A study of human muscle metabolism in relation to exercise, training and peripheral vascular disease.
2015-11-19T08:50:42Z (GMT) by
The introduction to this thesis comprises two parts. A comprehensive review of the mechanisms and control of human skeletal muscle metabolism with emphasis on anaerobic metabolism and the effects of training, and a review of atherosclerosis and peripheral vascular disease with special mention of skeletal muscle metabolism in vascular disease together with an account of areas in which drugs may help in its treatment. There follows a detailed account of the technique for biopsying human skeletal muscle together with the analytical methods for the fluorimetric assay of high energy phosphates, glycogen, glyclolytic intermediates and succinic dehydrogenase activity. Three experimental chapters are then presented. The first describes the Anaerobic Work Test (AWT) and the metabolic changes that occurred in the quadriceps muscle of man after 6 and 30 s of supra-maximal exercise. This showed that within 6 s of exercise of this magnitude more than 50% of ATP was already being supplied by glycolysis. Over a 30 s sprint of the same intensity almost 70% of the energy was supplied by glycolysis and marked reduction in ATP occurred in the presence of significant amounts of PCr. The second experimental chapter examined the influence of high intensity training on the 30 s AWT and a trend for the resulting improvement in performance to be associated with an increased glycolytic capacity was revealed. The final experimental chapter combined a study of metabolic changes in the gastrocnemius muscle of patients with ischaemic rest pain together with a trial of intravenous naftidrofuryl in its treatment. Changes in muscle metabolism observed in patients with rest pain (low glycogen, ATP, PCr and SDH levels) were felt to represent disuse rather than a direct effect of muscle ischaemia and the drug naftidrofuryl conferred no obvious metabolic benefit although it did appear to possess analgesic properties. In the final discussion an hypothesis on fuel supply as a mechanism for fatigue is presented in the light of the metabolic changes reported.