The metabolic consequences of reduced habitual activities in patients with muscle pain and disease.

Abstract

Abstract Activities of mitochondrial enzymes have been measured in percutaneous muscle biopsies obtained from 23 patients with non-specific muscle pains (e.g. effort syndromes and post-viral fatigue syndromes), in biopsies obtained from eight patients with McArdle's disease (myophosphorylase deficiency), an enzyme defect known to lead to muscle pain during exercise, and, for comparison, in biopsies obtained from 14 untrained controls. Exercise performance was studied during incremental cycle ergometry in six typical patients with non-specific muscle pains and in six patients with McArdle's disease. The patients in general had a lower content of mitochondria in their muscles than the controls. The patients with nonspecific pain studied during cycle ergometry could not exercise at high intensities and showed decreased endurance, tachycardia, a high degree of exercise stress and an increased dependence on glycolysis at low exercise intensities. Many of the biochemical changes during exercise and many of the symptoms of these patients could be a consequence of their reduced habitual activities. The patients with McArdle's disease also could not exercise at high intensities because of their metabolic defect. The most ‘active’ patients had a normal content of mitochondria in their muscles and performed better during cycle ergometry. Furthermore, in contrast to the others they managed to remain successful in their profession. This study appears to suggest that the physical and mental well-being of patients with muscle pain and disease could be improved by the enhancement of their habitual activity.