Sliding Filament Theory

The sliding filament theory explains how the muscles contract to generate force.

Recap on skeletal muscle ultrastructure

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 fibre adaptations

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.

Figure 1 The ultrastructure of a microfibre.

Another specialised structure seen in skeletal muscle fibre is T tubules (transverse tubules), protruding of 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.

Sarcomeres: bands, lines, and zones

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:

1. Troponin T: bind to tropomyosin.
2. Troponin I: bind to actin filaments.
3. 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.

Figure 2. Arrangement of filaments in sarcomeres. Source: OpenStax College, CC-BY-4.0.

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 bands 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.

The sliding filament theory

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. This process is known as the sliding filament theory.

Evidence for the sliding filament theory

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):

1. The distance between Z-discs is reduced, which confirms the shortening of sarcomeres during muscle contraction.
2. The H zone (region at the centre of A bands containing only myosin filaments) shortens.
3. The A band (the region where actin and myosin filaments overlap) remains the same.
4. The I band (the region containing only actin filaments) shortens too.

Figure 3. Changes in the length of sarcomere bands and zones during muscle contraction.

The sliding filament mechanism of muscle contraction

Muscle events can be broken down into three steps: muscle stimulation, muscle contraction, and muscle relaxation.

Muscle stimulation

1. An action potential arrives at the axon terminal of the presynaptic neurone, simultaneously reaching many neuromuscular junctions.
2. The action potential causes voltage-gated calcium ion channels on the presynaptic knob to open, driving an influx of calcium ions.
3. The calcium ions cause the synaptic vesicles to fuse with the presynaptic membrane, releasing acetylcholine (ACh) into the synaptic cleft.
4. ACh diffuses across the synaptic cleft and binds to ACh receptors on the muscle fibre, resulting in depolarisation of the sarcolemma.

Muscle contraction

1. The action potential spreads along the T tubules.
2. 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 Ca ions into the sarcoplasm.
3. Calcium ions bind to troponin C, causing a conformational change that leads to the movement of tropomyosin away from actin-binding sites.
4. High energy ADP-myosin molecules can now interact with actin filaments and form cross-bridges.
5. 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.
6. As new ATP binds to the myosin head, the cross-bridge between myosin and actin is broken.
7. Myosin head hydrolyses ATP to ADP and phosphate ion. The energy released returns the myosin head to its original position.
8. Steps 4 to 8 are repeated as long as calcium ions are present in the sarcoplasm (Figure 4). Continued pulling of actin filaments towards the M line causes the sarcomeres to shorten.

Muscle relaxation

1. As the nerve impulse stops, calcium ions pump back into the sarcoplasmic reticulum using the energy from ATP.
2. In response to the decrease in calcium ion concentration within the sarcoplasm, tropomyosin moves and blocks the actin-binding sites.
3. This response prevents any further cross bridges from forming between actin and myosin filaments, resulting in muscle relaxation.

Figure 4. Actin-myosin cross-bridge formation cycle.

Source of energy for muscle contraction

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:

1. Aerobic respiration of glucose and oxidative phosphorylation in the mitoƒhchondria.
2. Anaerobic respiration of glucose.
3. Regeneration of ATP using Phosphocreatine. (Phosphocreatine acts like a reserve of phosphate.)