= Solution
The <sodium> trace is a rapid inward current after depolarization, followed by loss of current even while <voltage> remains depolarized. A <voltage-gated sodium channel> therefore activates rapidly and then becomes unavailable through <Ion-channel inactivation>[inactivation]. Under ordinary cardiac ionic gradients, the test potential is below the <sodium> <reversal potential>, so opening carries inward positive charge. Rapid <sodium> entry supports the fast action-potential upstroke and propagation in working myocardium; <Ion-channel inactivation>[inactivation] and subsequent recovery contribute to <Neuronal refractory period>[refractoriness].
The <potassium> trace develops more slowly, is outward during the positive step, and remains approximately sustained until repolarization. It is consistent with a delayed outward <potassium> <Electrical conductance>[conductance]: activation counteracts depolarization, and deactivation follows the return towards the holding <voltage>. <Potassium> currents contribute to repolarization and stable diastolic <voltage>. The trace does not identify a unique cardiac <Voltage-gated potassium channel>[potassium-channel] subtype, and not all <potassium> channels lack <Ion-channel inactivation>[inactivation].
Together, fast inward activation initiates excitation and slower outward activation terminates it. Current direction is set by electrochemical driving <force> as well as gating: $I=N_{\rm ch}g_{\rm single}p_o(V_m-E_{\rm ion})$ in an ohmic approximation. A <voltage clamp> fixes $V_m$ and reveals those currents; in a freely firing cell the currents instead jointly determine the <voltage> through the membrane-capacitance equation. <Calcium> current is also important for the cardiac plateau, so these two traces alone are not a complete ventricular action-potential model. The sodium-potassium pump maintains long-term gradients but is not the fast gating mechanism seen in these recordings.
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