Based upon literature and our own experimentation on Goldblatt rats, the significance of a decrease of the maximal shortening velocity of the myocardium at zero load (Vmax) in the hypertrophied, chronically pressure-loaded heart is discussed. In the hypertrophied myocardium with varying concentrations of the contractile structures, the developed tension under isometric conditions (sigma) and the maximum rate of tension development (d sigma/dtmax) can indicate significant deviations from the values of controls of the same age, without, however, making it possible to draw from these changes absolute conclusions about the elementary contractile process. With the enhanced concentration of contractile proteins, the mentioned isometric values, as well as the maximum instantaneous power (cross-sectionally related) of the myocardium can be increased during a stage of hypertrophy in which Vmax is already reduced. The decrease of Vmax shows a rough correlation with the reduction of the specific ATPase activity of actomyosin and is already observed at moderate degrees of hypertrophy (30 to 50%). The time course of the change of both parameters in experimental hypertrophy suggests a causal relation between the changes of those two parameters and the failure of the myocardium in later stages of a chronic overload. Under the condition of reliable estimation, Vmax allows for, also with changed actomyosin concentration, an assessment of the elementary contractile process. On the other hand, Vmax does not present a sufficient measure for the cross-sectionally related power capacity of the hypertrophied myocardium. The possible dissociation between the unloaded shortening velocity and the cross-sectionally related power capacity could, in certain cases, explain an unsatisfactory correlation between Vmax and the clinical state of the heart. The so-called empirical indices of contractility, which are not always clearly related to basic physiological characteristics of the myocardium, should be interpreted with particular reserve in relation to the hypertrophied cardiac muscle.