Carefully read the prompt. The discussion is cardiac action potential formation, notcross-bridge formation. Just like with skeletal muscles, Ca2+regulates cardiac cross-bridge formation by binding to or separating from troponin. Ca2+does not influence cardiac action potential formation in its capacity as a cross-bridge regulator (troponin binding). Concepts tested: How concentration gradients are established How current influence the membrane potential (Lecture 3) Role of Ca2+in cardiac action potential formation (Lecture 6) Cardiac action potential vs. cross-bridge formation (Lecture 4) Ca2+current ensures sustained depolarizationduring the cardiac A/P. This appears as a flattening of the action potential called the plateau phase. When sodium channels close, incoming Na+current stops and depolarization is completed. Meanwhile, the incoming Na+ current opens voltage-gated potassium channels and voltage-gated calcium channels. When this happens, K+current flows outof the cell whereas Ca2+current flows intothe cell. These two cross-directional currents cancel each other out thus temporarilypreventing membrane repolarization. So, the +50 mV membrane potential established by incoming Na+current is maintained hence “sustained depolarization” until the calcium channels close. (It is important to note that there is no Na+current flowing during the “sustained depolarization” phase. When the calcium channels close, the potassium channels remain open at which point the exiting K+current repolarizes the membrane. The cardiac refractory period combined with the plateau phase ensure proper rhythm of chamber contraction and relaxation that optimizes ventricular filling, ejection of blood, and cellular perfusion. 14.