The depression of isometric force following active shortening is a well-accepted characteristic of skeletal muscle, yet its mechanisms remain unknown. While traditionally analyzed at steady-state, transient phenomena caused, at least in part, by cross-bridge kinetics, may provide novel insight into the mechanisms associated with force depression (FD). To identify the transient aspects of FD, and its relation to shortening speed, shortening amplitude, and muscle mechanical work, in situ experiments were conducted in soleus muscle-tendon units of anesthetized cats. The period immediately following shortening, in which force recovers toward steady-state, was fit using an exponential recovery function (R²>0.99). Statistical analyses revealed that steady-state FD (FD_ss) increased with shortening amplitude and mechanical work. This FD_ss increase was always accompanied by a significant decrease in force recovery rate. Furthermore, a significant reduction in stiffness was observed following all activated shortenings, presumably due to a reduced proportion of attached cross-bridges. These results were interpreted with respect to the two most prominent proposed mechanisms of force depression: sarcomere length non-uniformity theory (7, 32), and a stress-induced inhibition of cross-bridge binding in the newly-formed actin/myosin overlap zone (14, 28). We hypothesized that the latter could describe both steady-state and transient aspects of FD using a single scalar variable, the mechanical work done during shortening. As either excursion (overlap) or force (stress) is increased, mechanical work increases, and cross-bridge attachment would become more inhibited; as supported by this study in which an increase in mechanical work resulted in a slower recovery to a more depressed steady-state force.