T3 regulates many aspects of muscle metabolism and insufficiency or inadequate conversion of T4 to T3 may contribute to muscle weakness, cramping, atrophy, and even rhabdomyolysis.
Triiodothyronine (T3), the bioactive form of thyroid hormone, regulates many aspects of skeletal muscle metabolism including fiber composition, calcium mobilization, oxygen consumption, and glucose uptake, and adequate serum levels are needed to maintain muscle homeostasis (Ucci 2019).
Muscle synthesis and breakdown are also regulated by T3 availability. Conversion of T4 to T3 takes place within the muscle, as does the deactivation of both T3 and T4, actions that depend on the deiodinase enzymes at work. Therefore, intracellular levels of T3 may be a determining factor in muscle maintenance.
Both hypothyroidism and hyperthyroidism are associated with muscle complications that may range from cramping and myalgia to atrophy and rhabdomyolysis. Hypothyroid-related muscle loss may be connected to the thyroid hormone’s role in regulating muscle mitochondria while hyperthyroid-related muscle breakdown may be related to increased protein catabolism. Thyroid hormones also take part in muscle regeneration which can be impaired if thyroid hormone availability is compromised. Higher levels of circulating free T3 have been associated with better muscle maintenance while lower levels may be considered a marker of frailty in the elderly (De Stefano 2021).
Animal studies found that the administration of T3 was able to counteract the muscle atrophy associated with starvation and may provide a promising therapy for other types of muscle breakdown (Ucci 2019).
References
De Stefano, Maria Angela et al. “Thyroid Hormone Action in Muscle Atrophy.” Metabolites vol. 11,11 730. 25 Oct. 2021, doi:10.3390/metabo11110730
Ucci, Sarassunta et al. “Thyroid Hormone Protects from Fasting-Induced Skeletal Muscle Atrophy by Promoting Metabolic Adaptation.” International journal of molecular sciences vol. 20,22 5754. 15 Nov. 2019, doi:10.3390/ijms20225754