Role of thyroid hormone in skeletal muscle physiology

Abstract

Thyroid hormones (TH) are crucial for development, growth, differentiation, metabolism and thermogenesis. Skeletal muscle (SM) contractile function, myogenesis and bioenergetic metabolism are influenced by TH. These effects depend on the presence of the TH transporters MCT8 and MCT10 in the plasma membrane, the expression of TH receptors (THRA or THRB) and hormone availability, which is determined either by the activation of thyroxine (T 4 ) into triiodothyronine (T 3 ) by type 2 iodothyronine deiodinases (D2) or by the inactivation of T 4 into reverse T 3 by deiodinases type 3 (D3). SM relaxation and contraction rates depend on T 3 regulation of myosin expression and energy supplied by substrate oxidation in the mitochondria. The balance between D2 and D3 expression determines TH intracellular levels and thus influences the proliferation and differentiation of satellite cells, indicating an important role of TH in muscle repair and myogenesis. During critical illness, changes in TH levels and in THR and deiodinase expression negatively affect SM function and repair. This review will discuss the influence of TH action on SM contraction, bioenergetics metabolism, myogenesis and repair in health and illness conditions.

Inhibition of Type 1 Iodothyronine Deiodinase by Bisphenol A

“…In addition, TH are the primary regulators of the basal metabolic rate, and an imbalance in TH homeostasis can predispose to weight gain [38]. Moreover, TH also regulate the function of important organs and systems, including cardiovascular system [39] and skeletal muscle [40]. The main product of the thyroid gland is T4.…”

Bioengineered human skeletal muscle with a Pax7+ satellite cell niche capable of functional regeneration

“…Growth factors and steroid hormones are more likely to have cell type specific effects, with insulin having been shown in myoblasts to increase fusion and the expression of myogenic genes, as well as driving proliferation (Saini et al, 2018;Wu et al, 2014). Thyroid hormones have well established roles in regulating skeletal muscle growth and differentiation, with hypothyroidism leading to reduced muscle mass (Bloise et al, 2018). At a molecular level the action of T3 on the expression of myogenic genes, MyoD and Myogenin, has been clearly established suggesting T3 will drive myogenesis in engineered muscles (Muscat et al, 1994;Downes et al, 1993).…”

Moderate exercise prevents the cell atrophy caused by hypothyroidism in rats

“…Forced exercise can also induce anxiety-like behaviors independently of corticoid stimulation (Leasure and Jones, 2008). Since hypothyroidism affects muscular function (Bloise et al, 2018), we employed a moderate forced-exercise routine suitable for hypothyroid rats and aimed at not increasing the activity of the HPA axis and other markers of stress. At the end, this exercise program (5 m/min, 30 min/ day, 5 days/week) did not modify the plasma corticos-terone levels, the body temperature and weight or the thyroid activity, nor did it elevate the behavioral index of anxiety.…”

“…It is thus possible that moderate exercise, not involving glucocorticoid upsurge, would stimulate thyroid activity and reduce the adverse effects of thyroid deficiency. Since hypothyroidism affects muscle metabolism (Bloise et al, 2018) and increases its fatigability (Roy et al, 2003), the potential of modest exercising to counteract the cognitive outcomes under these circumstances is a particularly pertinent question. In the present study we assessed the effect of a moderate exercise routine on the development of a hypothyroid condition induced by antithyroid drugs in rats, and evaluated the effect of this exercise protocol on the integrity and function of the population of pyramidal cells of the hippocampus.…”