Decreased Ca²⁺ responsiveness of the myofilaments underlies myocardial stunning. Given that cross-bridge cycling is a major determinant of myofilament behavior, we quantified cross-bridge cycling rate in stunned myocardium. After stabilization, rat hearts were subjected to 20 minutes of no-flow global ischemia and 30 minutes of reperfusion at 37°C. Control hearts were perfused continuously at 37°C for 60 minutes. Trabeculae were dissected and chemically skinned with 1% triton X-100. The muscles were then activated with solutions of varied [Ca²⁺]. Force-[Ca²⁺] relations, rate of force redevelopment after release (k_tr), muscle stiffness (k_m), and myofilament ATP consumption were determined. Maximal Ca²⁺-activated force (F_max) was depressed in stunned myocardium (49±5 vs 82±5 mN/mm², p<0.01). Western immunobloting showed degradation of troponin I in stunned myocardium. k_tr at F_max was significantly increased in stunned muscles (21.3±2.47 vs 13.8±0.83 s^-1 , 22°C, p<0.01; 7.49±0.52 vs 5.81±0.54 s^-1, 10°C, p<0.05). The ratio of k_m measured at 100 Hz over that at 1 Hz, during F_max, is lower in stunned muscles (8.22±1.56 vs 12.94±0.71, p<0.05). In comparison with k_m at rigor, k_m at F_max is significantly lower in the stunned group (78.82±6.11% vs 96.27±3.03%, p<0.05). Myofilament ATP consumption at F_max did not change in stunned muscles (5901±952 vs 5596±972 pmol^.µl^-1.min^-1, p=0.49). These results show that cross-bridge cycling is increased in stunned myocardium. Such increases are likely the result of increased transition rate from force-generating states to non-force-generating states. Thus, stunned myocardium still maintains ATP consumption in spite of lower force development rationalizing the long-standing paradox of decreased force but unchanged oxygen consumption in the post-ischemic heart.