The sliding filament theory explains muscle contraction: thin actin filaments slide past thick myosin filaments, shortening each sarcomere without either filament becoming shorter. This process requires calcium ions and ATP.
The Mechanism
- A motor neuron stimulates a muscle fibre, producing an action potential that travels along the sarcolemma and into the transverse tubules.
- The sarcoplasmic reticulum releases calcium ions into the sarcoplasm.
- Calcium ions bind to troponin, changing its shape. This moves tropomyosin away from the myosin-binding sites on actin.
- Energized myosin heads bind to the exposed sites, forming cross-bridges.
- The release of inorganic phosphate causes each myosin head to pivot in a power stroke, pulling the actin filament towards the centre of the sarcomere. ADP is then released.
- A new ATP molecule binds to myosin, causing the cross-bridge to detach from actin.
- ATP is hydrolysed into ADP and inorganic phosphate. The released energy returns the myosin head to its energized position, allowing the cycle to repeat while calcium ions and ATP remain available.
- When stimulation ends, calcium ions are actively transported back into the sarcoplasmic reticulum. Tropomyosin covers the binding sites again, and the muscle fibre relaxes.
| Sarcomere feature | Change during contraction |
|---|---|
| Z-lines | Move closer together |
| I-band | Becomes narrower |
| H-zone | Becomes narrower and may disappear |
| A-band | Remains the same width |
| Actin and myosin filaments | Remain the same length |
A common misconception is that actin and myosin filaments contract or shorten. They do not: the sarcomere shortens because the filaments slide past one another and overlap more.
Exam Technique
For an IB SEHS HL explanation, present the sequence from calcium release to cross-bridge formation, power stroke, ATP-dependent detachment and re-cocking. Distinguish clearly between ATP's role in detachment and hydrolysis providing energy to re-energize the myosin head.
