Exercise in patients with intermittent claudication results in the generation of oxygen derived free radicals and endothelial damage

Peripheral vascular disease is a major cause of morbidity in Britain. Each year approximately 50,000 patients are admitted to hospital in Britain with a principal diagnosis of peripheral vascular disease and of these over 20,000 have major surgery, including amputations, with an operative mortality of about 10% (Department of Health and Social Security Office of Population Censuses and Surveys 1986). Intermittent claudication is the most common symptom of peripheral vascular disease (Dormandy et al, 1989) and is a symptom of cramp-like muscle pain, brought on by walking, relieved by rest and reproduced by further exercise. It may affect the calf, thigh or buttock muscle groups depending upon the level and degree of vascular obstruction. Intermittent claudication is caused by an inadequate blood supply to the exercising muscles of the lower limb, although the exact pathophysiological mechanism responsible for the symptom remains unknown (Lorentsen, 1973). Five per cent of men over 50 years suffer from intermittent claudication (Dormandy et al,1989). Claudication itself does not cause death, however, the mortality of claudicants is approximately three times that of age and sex matched individuals (Dormandy et al,1989), being about 50% after ten years (Dormandy et al, 1986). Seventy-five per cent of these deaths are due to cardiovascular disease, such as. myocardial infarction, cerebrovascular accidents and aortic aneurysms (Dormandy et al,1989). Paradoxically the disease seems to stabilise symptomatically in seventy-five per cent of patients soon after onset (Dormandy et al,1989) and few claudicants progress to limb threatening ischaemia (Cronenwett et al,1984).