At the neuromuscular junction, ACh released by the synaptic terminal binds to receptors on sarcolemma.
Step 2 (Contraction)
The resulting change in the transmembrane potential of the muscle fiber leads to the production of an action potential that spreads across the entire surface of the muscle fiber and along the T-tubules.
Step 3 (Contraction)
The sarcoplasmic reticulum releases stored calcium ions, increasing the calcium concentration of the sarcoplasm in and around the sarcomeres.
Step 4 (Contraction)
Calcium ions bind to troponin, producing a change in the orientation of troponin-tropomyosin complex that exposes active sites on the thin filaments. Cross-bridges form when myosin heads bind to active sites on actin.
Step 5 (Contraction)
The contraction begins as repeated cycles of cross-bridge binding, pivoting, and detachment occur, powered by the hydrolysis of ATP. These events produce filament sliding, and the muscle fiber shortens.
Step 6 (Relaxation)
ACh is broken down by AChE, ending action potential generation in the sarcolemma.
Step 7 (Relaxation)
The sarcoplasmic reticulum reabsorbs calcium ions, and the concentration of calcium ions in the sarcoplasm declines.
Step 8 (Relaxation)
When calcium ion concentrations approach normal resting levels, the troponin-tropomyosin complex returns to its normal position. This change re-covers the active sites and prevents further cross-bridge interaction.
Step 9 (Relaxation)
Without cross-bridge interactions, further sliding cannot take place, and the contraction ends.
Step 10 (Relaxation)
Muscle relaxation occurs, and the muscle returns passively to its resting length.