 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 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; inactivation and subsequent recovery contribute to 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 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 potassium-channel subtype, and not all potassium channels lack 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: $I=N_{\mathrm{ch}}{g}_{\mathrm{single}}{p}_o(V_m-E_{\mathrm{ion}})$ 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.