Cardiac-specific Na⁺–Ca²⁺ exchanger (NCX) knockout (KO) mice surprisingly survive into adulthood without compensatory changes in protein expression levels. To determine how cardiac function is maintained in the absence of NCX, we investigated membrane currents, intracellular Ca²⁺, and action potentials (APs) in whole cell patch-clamped myocytes from wild-type (WT) and NCX knockout mice. There was no difference in resting Ca²⁺ or sarcoplasmic reticular Ca²⁺ load between KO and WT. During prolonged caffeine exposure, the decrease of the Ca²⁺ transient was drastically slowed in KO versus WT myocytes, indicating that no alternative Ca²⁺-extrusion mechanism is upregulated to compensate for the absence of NCX. Peak L-type Ca²⁺ current (I_Ca) was reduced by 62% in KO myocytes compared with WT. Nevertheless, the corresponding Ca²⁺ transients were similar, implying an increase in the gain of excitation–contraction coupling in KO cells. APs recorded from KO cells repolarized more rapidly than in WT. In WT myocytes, applying a KO AP waveform voltage clamp reduced Ca²⁺ influx via I_Ca by 59% compared with WT AP waveform clamps. Again, the corresponding Ca²⁺ transients remained similar. Our findings indicate that NCX KO myocytes limit Ca²⁺ influx to &20% of that in WT by reducing I_Ca and by abbreviating the AP. Contractility is maintained by an increase in the gain of excitation–contraction coupling resulting from both a more rapid repolarization of the AP and an as yet unidentified AP-independent mechanism.