CHRONIC ALCOHOLIC PROXIMAL WASTING: PHYSIOLOGICAL, MORPHOLOGICAL AND BIOCHEMICAL STUDIES IN SKELETAL MUSCLE
Article first published online: 25 MAR 2008
Australian and New Zealand Journal of Medicine
Volume 17, Issue 4, pages 413–419, August 1987
How to Cite
TROUNCE, I., BYRNE, E., DENNETT, X., SANTAMARIA, J., DOERY, J. and PEPPARD, R. (1987), CHRONIC ALCOHOLIC PROXIMAL WASTING: PHYSIOLOGICAL, MORPHOLOGICAL AND BIOCHEMICAL STUDIES IN SKELETAL MUSCLE. Australian and New Zealand Journal of Medicine, 17: 413–419. doi: 10.1111/j.1445-5994.1987.tb00078.x
- Issue published online: 25 MAR 2008
- Article first published online: 25 MAR 2008
- Accepted for publication: 10 April 1987
- Alcoholic myopathy;
- glycolytic enzymes;
- mitochondrial studies.
Abstract Electromyography, muscle histochemistry and assay of all glycolytic enzymes, phosphorylase, glycogen, carnitine and several mitochondrial marker enzymes in skeletal muscle (vastus lateralis) were carried out in two groups. One group comprised chronic alcoholic patients with prominent proximal wasting, the other was an alcoholic group with normal neuromuscular examination. Biochemical results were compared with data from control groups with normal muscle histology and with non-alcohol related type 2b fibre atrophy. Either 2b atrophy factor or 2b variability coefficient were increased in all wasted alcoholic patients, with normal values in alcoholics without wasting. Electromyography studies were usually normal in proximal muscles, although several patients had mild distal neuropathies. A significant fall in activity of phosphorylase and all glycolytic enzymes was found in wasted alcoholics with reference to normal controls. In the non-ethanolic 2b atrophy group the activity of several glycolytic enzymes was also significantly lower, but for each enzyme the mean activity was not depressed to the same extent as in the wasted alcoholic group. Muscle glycogen, carnitine, and mitochondrial marker enzyme activities (isocitrate dehydrogenase, monoamine oxidase, cytochrome oxidase) were normal in alcoholics with proximal wasting. It is concluded that there is no deficiency of mitochondrial marker enzymes in wasted alcoholics and that a significant depression in glycogenolytic and glycolytic enzyme activity is seen which is explained in part, but probably not fully, by 2b fibre atrophy.