To determine whether hyperthyroidism selectively increases beta-adrenergic receptor density in vessels or fibers of human skeletal muscle, we characterized beta-receptor distribution autoradiographically in muscle biopsies of 18 subjects aged 26 +/- 1 yr before and after daily administration of 100 micrograms 3,5,3'-triiodothyronine (T3) for 2 wk. To establish whether vascular and metabolic responses to beta-adrenergic stimulation are concomitantly altered, we quantified calf blood flow and plasma concentrations of glucose, lactate, glycerol, free fatty acids (FFA), insulin, and C-peptide during graded-dose isoproterenol infusion in eight of these individuals. Differences in beta-adrenergic receptor density among muscle fiber types and vascular components were highly significant (type I greater than type IIa greater than type IIb muscle fibers, P less than 0.001; and type I muscle fibers greater than resistance arterioles, P less than 0.05). Hyperthyroidism increased beta-adrenergic receptor density in all types of muscle fibers (+31-50%; P less than 0.01) but not in resistance arterioles. There was no change in calf blood flow or plasma glucose, glycerol, FFA, insulin, or C-peptide responses to isoproterenol. A rise in lactate during stages 3 and 4 of isoproterenol infusion (P less than 0.01) was observed before but not after T3 administration. Thus hyperthyroidism increases beta-adrenergic receptor density in fibers but not vessels of human skeletal muscle without increasing either metabolic or vascular responses to selective beta-adrenergic stimulation.
Carbonic anhydrase III in skeletal muscle fibers: an immunocytochemical and biochemical study.