in a sort of rowing motion. This is how muscle shortening takes place during contraction. Finally, in the detachment phase, ATP binds to the myosin head, causing it to detach from the myosin binding site on the actin filament.

Note that the conformational change due to the binding of calcium goes both ways; the DETACHMENT of calcium from the troponin complex ALSO causes a conformational change, causing the tropomyosin to cover the myosin binding sites.

This happens on a massive scale upon muscle contraction, with thousands of cross bridges being formed/destroyed in a single second and millions of muscle fibrils being stimulated at once by an arriving action potential with the final aim of contracting the muscle.

Hope this helps!

The sliding filament model shows the overlapping myosin and actin fibres that are found within a sarcomere. When a muscle contracts, the actin and myosin form cross-bridges, increasing the amount of overlap, and make the sarcomere shorter. These cross-bridges can only form when the cross bridge binding sites are exposed on the actin fibre. Tropomyosin is a protein that covers the cross-bridge binding sites on the actin fibre, preventing contraction.