In skeletal muscle, steady-state force is consistently greater following active stretch than during a purely isometric contraction at the same length (residual force enhancement; RFE). Similarly, when deactivated, the force remains higher following active stretch than following an isometric condition (passive force enhancement; PFE). RFE and PFE have been associated with the sarcomere protein titin, but skeletal and cardiac titin have different structures, and results regarding RFE in cardiac muscle have been inconsistent and contradictory. Therefore, the purpose of this study was to determine if cardiac muscle exhibits RFE and PFE. Skinned fibre bundles (n = 10) were activated isometrically at a sarcomere length of 2.2 μm and actively stretched by 15% of their length. The resultant active and passive forces were compared to the corresponding forces obtained for purely isometric contractions at the long length. RFE was observed in all fibre bundles, averaging 5.5 ± 2.5% (ranging from 2.3 to 9.4%). PFE was observed in nine of the ten bundles, averaging 11.1 ± 6.5% (ranging from -2.1 to 18.7%). Stiffness was not different between the active isometric and the force enhanced conditions, but was higher following deactivation from the force-enhanced compared to the isometric reference state. We conclude that there is RFE and PFE in cardiac muscle. We speculate that cardiac muscle has the same RFE capability as skeletal muscle, and that the most likely mechanism for the RFE and PFE is the engagement of a passive structural element during active stretching.