sarcomere. The sarcoplasmic reticulum is extremely sensitive to changes in polarization. When polarization is reversed, the terminal cisternae become permeable to ions and release their large stores of these ions into the sarcomeres. The ions bind to troponin enabling the troponin to bind with tropomyosin and shift it from myosin's binding sites on the actin proteins. Once bound to actin, myosin can break down ATP and release the energy needed for its power-stroke that pulls the actin filaments toward the center of the sarcomere. These power-strokes will continue and, thus, muscle contraction will continue as long as there is free in the sarcomeres. When nervous stimulation stops, however, the membrane of the terminal cisternae rapidly pumps the remaining free back into the cisternae. Without the presence of ions, troponin is no longer able to bind to tropomyosin, tropomyosin again blocks myosin's binding sites on the actin proteins, and contraction ceases.
