The sliding filament theory given by A. F. Huxley and R. Niedergerke (1954), and H. E. Huxley and J. Hanson (1954) explains 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.
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.
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 fibres 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 neurons axon and the muscle fibres it stimulates.
When an impulse stimulates the muscle fibres 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 centre of the sarcomere. This process is carried out simultaneously in all sarcomere and the end process is the shortening of all sarcomeres.
Troponin, which is a complex of 3 proteins which 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 themselves with troponin which causes a change in the muscle cell that moves tropomyosin out of the way to the cross-bridges can attach and produce muscle contraction.
In Summary, the Sliding Filament Theory Steps are as Followed:
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.
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Q: What are Cross Bridges?
A: With respect to muscular contraction, a cross-bridge refers to the attachment of myosin with actin within the muscle cell. All types of muscles - whether discussing skeletal, cardiac or smooth - contract by cross-bridge cycling - that is, repeated attachment of actin and myosin within the cell.
Q: What is the Role of Troponin?
A: Troponin is a protein complex that attaches to the protein tropomyosin and lies between actin filaments in the muscle. The protein tropomyosin blocks the attachment site for myosin head and prevents the contraction of a relaxed muscle.
Q: What is the Sliding Filament Theory of Muscle Contraction?
A: Please refer to the first part of the article.
Q: What is the Part of ATP Molecules in Sliding Filament Theory in Muscle Contraction?
A: ATP, the energy currency of the cell, releases myosin from actin filaments. During muscle contraction, myosin attaches to actin filaments and ATP attaches to the myosin head, in turn, releasing the actin molecule, and causing muscle relaxation.
Q: What can Stop a Muscle Contraction?
Energy System Fatigue: There is no more ATP left in the muscle cell so it can not contract.
Nervous System Fatigue: The nervous system is not able to create action potential sufficiently to maintain the stimulus and cause calcium release.
Voluntary Nervous System Control: The nerve that sends signals to the muscle to contract stops sending that signal. Hence, no more calcium ions will enter the muscle cell and the contraction stops.
Sensory Nervous System Information: A sensory neuron provides feedback to the brain indicating that a muscle is injured while the human body is trying to lift a heavyweight. As a result, the impulse to that muscle telling it to contract is stopped.