Fatigue in human metabolic myopathy
Deutscher übersetzter Titel: | Muskelermuedung bei metabolischer Myopathie beim Menschen |
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Autor: | Wiles, C.M.; Jones, D.A.; Edwards, R.H.T. |
Herausgeber: | Porter, Ruth; Whelan, Julie |
Erschienen in: | Human muscle fatigue. Physiological mechanisms |
Veröffentlicht: | : Pitman Medical (Verlag), 1981, S. 264-282 |
Format: | Literatur (SPOLIT) |
Publikationstyp: | Sammelwerksbeitrag |
Medienart: | Gedruckte Ressource |
Sprache: | Englisch |
Schlagworte: | |
Online Zugang: | |
Erfassungsnummer: | PU198205016693 |
Quelle: | BISp |
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