1. Action potential opens presynaptic voltage-gated Ca²⁺ channels, inducing acetylcholine (ACh) release.
2. Postsynaptic ACh binding leads to muscle cell depolarization at the motor end plate.
3. Depolarization travels over the entire muscle cell and deep into the muscle via the T-tubules.
4. Membrane depolarization induces conformational changes in the voltage-sensitive dihydropyridine receptor (DHPR) and its mechanically coupled ryanodine receptor (RR) → Ca²⁺ release from the sarcoplasmic reticulum (buffered by calsequestrin) into the cytoplasm.
5. Tropomyosin is blocking myosin-binding sites on the actin filament. Released Ca²⁺ binds to troponin C (TnC), shifting tropomyosin to expose the myosin-binding sites.
6. Myosin head binds strongly to actin (crossbridge). P_i released, initiating power stroke.
7. During the power stroke, force is produced as myosin pulls on the thin filament A. Muscle shortening occurs, with shortening of H and I bands and between Z lines (HI, I’m wearing shortZ). The A band remains the same length (A band is Always the same length). ADP is released at the end of the power stroke.
8. Binding of new ATP molecule causes detachment of myosin head from actin filament. Ca²⁺ is resequestered.
9. ATP hydrolysis into ADP and P_i results in myosin head returning to high-energy position (cocked). The myosin head can bind to a new site on actin to form a crossbridge if Ca²⁺ remains available.
10. Reuptake of calcium by sarco(endo)plasmic reticulum Ca²⁺ ATPase (SERCA) → muscle relaxation.