Effects of thyroid hormone on Ca2+ efflux and Ca2+ transport capacity in rat skeletal muscle

The present study was undertaken to investigate the effects of 3,5,3'-triiodothyronine (T3) treatment on passive Ca2+ efflux, Ca2(+)-dependent Mg2(+)-ATPase (Ca2(+)-ATPase) concentration and active Ca2+ transport in isolated rat skeletal muscle. In addition, the question was examined whether changes in Ca2+ efflux at rest and during electrical stimulation in the hyperthyroid state were accompanied by parallel changes in 3-O-methylglucose efflux. The resting Ca2+ efflux from rat soleus muscle was increased by 25% after 8 days of treatment with T3 (20 micrograms/100 g body weight). This was associated with a 78% increase in the basal efflux of 3-O-methylglucose. Electrical stimulation resulted in a rapid stimulation of Ca2+ efflux and 3-O-methylglucose efflux in the two groups of rats, and the levels obtained were significantly higher in the T3-treated group. The stimulating effect of the alkaloid veratridine on Ca2+ efflux was 60% larger in 8-day hyperthyroid rats. Within 24 h after the start of T3 treatment, a significant (21%) increase in Ca2(+)-ATPase concentration was detected. Significant increases in active Ca2+ uptake and passive Ca2+ efflux were not observed until after 2 and 3 days of T3 treatment, respectively. It is concluded that T3 stimulates the synthesis of Ca2+ ATPase and augments the intracellular Ca2+ pools (sarcoplasmic reticulum and mitochondria). The latter results in enhancement of the passive Ca2+ leak, which in turn, may lead to activation of substrate transport systems. The suggested increase in intracellular Ca2+ cycling after T3 treatment may, at least partly, explain the T3-induced stimulation of energy metabolism.