In this report we have emphasized the significant influence of loading conditions on LV relaxation. Changes in inotropic state, ischemia, hypertrophy, and a host of other factors were not discussed herein. Ventricular asynchrony is likewise beyond the scope of this review, but it should be recognized that complex loading interactions among fibers within the LV wall influence relaxation and filling in ventricles that contract and relax nonsynchronously. Intact heart and isolated muscle experiments indicate that changes in preload do not influence relaxation rates when systolic pressure or total load remains constant. It appears, therefore, that the relaxation changes that occur with volume loading are primarily due to changes in systolic pressure or load. Indeed, an increase in systolic pressure may cause a substantial decrease in isovolumic relaxation rate, especially if there is a slow rise and a late peak in LV pressure. By contrast, an abrupt increase in late systolic load augments relaxation rate. Intact heart studies indicate that an abrupt load increment near the end of ejection results in premature and more rapid isovolumic relaxation, while an increase in left atrial pressure increases the filling rate; isolated muscle studies indicate that a load increment at the end of isometric relaxation causes an increase in isotonic relaxation rate. Thus, loading conditions during the periods of ejection, isovolumic relaxation, and filling can influence relaxation parameters and should be considered in clinical and experimental studies of LV relaxation.