Answer
When the end plate potential (EPP) is created in the sarcolemma, the change in voltage causes the voltage-gated ion channels in the sarcolemma to open. This results in an inflow or diffusion of sodium ions -- down their electrochemical gradient-- and soon after an outflow of K+ ions. Rapid changes in ion concentration between the outside and the inside of the myofiber results in the depolarization and repolarization of the cell , in other words, an action potential (AP) is generated.
The action potential is propagated in along the sarcolemma, spreads to the terminal cisternae, and is conducted by T-tubules into the interior of the myofiber.
The AP opens voltage-gated calcium channels in the terminal cisternae and the sarcoplasmic reticulum(SR)
As a consequence Ca++ ions pour out of the SR -- down their concentration gradient--into the cytoplasm ( sarcoplasm) of the myofiber. The released Ca++ ions bind to the troponin, which is attached to tropomyosin molecules of thin filaments. This binding causes the tropomyosin-troponin complex to change conformation , and this change in shape exposes the active sites on the actin filament. Now the myosin is able to bind to these exposed and available actin sites
Work Step by Step
The combined effect of the EPP and the AP is to cause excitation of the myofiber. The binding of calcium to the tropomyosin-troponin complex exposes the active sites of the actin filaments and makes the myocyte ready for binding myosin heads and contracting under the power of energy supplied by ATP.
