We examined the effects of pharmacologically altering Ca²⁺ sources on the mechanical and energetic properties of paired-pulse ("bigeminic") contractions. The fraction of heat released that is related to pressure development and pressure-independent heat release were measured during isovolumic contractions in arterially perfused rat ventricles. The heat release by both regular and bigeminic contractions showed two brief pressure-independent components (H1 and H2) and a pressure-dependent component (H3). We used active heat (H[[rad]]a) over pressure-time integral (PtI) and H3 over PtI ratios to estimate the energetic cost of muscle contraction (overall economy) and pressure maintenance (contractile economy) respectively. None of these ratios was affected by the stimulation pattern "per se". CAFFEINE (an inhibitor of SR function) significantly decreased mechanical responses and increased the energetic cost of contraction (: 101±12.6%). VERAPAMIL (L-type Ca²⁺ channel blocker) decreased pressure maintenance of both extrasystolic (:43.4±3.7%) and postextrasystolic (:37.5±3.5%) contractions without affecting postextrasystolic potentiation, suggesting that a VERAPAMIL-insensitive fraction is responsible for the potentiation. The latter fraction (VERAPAMIL-insensitive) was further studied in the presence of Lithium (45 mM) and KB-R7943 (5 µM) (inhibitors of the Na⁺/Ca²⁺ exchanger). Both agents decreased all mechanical responses including the postextrasystolic potentiation (:67.3±3.3%) without altering neither overall nor contractile economies, suggesting an association of the VERAPAMIL-insensitive Ca²⁺ fraction to the sarcolemmal Na⁺/Ca²⁺ exchanger. The effect of the inhibitors of the Na⁺/Ca²⁺ exchanger on the potentiation suggests an increased participation of extracellular Ca²⁺ (and thus a redistribution of the relative participation of the Ca²⁺ pools) during bigeminic contractions in rat myocardium.