We have shown previously that the physiologic, mechanical cardiac cycle is associated with a parallel, cardiac cycle-dependent variation of integrated backscatter (IB). However, the mechanisms responsible are not known. The mathematical and physiological considerations explored in the present study suggest that the relationship between backscatter and myocardial contractile function reflects cyclic alterations in myofibrillar elastic parameters, with the juxtaposition of intracellular and extracellular elastic elements that have different intrinsic acoustic impedances providing an appropriately sized scattering interface at the cellular level. Cardiac cycle-dependent changes in the degree of local acoustic impedance mismatch therefore may elicit concomitant changes in backscatter. Because acoustic impedance is determined partly by elastic modulus, changes in local elastic moduli resulting from the non-Hookian behavior of myocardial elastic elements exposed to stretch may alter the extent of impedance mismatch. When cardiac cell mechanical behavior is represented by a three-component Maxwell-type model of muscle mechanics, the systolic decrease in IB that we have observed experimentally is predicted. Our prior observations of regional intramural differences in IB and the dependence of IB on global contractile function are accounted for as well. When the model is tested experimentally by assessing its ability to predict the regional and global behavior of backscatter in response to passive left ventricular distention, good concordance is observed.