History-dependent properties, such as residual force depression (rFD;​ i.e., the decrease in steady-state isometric force of a muscle, following active shortening, compared to the corresponding force of a purely isometric contraction) have been consistently observed in skeletal muscle. However, the corresponding work on history-dependent properties in cardiac muscle is limited and controversial, and the rFD property specifically remains unexplored. Therefore, the purpose of this study was to examine rFD in cardiac myofibrils.

Myofibrils (n = 10) isolated from the left ventricle of rabbits were held at an average sarcomere length (SL) of 2.2 µm. Myofibrils were then activated, and actively shortened to an average SL of 1.8 µm, held constant at this length until the force reached a steady-state. The myofibrils were then deactivated and allowed to recover for 10 mins. Finally, myofibrils were activated again at an average SL of 1.8 µm, to measure the purely isometric force at this length.

All ten myofibrils exhibited rFD, averaging 23.0 % (± 9.4 %) of the purely isometric reference force. This result suggests that rFD occurs in cardiac muscle within a physiologically relevant range of function, and that similar to skeletal muscle, the molecular mechanisms underlying cardiac rFD originate, at least in part, from the sarcomere.