Abstract

The ability of muscle fibres to sustain force can be related to their economy of energy utilization and to their capacity to regenerate energy. The patho-physiology of muscle fatigue is analysed in patients with thyroid dysfunction and with impaired glycogenolysis, and in a patient with abnormal mitochondrialfunction. Muscle from hypothyroid patients is slow in relaxing and shows a reduced energy requirement and reduced fatiguability, whereas muscle of hyper-thyroid patients may show the opposite features. In myophosphorylase defi- ciency the energy economy is normal in the fresh state and increases as con- traction proceeds; however, fatigue is premature and associated with impaired excitation rather than an overall depletion of energy stores. With abnormal mitochondrial function the muscle tends to be effectively anaerobic and fa- tigue is associated with impaired excitation-contraction coupling. This appears to result from either muscle ischaemia or the dominant use of anaero- bic metabolism for energy regeneration. Fatigue in these disorders of energy metabolism may ultimately be due to a reduced supply of ATP but direct evi- dence of this is lacking and, if it occurs, its physiological expression is probably variable. Verf.-Referat