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Peripheral arterial disease results in varying degrees of functional disability. Although principally a disease of the vascular tree, evidence demonstrates a significant contribution from metabolic alterations within ischaemically affected skeletal muscle. This thesis was concerned with better characterising the nature of these metabolic alterations, and their contribution to the functional disability in PAD patients. It also examined the efficacy of dietary carbohydrate supplementation as a therapeutic intervention in PAD. The activity of the pyruvate dehydrogenase complex (PDH) is an important determinant of carbohydrate metabolism, experiment I examined the possibility that the active fraction of PDH (PDHa) is lower than normal in skeletal muscle of patients with intermittent claudication (IC) or patients with chronic limb ischaemia and rest pain (RP). A resting muscle biopsy was taken from the medial gastrocnemius of 11 patients with IC, seven patients with RP and eight healthy control subjects (CON). Biopsies were analysed for PDHa, acetylcarnitine, glycogen and phosphocreatine. In the RP group resting PDHa was 60 percent lower than CON (0.19 ± 0.21 versus 0.53 ± 0.27 mmol.min·1.kg·1 wet wt), but not significantly different (p = 0.09) from IC (0.42 ± 0. i 7 mmol.min·1.kg·1 wet wt); PDHa was not different between IC and CON (p = 0.54). There was no difference in muscle acetylcarnitine and glycogen between the groups, nor were there any associations between PDHa and resting acetylcamitine. Further work is warranted in determining the significance of the reduction in PDHa in the RP group, its relationship to symptoms and amenability to treatment. Study two examined the extent to which resting metabolic changes within ischaemic muscle account for the exercise intolerance in PAD patients with intermittent claudication. Specifically, study two tested the hypothesis that walking intolerance in intermittent claudication (IC) is related to both slowed whole body V02 kin