Effects of varying I_NCX density on the simulated calcium signals and membrane voltage of embryonic cardiomyocytes. Decreased I_NCX (0.25× control) causes cytosolic calcium accumulation and stops the spontaneous activity (middle) by altering calcium flux through RyRs (J_RyR, insert). Upon simulated external electrical stimulation, the model produces cytosolic calcium transients and APs, where calcium transients rely on calcium flux through voltage-activated calcium channels. Increased I_NCX (3× control) enhances calcium extrusion, depleting the SR calcium stores (insert), thus stopping the spontaneous activity. The model cell retains its excitability, but due to lower [Ca²⁺]_i levels facing RyRs, calcium influx can only induce sporadic SR calcium releases, thus causing irregular activity (right panels).