Kaminsky P, Klein M, Duc M
Service de Médecine J, Hôpitaux de Brabois, CHRU de Nancy, Vandoeuvre.
Presse Med. 1993;22(16):774-8.
Thyroid hormones control the expression of genes coding for myosin isoforms, the Na-K ATPase pumps and the Ca-ATPase canals of the sarcoplasmic reticulum. This explains the increase of contractility and relaxation of skeletal muscles observed in hyperthyroidism, as opposed to hypothyroidism. Control of key-enzymes of the main energetic pathways accounts for inhibition of oxidative metabolisms in hypothyroidism and excessive glycolysis recruitment in hyperthyroidism. In both cases muscle performance is reduced, with accumulation of lactic acid at exercise. This is due to defective pyruvate oxidation and proton expulsion in hypothyroidism, and to acceleration of glycolysis in hyperthyroidism. These abnormalities partly explain why subjects with dysthyroidism are intolerant to exertion.
甲状腺激素控制着编码肌球蛋白同工型、钠钾ATP酶泵以及肌浆网钙ATP酶通道的基因的表达。这就解释了甲状腺功能亢进时观察到的骨骼肌收缩性和舒张性增加，与甲状腺功能减退相反。对主要能量代谢途径关键酶的控制导致甲状腺功能减退时氧化代谢受到抑制，而甲状腺功能亢进时糖酵解过度激活。在这两种情况下，肌肉功能都会降低，运动时会有乳酸堆积。这是由于甲状腺功能减退时丙酮酸氧化和质子排出存在缺陷，以及甲状腺功能亢进时糖酵解加速。这些异常部分解释了甲状腺功能紊乱患者不耐运动的原因。
