· In thyroid overactivity, an elevation of metabolic activity that results in increased catabolism in muscle cells, may lead to myopathy. · In thyroid underactivity, glucosaminoglycan deposition in type II and type I muscle fibers leads to impaired contractility of the actin-myosin unit, decreased myosin ATPase activity, and a slower ATP turnover, all of which may lead to myopathy. This evidence concerns the gene MYH14 and myopathy.