1. The steady-state heat production rate (E) of soleus muscles obtained from adult mice in various thyroid states was measured in a perfused microcalorimeter. The ouabain-suppressible fractions of E and 42K influx were compared and the energetic efficiency of active Na-K transport assessed. 2. Hypothyroidism with plasma thyroxine concentrations below 1 microgram/100 ml. was induced by pretreatment with 131I or perchlorate. In soleus muscles isolated from treated animals, mean E values were 25.1 +/- 0.7 and 24.2 +/- 0.5 mcal.g wet wt.-1.min-1 for the 131I and the perchlorate series respectively, i.e. about 30% lower than the control level (36.3 +/- 1.5 mcal.g wet wt.-1.min-1). Following triiodothyronine treatment, E was increased by about 45%. 3. In muscles from hypothyroid (131I and perchlorate series), euthyroid and hyperthyroid mice ouabain (10(-3) M) induced a rapid decrease in E of 1.6 +/- 0.1 and 1.4 +/- 0.1, 2.5 +/- 0.2, and 4.3 +/- 0.6 mcal.g wet wt.-1.min-1 respectively, i.e. between 6 and 8% of E. 4. In muscles obtained from hypothyroid, euthyroid and hyperthyroid mice, the ouabain-suppressible component of 42K influx was 0.17 +/- 0.04, 0.31 +/- 0.02 and 0.45 +/- 0.02 micromole. g wet wt.-1.min-1 respectively. Whereas the total number of ouabain binding sites varied appreciably with the thyroid status, the Na-K contents of soleus or diaphragm muscles showed no significant changes. 5. Notwithstanding the parallelism between the changes in basal E and ouabain-sensitive components of E and K influx with the thyroid status, it is concluded that active NA-K transport cannot be considered a primary effector of thyroid thermogenesis in intact mammalian skeletal muscle. The direct contribution of active NA-K transport to this thermogenesis was indeed small compared with the over-all cellular energy dissipation. 6. The minimum over-all energetic efficiency of the transport process in the intact muscles (30--35%) was not dependent on the thyroid status.