The sliding filament theory is given by A. F. Huxley and R. Niedergerke (1954), and H. E. Huxley and J. Hanson (1954) explain how muscles in the human body contract to produce force.). In 1954, using high-resolution microscopy, these scientists noticed changes in the sarcomeres as muscle tissue shortened. They observed that during contraction, one zone of the repeated sarcomere arrangement, the ‘A band’, remained relatively constant in length.
The ‘A band’ contains thick filaments of myosin which suggests that the myosin remained central and constant throughout the length while other regions of the sarcomere shortened. The investigators observed that the ‘I’ band, which is rich in thin filaments made of actin, changed its length along with the sarcomere.
These observations led them to propose the sliding filament theory or the muscle contraction theory. The theory states that the sliding of actin past myosin generates muscle tension. As actin is tethered to structures located at the lateral ends of each sarcomere (Z discs or ‘Z’ bands) any shortening of this filament length would result in a shortening of the sarcomere which would, in turn, shorten the muscle.
Sarcomere
When muscle cells are viewed under the microscope, a striped pattern (striations) can be observed. This pattern is formed by a series of basic units called sarcomeres.
The sarcomeres are arranged in a stacked pattern throughout muscle tissue and a single muscle cell can have thousands of them. Sarcomeres are highly stereotyped and are repeated throughout muscle cells, and the proteins within them can change in length. The change in length causes the overall length of a muscle to change.
An individual sarcomere contains many parallel myosin and actin filaments. The interaction of these proteins is at the core of the sliding filament theory.
Sliding Theory of Muscle Contraction
The sliding filament theory can be best explained as the following. For a muscle contraction to take place, there must be a stimulation first to form an impulse (action potential) from a neuron that connects to the muscle. The individual motor neuron plus and the muscle fibers it stimulates, in a combination is called a motor unit. The motor endplate which is also known as the neuromuscular junction is the location of the motor neuron’s axon and the muscle fibers it stimulates.
When an impulse stimulates the muscle fibers of a motor unit, it starts a reaction in each sarcomere between the myosin and actin filaments. It results in the start of a contraction and the sliding filament theory.
The reaction, created from the arrival of an impulse stimulates the ‘heads’ on the myosin filament to reach forward, attach to the actin filament and pull actin towards the center of the sarcomere. This process is carried out simultaneously in all sarcomeres and the end process is the shortening of all sarcomeres.
Troponin, which is a complex of 3 proteins that are integral to muscle contraction. This complex is attached to the protein tropomyosin within the actin filaments. When a muscle is relaxed tropomyosin blocks the attachment sites for the myosin cross-bridges (heads), thus preventing contraction.
When a muscle is stimulated to contract by the action potential, calcium channels open in the sarcoplasmic reticulum and release calcium into the sarcoplasm. Some of this released calcium attaches itself with troponin which causes a change in the muscle cell that moves tropomyosin out of the way to the cross-bridges that can attach and produce muscle contraction.
In Summary, the Sliding Filament Theory Steps are as follows
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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.
Muscle Contraction
The thin filaments move across the thick filaments during contraction. Muscle contraction is initiated by a signal sent by the central nervous system via a motor neuron. The neuromuscular junction connects a motor neuron to the sarcolemma. When a brain signal reaches this junction, acetylcholine is released and an action potential is formed in the sarcolemma. Calcium ion is released in the sarcoplasm as this moves across the muscle fiber. Calcium then binds to troponin on actin filaments, exposing myosin active sites. Using energy from ATP hydrolysis, myosin binds to the exposed active site on actin. This attracts action to the center. The Z lines that are connected to them are likewise pulled, causing contraction. Myosin is in a state of relaxation.
As a result, the hydrolysis of ATP at the myosin head proceeds, causing more sliding. This is repeated until calcium ions are pushed back to the sarcolemma, resulting in the actin sites being covered again. The Z lines revert to their initial places. This results in relaxation. Muscular fatigue develops as a result of recurrent muscle activation, which results in the accumulation of lactic acid.
Muscles are red because of a pigment called myoglobin. Red fibers are myoglobin-rich muscles. They also have a large number of mitochondria, which may be used for energy production. White fibers are muscles that lack myoglobin and are white.