Both intracellular calcium and strongly bound crossbridges contribute to thin filament activation in the heart, but the magnitude and the duration of the effects due to crossbridges are not well characterized. In this study, crossbridge attachment was altered in tetanized ferret papillary muscles and changes in the rate constant for the recovery of force (k (TR)) and unloaded shortening velocity (V (U)) were measured to track thin filament activation. k (TR) decreased as the time the muscles spent at low levels of crossbridge attachment (shortening deactivation) increased (0.02 s=17.9+/-2.3 s(-1), 0.32 s=3.3+/-0.4 s(-1); half-time=0.052 s; P<0.05). Furthermore, the deactivation was reversible and k (TR) recovered when muscles were allowed to regenerate force isometrically during the same tetanus. V (U) also decreased when the preceding load was lower (isometric load, V (U)=1.93+/-0.26 muscle lengths/s (ML/s); zero load, V (U)=0.93+/-0.14 ML/s, P<0.05) and as the length of time the muscle spent unloaded increased (>60% decline after 0.3 s). In addition, V (U) recovered when the muscle was allowed to regenerate force isometrically. These results indicate that crossbridge attachment increases thin filament activation as reflected in measurements of V (U) and k (TR). This 'extra' activation by crossbridges appears to be a dynamic process that decays during unloaded shortening and redevelops during isometric contraction.