This theory, proposed by Andrew and Hugh Huxley, explains how muscles contract without the actual filaments getting shorter—they simply slide past one another (actin slides over myosin).
The Sliding Filament Theory
- Neural Signal: The process begins when a motor neuron releases the neurotransmitter Acetylcholine (ACh) at the neuromuscular junction, triggering an action potential in the muscle fiber.
- Calcium Release: The action potential travels down the T-tubules, causing the sarcoplasmic reticulum to release stored Calcium ions into the sarcoplasm.
- Binding Site Exposure: Calcium binds to Troponin, which causes a conformational change that moves Tropomyosin away from the active binding sites on the Actin (thin) filaments.
- ATP Activation: Before binding, the Myosin (thick) head hydrolyzes ATP into ADP and inorganic phosphate, putting the myosin head in a “cocked” or high-energy state.
- Cross-Bridge Formation: The energized myosin head binds to the exposed active site on the actin filament, forming a Cross-Bridge.
- The Power Stroke: The myosin head releases the ADP and Pi, causing it to pivot and pull the actin filament toward the center of the Sarcomere (the M-line).
- Detachment: A new molecule of ATP binds to the myosin head, causing it to release its grip on the actin filament.
- Re-activation: The myosin head hydrolyzes the new ATP again, returning to its cocked position, ready for the next cycle.
- Sarcomere Shortening: As this cycle repeats thousands of times (“rowing”), the Z-lines are pulled closer together, the H-zone disappears, and the I-band shortens, while the A-band remains the same length.
- Relaxation: When the neural signal stops, calcium is pumped back into the sarcoplasmic reticulum, tropomyosin covers the binding sites again, and the muscle relaxes.
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