A long rod shaped region that acts as a flexible hinge.
A myosin head. The head has an ATP binding site and a region complementary to actin.
Actin
Actin is made of 2 protein strands twisted around each other. Actin has binding sites for myosin. At rest the binding sites are blocked by tropomyosin molecules.
The Sliding Filament Theory P1:
An action potential arrives at the neuromuscular junction causing acetylcholine to be released.
Acetylcholine diffuses across the cleft and binds to receptor proteins in the sarcolemma, this opens Na+ channels & allows Na+ to enter and depolarise the sarcolemma.
The depolarisation is carried inwards by T-tubules into the sarcoplasm.
The Sliding Filament Theory P2:
This causes Ca 2+ channels to open on the sarcoplasmic reticulum allowing Ca 2+ to diffuse out of it and enter the sarcoplasm.
Ca 2+ causes:
The tropomyosin molecules to move and so expose the myosin binding site on the actin molecule.
The activation of ATP hydrase causing ATP -> ADP + Pi. The energy is used to move the myosin head into a 'cocked' position.
The Sliding Filament Theory P3:
The myosin head binds to actin, forming an actomyosin crossbridge. This binding and the release of ADP from the myosin head causes the myosin head to tilt and pull on the actin (the 'power-stroke').
ATP is reformed (in respiration) and binds to the myosin head again. This binding causes the actinomysin crossbridge to detach.
ATP is hydrolysed the myosin head recocks again. If Ca 2+ opens are still present the myosin can bind to the next binding site so the molecules shorten again.