STRUCTURAL AND FUNCTIONAL-CHANGES IN SKELETAL-MUSCLE IN ANOREXIA-NERVOSA

Protein-energy malnutrition in anorexia nervosa is an under-recognised cause of muscle dysfunction. To characterise the skeletal myopathy th at occurs in patients with severe anorexia nervosa, muscle function an d structure were comprehensively examined in eight young adult female patients with severe (40%) self-induced weight loss. All of the patien ts showed impaired muscle function on strength and exercise measuremen t. The maximum voluntary contraction force for the patient group was s ignificantly less than predicted values. Electromyography revealed myo pathy in five of the patients, four of whom also had electro-physiolog ical evidence of neuropathy. However, muscle biopsy specimens consiste ntly Introduction showed myopathic changes with severe type 2 fibre at rophy but with no evidence of neuropathic changes. Ultrastructurally, there was separation and segmental loss of myofibrils and most biopsy samples contained abundant glycogen granules; we have previously repor ted that one of the most consistent biochemical abnormalities in these patients is impaired ischaemic lactate responses to forearm exercise. The result of severe protein-energy malnutrition on the musculo-skele tal system is a metabolic myopathy. Although the patients admitted to a variety of abnormal dieting behaviours, such as over-exercising and self-induced vomiting, no association was found between any of these a nd quantitative histological changes in the muscle biopsy samples. It is recommended that myopathy in anorexia nervosa be treated by institu ting an appropriate refeeding programme.