Muscle contraction is a highly coordinated process that involves electrical signals, ion exchange, and interaction between proteins. The main mechanism of muscle contraction is based on the sliding filament theory, which describes how actin (thin filaments) and myosin (thick filaments) interact to produce contraction. Below is a detailed step-by-step explanation of how muscle contraction occurs in skeletal muscles.

1. Neuromuscular Junction and Signal Transmission

Muscle contraction begins when an action potential (electrical impulse) is sent from the brain or spinal cord through the motor neuron to the neuromuscular junction (NMJ), which is the synapse (connection) between the motor neuron and the muscle fiber.

1. Action Potential and Release of Acetylcholine

• Action potential travels down the motor neuron and reaches the axon terminal at the neuromuscular junction.
• This causes the release of the neurotransmitter acetylcholine (ACh) into the synaptic cleft (the gap between the neuron and the muscle fiber).

1. Depolarization of Sarcolemma

• ACh binds to receptors on the sarcolemma (muscle cell membrane), leading to an influx of sodium ions (Na⁺) into the muscle fiber, which generates a new action potential in the muscle fiber.
• The action potential travels across the sarcolemma and into the T-tubules (transverse tubules), which are extensions of the cell membrane that penetrate the muscle fiber.

2. Release of Calcium Ions (Ca²⁺) from the Sarcoplasmic Reticulum

The T-tubules carry the action potential deep into the muscle fiber, which triggers the release of calcium ions (Ca²⁺) from the sarcoplasmic reticulum (SR), a specialized form of endoplasmic reticulum that stores calcium ions.

1. Role of Calcium in Muscle Contraction

• Calcium ions bind to the troponin complex, which is a protein located on the actin filaments. This binding causes a conformational change in the troponin-tropomyosin complex.
• Tropomyosin, which normally blocks the binding sites on actin, shifts out of the way, exposing the myosin-binding sites on actin.

3. Cross-Bridge Formation

Once the myosin-binding sites on actin are exposed, myosin heads, which are part of the thick myosin filaments, can bind to the actin filaments to form a cross-bridge.

1. ATP Binding and Hydrolysis

• Before the cross-bridge formation, ATP binds to the myosin head, causing it to detach from the actin filament if it was previously bound.
• The enzyme ATPase in the myosin head hydrolyzes ATP into ADP and inorganic phosphate (Pi), which provides energy for the myosin head to “cock” into a high-energy state.

4. Power Stroke and Sliding of Filaments

Once the myosin head binds to the exposed actin site, the power stroke occurs:

• The myosin head pivots, pulling the actin filament toward the center of the sarcomere (the basic contractile unit of the muscle).
• This action is powered by the energy from ATP hydrolysis.
• The sliding filament mechanism describes the movement of actin and myosin filaments past each other, shortening the sarcomere, and thus contracting the muscle.

Key Points:

• Sarcomere Shortening: As the actin filaments are pulled towards the center, the Z-lines (the boundaries of the sarcomere) come closer together, causing the sarcomere to shorten and resulting in muscle contraction.
• ATP Consumption: Each cycle of cross-bridge formation and power stroke requires the hydrolysis of ATP, which provides the energy for contraction.

5. Detachment of Myosin and Resetting of the Myosin Head

• After the power stroke, ADP and Pi are released from the myosin head.
• A new molecule of ATP binds to the myosin head, causing it to release from the actin filament.
• The myosin head repositions itself (re-cocks) to its high-energy state, ready to bind to another actin site further along the filament.

6. Relaxation of the Muscle

Muscle contraction continues as long as there is an action potential, calcium in the sarcoplasm, and ATP available. Once the action potential ceases, the following processes occur:

1. Calcium Reuptake

• Calcium ions are actively pumped back into the sarcoplasmic reticulum by calcium ATPase pumps (this process requires ATP).
• As calcium is removed from the sarcoplasm, the troponin-tropomyosin complex returns to its resting conformation, blocking the myosin-binding sites on actin.

1. Muscle Relaxation

• As the myosin-binding sites are covered, the cross-bridges between myosin and actin are broken, and the muscle relaxes. The sarcomeres lengthen, and the muscle returns to its resting state.

7. Summary of the Muscle Contraction Process

1. Signal Transmission: Action potential from the motor neuron reaches the muscle fiber at the neuromuscular junction.
2. Calcium Release: The action potential travels down the T-tubules, causing calcium ions to be released from the sarcoplasmic reticulum.
3. Cross-Bridge Formation: Calcium binds to troponin, shifting tropomyosin and exposing myosin-binding sites on actin. Myosin heads bind to actin, forming cross-bridges.
4. Power Stroke: Myosin heads pivot, pulling actin filaments toward the center of the sarcomere, causing muscle contraction.
5. Detachment and Resetting: ATP binds to the myosin head, causing detachment from actin and resetting of the myosin head for another cycle.
6. Relaxation: Calcium ions are reabsorbed into the sarcoplasmic reticulum, and the muscle relaxes.

Conclusion

Muscle contraction is a highly regulated and energy-dependent process that involves the interaction of myosin and actin filaments within the sarcomere. It is initiated by an action potential from the nervous system and is dependent on calcium and ATP to enable the sliding filament mechanism. The continuous cycles of cross-bridge formation, power stroke, and detachment lead to muscle shortening and movement. When the stimulus stops, the muscle relaxes as calcium is pumped back into the sarcoplasmic reticulum and the cross-bridges are broken. This intricate process allows for voluntary control of movement and is fundamental to all forms of skeletal muscle activity.