The consequences of an extrasystole (ES) on cardiac muscle's energetics and Ca²⁺ homeostasis were investigated in the beating heart. The fraction of heat release related to pressure development (pressure dependent) and pressure-independent heat release were measured during isovolumic contractions in arterially perfused rat ventricle. The heat release by a contraction showed two pressure-independent components (H1 and H2) of short evolution and a pressure-dependent component (H3). The additional heat released by ES was decomposed into one pressure-independent (H'₂) and one pressure-dependent (H'₃) component with time courses similar to those of control components H2 and H3. ES also induced the potentiation of pressure development (P) and heat release during the postextrasystolic (PES) beat. The slope of the linear relationship between pressure-dependent heat and pressure maintenance was similar in control, ES, and PES contractions (0.08 ± 0.01, 0.10 ± 0.02, and 0.08 ± 0.01 mJ · g¹ · mmHg¹ · s¹, respectively). The potentiation of H2 (heat component related with Ca²⁺ removal processes) in PES was equal to H'₂ at 0.3, 0.5, 1, and 2 mM Ca²⁺, suggesting that the extra amount of Ca²⁺ mobilized during ES was recycled in PES. Pretreatment with 1 mM caffeine to deplete sarcoplasmic reticulum Ca²⁺ content inhibited both the mechanical and energetic potentiation of PES. However, the heat released and the pressure developed during ES were not changed by sarcoplasmic reticulum depletion. The results suggest that 1) the source of Ca²⁺ for ES would be entirely extracellular, 2) the Ca²⁺ entered during ES is accumulated in the sarcoplasmic reticulum, and 3) the Ca²⁺ stored by the sarcoplasmic reticulum during ES induces an increased contribution of this organelle during PES compared with the normal contraction.