By means of rapid planar Hill type antimony-bismuth thermophiles the initial heat liberated by papillary muscles was measured synchronously with developed tension for control (C), pressure-overload (GOP), and hypothyrotic (PTU) rat myocardium (chronic experiments) and after application of 10(-6) M isoproterenol or 200 10(-6) M UDCG-115. Economy of force production was analyzed by the ratio of initial heat versus developed tension-time integral. This ratio was found to be reduced by 34% in GOP and by 43% in PTU myocardium (P less than 0.01, respectively) indicating increased economy of force production. In contrast, isoproterenol increased initial heat versus tension-time integral by 70% (P less than 0.01) indicating reduced economy of force production. No change in this ratio was found for UDCG-115. The presented data indicates that long and short term modulation of myocardial energetic costs of force generation is possible. The basic mechanisms for these myocardial alterations are discussed.