Chronic Fatigue Syndrome: Metabolic and Electrophysiological Muscle Responses to Exercise pp. 89-102
Authors: Yves Jammes, Stéphane Delliaux, Jean Guillaume Steinberg, Fabienne Brégeon, of Mediterranée and Lung Function Laboratory, North Hospital, Assistance Publique – Hôpitaux de Marseille, Marseille, France
Abstract: Because chronic fatigue syndrome (CFS) is often diagnosed in later life of subjects who exercise frequently, exercise-induced causes of CFS are highly suspected. Muscle metabolism at rest, during, and after muscle contraction was explored in CFS patients using physiological (oxygen uptake (VO2), arterio-venous oxygen difference) and biochemical assessment (31P resonance magnetic spectroscopy, lactic acid, blood markers of oxidative stress, cytokines, and heat shock proteins, Hsp). In the majority of CFS patients, 1) muscle glycolysis is unaltered, 2) the aerobic capacity is often enhanced and about one-fourth of patients have an increased proportion of type 1 oxidative muscle fibre, 3) exercise-induced production of reactive oxygen species (ROS) is accentuated with reduction of antioxidant defences, 4) the immune response to exercise is rarely modified, 5) recent observations indicate a marked reduction of heat shock proteins (Hsp) expression in response to exercise. Because, in healthy individuals, Hsp protect the cells against the deleterious effects of ROS, it is tempting to speculate that the elevated oxidative stress in CFS patients might result from reduced Hsp expression. CFS patients have also reduced muscle excitability in response to direct stimulation (M wave) and a deregulation of the Na+/K+ and Ca2+-ATPase pumps. M wave alterations are correlated with both the magnitude of reduced K+ outflow from contracting muscles and accentuated oxidative stress. Thus, CFS is characterized by an altered muscle response to exercise which might result from an accentuated oxidative stress, possibly due to reduced Hsp expression.