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Jetzt kostenlos anmeldenThe sliding filament theory explains how the muscles contract to generate force, based on the movements of thin filaments (actin) along thick filaments (myosin).
Before diving into the sliding filament theory, let's review the Skeletal Muscle structure. Skeletal muscle cells are long and cylindrical. Due to their appearance, they are referred to as muscle fibres or myofibers. Skeletal Muscle fibres are multinucleated cells, meaning that they consist of multiple nuclei (singular nucleus) because of the fusion of hundreds of precursor muscle cells (embryonic myoblasts) during early development.
Moreover, these muscles can be pretty large in humans.
Muscle fibres are highly differentiated. They have acquired particular adaptations, making them efficient for contraction. Muscle fibres consist of the plasma membrane in muscle fibres is called the sarcolemma, and the cytoplasm is called the sarcoplasm. As well as, myofibers which possess a specialised smooth endoplasmic reticulum called the sarcoplasmic reticulum (SR), adapted for storing, releasing, and reabsorbing calcium ions.
Myofibers contain many contractile protein bundles called myofibrils, which extend along with the skeletal muscle fibre. These myofibrils are composed of thick myosin and thin actin myofilaments, which are the critical proteins for Muscle Contraction, and their arrangement gives the muscle fibre its striped appearance. It is important not to confuse myofibers with myofibrils.
Fig. 1 - The ultrastructure of a microfibre
Another specialised structure seen in skeletal muscle fibre is T tubules (transverse tubules), protruding off the sarcoplasm into the centre of the myofibers (Figure 1). T tubules play a crucial role in coupling muscle excitation with contraction. We will elaborate further on their roles further on in this article.
Skeletal muscle fibres contain many mitochondria to supply a large amount of ATP needed for Muscle Contraction. Furthermore, having multiple nuclei allows muscle fibres to produce large amounts of proteins and enzymes required for Muscle Contraction.
Skeletal myofibers have a striated appearance due to the sequential arrangement of thick and thin myofilaments in myofibrils. Each group of these myofilaments is called sarcomere, and it is the contractile unit of a myofiber.
The sarcomere is approximately 2 μm (micrometres) in length and has a 3D cylindrical arrangement. Z-lines (also called Z-discs) to which the thin actin and myofilaments are attached border each sarcomere. In addition to actin and myosin, there are two other proteins found in sarcomeres that play a critical role in regulating the function of actin filaments in muscle contraction. These proteins are tropomyosin and troponin. During muscle relaxation, tropomyosin binds along actin filaments blocking the actin-myosin interactions.
Troponin is composed of three subunits:
Troponin T: bind to tropomyosin.
Troponin I: bind to actin filaments.
Troponin C: binds to calcium ions.
Since actin and its associated proteins form filaments thinner in size than the myosin, it is referred to as the thin filament.
On the other hand, the myosin strands are thicker due to their larger size and multiple heads that protrude outwards. For this reason, myosin strands are called thick filaments.
The organisation of thick and thin filaments in sarcomeres gives rise to bands, lines, and zones within sarcomeres.
Fig. 2 - Arrangement of filaments in sarcomeres
The sarcomere is split into the A and I bands, H zones, M lines, and Z discs.
A band: Darker coloured band where thick myosin filaments and thin actin filaments overlap.
I band: Lighter coloured band with no thick filaments, only thin actin filaments.
H zone: Area at the centre of A band with only myosin filaments.
M line: Disc in the middle of the H zone that the myosin filaments are anchored to.
Z-disc: Disc where the thin actin filaments are anchored to. The Z-disc Marks the border of adjacent sarcomeres.
Energy in the form of ATP is needed for the movement of myosin heads and the active transportation of Ca ions into the sarcoplasmic reticulum. This energy is generated in three ways:
Aerobic Respiration of glucose and oxidative phosphorylation in the mitoƒhchondria.
Anaerobic Respiration of glucose.
Regeneration of ATP using Phosphocreatine. (Phosphocreatine acts like a reserve of phosphate.)
The sliding filament theory suggests that striated muscles contract through the overlapping of actin and myosin filaments, resulting in a shortening of the muscle fibre length. Cellular movement is controlled by actin (thin filaments) and myosin (thick filaments).
In other words, for a skeletal muscle to contract, its sarcomeres must shorten in length. The thick and thin filaments do not change; instead, they slide past one another, causing the sarcomere to shorten.
The sliding filament theory involves different steps. The step by step of the sliding filament theory is:
Step 1: An Action Potential signal arrives at the axon terminal of the presynaptic neuron, simultaneously reaching many neuromuscular junctions. Then, the Action Potential causes voltage-gated calcium ion channels on the presynaptic knob to open, driving an influx of calcium ions (Ca2+).
Step 2: The calcium ions cause the synaptic vesicles to fuse with the presynaptic membrane, releasing acetylcholine (ACh) into the synaptic cleft. Acetylcholine is a neurotransmitter that tells the muscle to contract. ACh diffuses across the synaptic cleft and binds to ACh receptors on the muscle fibre, resulting in depolarisation (more negative charge) of the sarcolemma (cell membrane of the muscle cell).
Step 3: The action potential then spreads along the T tubules made by the sarcolemma. These T tubules connect to the sarcoplasmic reticulum. Calcium channels on the sarcoplasmic reticulum open in response to the action potential they receive, resulting in the influx of calcium ions (Ca2+) into the sarcoplasm.
Step 4: Calcium ions bind to troponin C, causing a conformational change that leads to the movement of tropomyosin away from actin-binding sites.
Step 5: High-energy ADP-myosin molecules can now interact with actin filaments and form cross-bridges. The energy is released in a power stroke, pulling actin towards the M line. Also, ADP and the phosphate ion dissociate from the myosin head.
Step 6: As new ATP binds to the myosin head, the cross-bridge between myosin and actin is broken. Myosin head hydrolyses ATP to ADP and phosphate ion. The energy released returns the myosin head to its original position.
Step 7: Myosin head hydrolyses ATP to ADP and phosphate ion. The energy released returns the myosin head to its original position. Steps 4 to 7 are repeated as long as calcium ions are present in the sarcoplasm (Figure 4).
Step 8: Continued pulling of actin filaments towards the M line causes the sarcomeres to shorten.
Step 9: As the nerve impulse stops, calcium ions pump back into the sarcoplasmic reticulum using the energy from ATP.
Step 10: In response to the decrease in calcium ion concentration within the sarcoplasm, tropomyosin moves and blocks the actin-binding sites. This response prevents any further cross bridges from forming between actin and myosin filaments, resulting in muscle relaxation.
Fig 4. Actin-myosin cross-bridge formation cycle.
As the sarcomere shortens, some zones and bands contract while others stay the same. Here are some of the main observations during contraction (Figure 3):
The distance between Z-discs is reduced, which confirms the shortening of sarcomeres during muscle contraction.
The H zone (region at the centre of A bands containing only myosin filaments) shortens.
The A band (the region where actin and myosin filaments overlap) remains the same.
The I band (the region containing only actin filaments) shortens too.
Fig. 3 - Changes in the length of sarcomere bands and zones during muscle contraction
Z disc: Disc where the thin actin filaments are anchored. The Z-disc marks the border of the adjacent sarcomeres.
According to the sliding filament theory, a myofiber contracts when myosin filaments pull actin filaments closer towards the M line and shorten sarcomeres within a fibre. When all the sarcomeres in a myofiber shorten, the myofiber contracts.
Yes, the sliding filament theory applies to striated muscles.
The sliding filament theory explains the mechanism of muscle contraction based on actin and myosin filaments that slide past each other and cause sarcomere shortening. This translates to muscle contraction and muscle fibre shortening.
Step 1: Calcium ions are released from the sarcoplasmic reticulum into the sarcoplasm. Myosin head does not move.
Step 2: Calcium ions cause tropomyosin to unblock actin-binding sites and permit cross bridges to form between actin filament and myosin head.
Step 3: Myosin head utilises ATP to pull on actin filament toward the line.
Step 4: Sliding of actin filaments past myosin strands results in shortening of sarcomeres. This translates to contraction of the muscle.
Step 5: When calcium ions are removed from the sarcoplasm, tropomyosin moves back to block calcium-binding sites.
Step 6: Cross bridges between actin and myosin are broken. Hence, the thin and thick filaments slide away from each other and the sarcomere returns to its original length.
According to the sliding filament theory, myosin binds to actin. The myosin then alters its configuration using ATP, resulting in a power stroke that pulls on the actin filament and causes it to slide across the myosin filament towards the M line. This causes the sarcomeres to shorten.
Flashcards in Sliding Filament Theory10
Start learningThe sliding filament theory involves the act of five different molecules + calcium ions. Name them.
1.Myosin
2.Actin
3.Tropomyosin
4.Troponin,
5.ATP
+ 6.Calcium ions
What are the six steps of the cross-bridge formation cycle?
1. The influx of calcium ions 🡺 triggers the unblocking of the actin-binding sites.
2. Myosin head binds to actin.
3. The power stroke of the myosin head causes the sliding of the thin actin filaments.
4. The binding of ATP to myosin head resulting in the cross-bridge detachment.
5. The hydrolysis of ATP, which re-energizes the myosin head and makes it ready for the next cycle.
6. The transport of calcium ions back to the SR.
An ___brings about the release of calcium ions from the _______.
Calcium ions flood into the sarcoplasm and _____, causing a ________of the troponin-tropomyosin complex.
This conformation change ____the binding sites on ____.
The binding of myosin to actin brings about a _____ of the cross bride, resulting in the release of ___and___.
At the same time, the cross-bridge ___, pulling the ____inward toward the _____. This movement is called the "_____."
The _____has been transformed into the ____of contraction.
The release of the myosin cross-bridge from actin triggers the ____of the ATP molecule into ___ and ___.
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