Sliding Filament Theory
Phase 1 
A nervous impulse arrives at the neuromuscular 
junction (NMJ) – this causes a release of a 
chemical called acetylcholine. Acetylcholine 
causes the depolarisation of the motor end 
plate which travels throughout the muscle. 
Calcium (Ca+) is then released from the 
sarcoplasmic reticulum (this encircles each 
myofibril). This calcium triggers a muscle 
contraction.
Phase 2 
If there is a lot of calcium, it binds to troponin. 
This causes the troponin-tropomyosin to move 
away from the actin. This means the myosin can 
now attach to the actin – this forms a cross-bridge.
Phase 3 
ATP is broken down (into ADP and P) so energy is released. 
The myosin pulls the actin inwards (the Z-line/Z-discs move 
closer together) and the sarcomere shortens e.g. the muscle 
shortens. 
The length of the thin and thick filaments do not change – 
they (actin and myosin) just move closer together / overlap 
and shorten the whole muscle fibre. 
The release of the P triggers what we call the ‘power-stroke’ 
of contraction!!! This is because the ADP which is still 
attached causes the myosin head to rotate, pulling the actin 
filaments past the myosin filaments and towards the M-line.
The myosin then detaches from the actin 
breaking the cross-bridge as the ATP binds again 
to the myosin head. 
The whole process is repeated when the myosin 
head attaches to an actin-binding site further 
down the actin filament - another ‘power-stroke’ 
occurs. 
Phase 4
Phase 5 
Muscular contraction can continue so long as 
there is ATP and enough calcium in the 
sarcoplasm. 
If the nervous impulse STOPS, the calcium 
goes back to the sarcoplasmic reticulum and the 
actin returns to resting position e.g. the muscle 
lengthens and relaxes.
TextWall 
Answer the question given to you in the lesson 
or the one that appears on the text wall

Sliding filament theory overview

  • 1.
  • 2.
    Phase 1 Anervous impulse arrives at the neuromuscular junction (NMJ) – this causes a release of a chemical called acetylcholine. Acetylcholine causes the depolarisation of the motor end plate which travels throughout the muscle. Calcium (Ca+) is then released from the sarcoplasmic reticulum (this encircles each myofibril). This calcium triggers a muscle contraction.
  • 3.
    Phase 2 Ifthere is a lot of calcium, it binds to troponin. This causes the troponin-tropomyosin to move away from the actin. This means the myosin can now attach to the actin – this forms a cross-bridge.
  • 4.
    Phase 3 ATPis broken down (into ADP and P) so energy is released. The myosin pulls the actin inwards (the Z-line/Z-discs move closer together) and the sarcomere shortens e.g. the muscle shortens. The length of the thin and thick filaments do not change – they (actin and myosin) just move closer together / overlap and shorten the whole muscle fibre. The release of the P triggers what we call the ‘power-stroke’ of contraction!!! This is because the ADP which is still attached causes the myosin head to rotate, pulling the actin filaments past the myosin filaments and towards the M-line.
  • 5.
    The myosin thendetaches from the actin breaking the cross-bridge as the ATP binds again to the myosin head. The whole process is repeated when the myosin head attaches to an actin-binding site further down the actin filament - another ‘power-stroke’ occurs. Phase 4
  • 6.
    Phase 5 Muscularcontraction can continue so long as there is ATP and enough calcium in the sarcoplasm. If the nervous impulse STOPS, the calcium goes back to the sarcoplasmic reticulum and the actin returns to resting position e.g. the muscle lengthens and relaxes.
  • 7.
    TextWall Answer thequestion given to you in the lesson or the one that appears on the text wall