Reduced metabolic efficiency of skeletal muscle energetics in hyperthyroid patients evidenced quantitatively by in vivo phosphorus-31 magnetic resonance spectroscopy.

Skeletal muscle energetics of seven hyperthyroid patients were investigated throughout a rest-exercise-recovery protocol using phosphorus-31 magnetic resonance spectroscopy (31P MRS) to quantitatively document in vivo the metabolic bases of impaired muscle performance in hyperthyroidism. The contributions of the main pathways of adenosine triphosphate (ATP) synthesis to energy production and proton efflux were measured and compared with results from normal muscle. At rest, a reduced concentration of phosphocreatine (PCr) was calculated for hyperthyroid patients when compared with controls, whereas pH and concentrations of inorganic phosphate (Pi) and phosphomonoesters (PME) were not different from controls. During exercise, the analysis of changes in pH and PCr concentration demonstrated that (1) at the onset of exercise, the magnitude of glycolysis activation is significantly larger for patients, resulting in a marked pH decrease; (2) the energy cost of exercise is higher for patients as compared with controls performing the same amount of work; and (3) both anaerobic and aerobic pathways are significantly more activated in the hyperthyroid group throughout the 3 minutes of exercise. During recovery, the rates of proton efflux and PCr resynthesis were similar in both groups, excluding any alteration in oxidative function and proton handling as a cause of initial glycolytic hyperactivation. The increased energy cost measured for patients during exercise evidences an increased need for energy, which is (1) probably linked to the existence of additional ATP-consuming mechanism(s), and (2) supported by hyperactivation of both aerobic and anaerobic pathways. These findings imply that, all things equal, a hyperthyroid muscle requires more energy to function than normal, and as a result is potentially more fatiguable.