The role of thyroid hormone on the heart in terms of contractility, induction of growth, and selective synthesis of cardiac isomyosins was studied. After transplanting rat hearts from inbred hypothyroid donors into the abdomen of hypothyroid recipients of the same strain, two hearts were obtained in the same animal, both having reduced heart rate (200–250 bpm), decreased maximum rate of force, and high predominance of V3isomyosin. The heart in situ carried a full load, while the transplant was denervated, beat isovolumically with minimum external work. After surgery, the recipient rats were put either on normal diet only (controls) or injected with a daily dose of T3(average 200 μg/kg), which increased the heart rate to 340 bpm in 3 days (euthyroid level) and to 450 bpm in 7 days (hyperthyroid level). In T3-treated rats, the contractility of both hearts normalized in 7 days and showed hyperthyroid pattern in 14 days, while the mass of the in situ hearts increased to normal values in 7 days (+130 mg) and hypertrophied in 14 days (+ 340 mg), in contrast to the transplanted heart, which underwent atrophy (−90 mg and −210 mg) similar to that of control group (−225 mg). The predominant V3isomyosin was completely reversed to V1in two weeks in both hearts. Thus, T3can neither stimulate cardiac growth nor can it attenuate the rate of atrophy in the denervated ``nonworking'' heart in spite of its direct effect on contractility and synthesis of isomyosins, which was similar to that observed in the in situ heart.