Developmental changes in the myocardial contractile system were evaluated in the fetus at 18, 21, and 28 days of gestation (full term 31 days) and in 3- to 5-day-old newborn rabbits. Mechanical function was studied using the isolated arterially perfused heart. Perfusion with ryanodine (10(-5) M), an inhibitor of Ca release from the sarcoplasmic reticulum, decreased contractile force and increased the time to peak tension in the 28-day fetus and newborn but these changes were minimal in the 18- and 21-day fetus. Postextrasystolic potentiation, which is thought to be caused by Ca release from the sarcoplasmic reticulum, was observed in the 28-day fetus and the newborn, but was not significant in the 18- and 21-day fetus. An ultrastructural study showed poorly developed sarcoplasmic reticulum and myofibrils in the 18- and 21-day fetus. Although the maximum developed tension observed at high extracellular calcium increased with development, the relative value of developed tension at various extracellular calcium was similar in the three fetal groups and only in the newborn the extracellular calcium-developed tension curve shifted to the right. Myofibrillar yield increased with development but sensitivity of myofibrillar ATPase activity to Ca was similar in the fetus and newborn. These data suggest that 1) the sarcoplasmic reticulum does not function significantly in the 18- and 21-day fetus, 2) although sarcoplasmic reticulum starts to function at late gestation, it does not cause significant changes in intracellular calcium in the fetal period, 3) myocardial contractility remains similar in the fetus from the 18th to 28th day of gestation and major changes in contractility occur after birth.