The rate of cross-bridge cycling represents the speed at which actin and myosin attach and detach in cardiac myofilaments. This rate is thought to be decreased in dilated cardiomyopathy, but little is known about how it changes at different stimulation frequencies. This may be important in heart failure because the patients typically exhibit symptoms due to physical exertion as the heart cannot appropriately respond to the increased heart rate to increase contractility. We hypothesized that failing hearts will have slower cross-bridge cycling rates compared to non-failing hearts as stimulation frequency is increased. We isolated intact human left ventricular trabeculae from failing hearts and measured the rate of tension redevelopment (ktr), an often-used index of rate of cross-bridge cycling. Etiologies of heart failure can be categorized into two types: ischemic cardiomyopathy (ICM) and non-ischemic cardiomyopathy (NICM). Here, we present our preliminary data that suggest that failing hearts with ICM and NICM may have different kinetic parameters, especially at high stimulation frequencies. When normalized to the baseline ktr at 0.5 Hz, ktr in failing left ventricular trabeculae with NICM collected at maximal calcium activation are slower at high stimulation frequencies (2 and 3 Hz) compared to non-failing samples. In addition, preliminary data suggest failing left ventricular trabeculae with ICM do not have significantly different ktr across the in vivo range of frequencies (0.5 Hz to 3 Hz) compared to non-failing samples. Due to the small sample size and individual variability of human myocardium, we currently cannot make any definitive conclusions regarding the differences in the ktr of NICM and ICM left ventricular trabeculae. However, we will continue to collect more human myocardium data to better understand the kinetics of cross-bridge cycling.