Mitral regurgitation (MR) causes ventricular dilation, a blunted myocardial force-frequency relation, and increased crossbridge force-time integral (FTI). The mechanism of FTI increase was investigated using sinusoidal length perturbation analysis to compare crossbridge function in skinned left ventricular (LV) epicardial muscle strips from 5 MR and 5 nonfailing (NF) control hearts. Myocardial dynamic stiffness was modeled as 3 parallel viscoelastic processes. Two processes characterize intermediate crossbridge cycle transitions,B(work producing) andC(work absorbing) with Q10s of 4 to 5. No significant differences in moduli or kinetic constants of these processes were observed between MR and NF. The third process,A, characterizes a nonenzymatic (Q10=0.9) work-absorbing viscoelasticity, whose modulus increases sigmoidally with [Ca2+]. Effects of temperature, crossbridge inhibition, or variation in [MgATP] support associating the calcium-dependent portion ofAwith the structural “backbone” of the myosin crossbridge. Extension of the conventional sinusoidal length perturbation analysis allowed using the A modulus to index the lifetime of the prerigor, AMADP crossbridge. This index was 75% greater in MR than in NF (P=0.02), suggesting a mechanism for the previously observed increase in crossbridge FTI. Notably, theA-process modulus was inversely correlated (r2=0.84,P=0.03) with in vivo LV ejection fraction in MR patients. The longer prerigor dwell time in MR may be clinically relevant not only for its potential role as a compensatory mechanism (increased economy of tension maintenance and increased resistance to ventricular dilation) but also for a potentially deleterious effect (reduced elastance and ejection fraction).