Modification of the functional capacity of sarcoplasmic reticulum membranes in patients suffering from chronic fatigue syndrome
Authors
Fulle S, Beliab S, Vecchieta J, Morabitoa C, Vecchieta L, Fano G
Institution
Laboratorio Interuniversitario di Miologia, Universita “G d’Annunzio”, Nuovo Polo Didattico, Via dei Vestini, 31, 66013 Chieti Scalo, Italy; and Universita degli Studi, Perugia, Italy
Summary
In chronic fatigue syndrome, several reported alterations may be related to specific oxidative modifications in muscle. Since sarcoplasmic reticulum membranes are the basic structures involved in excitation–contraction coupling and the thiol groups of Ca2+ channels of SR terminal cisternae are specific targets for reactive oxygen species, it is possible that excitation–contraction coupling is involved in this pathology.
We investigated the possibility that abnormalities in this compartment are involved in the pathogenesis of chronic fatigue syndrome and consequently responsible for characteristic fatigue.
The data presented here support this hypothesis and indicate that the sarcolemmal conduction system and some aspects of Ca2+ transport are negatively influenced in chronic fatigue syndrome. In fact, both deregulation of pump activities (Na+/K+ and Ca2+-ATPase) and alteration in the opening status of ryanodine channels may result from increased membrane fluidity involving sarcoplasmic reticulum membranes.
Publication
Neuromuscular Disorders 2003; 13: 479–84. Published by Elsevier Science.
Comment from ME Research UK
A new and exciting development in the biological basis of CFS comes from a team in Italy who have demonstrated significant changes to the physiology of muscle. This is the same team who, in 2000, published evidence of oxidative damage within the vastus lateralis muscles of CFS patients, probably as a consequence of oxygen free radical damage stemming from dysfunctional muscle cell mitochondria. In this most recent study, they suggest that the post-exertional fatigue that is so characteristic of CFS is linked to the basic structures involved in excitation and contraction (E-C) coupling of muscles. Specifically, they hypothesised that the rapid onset of fatigue and accompanying muscle pain are due to modifications of the fluidity of membranes associated with the sarcoplasmic reticulum of the muscle cell. These membranes are central to the spread of action potentials towards the interior of the cell and to the transport of calcium (Ca2+) that initiates contraction of the muscle.
The data reported by the Italian group provides novel evidence of disruption to Ca2+ transport in the muscle of ME/CFS patients. This disruption may be a consequence of the energy status of the cell or to gates in the cell membrane, known as ryanodine channels.
The study was carried out on a small number of CFS patients who were selected on precise clinical criteria along with a similar number of fibromyalgia patients and controls. It is interesting to note that the abnormalities were found only in the CFS group and not the FMS patients, despite the apparent similarity in some symptoms.
