Biochemical and inflammatory changes in the exercising claudicant

Intermittent claudication is an early manifestation of atherosclerosis in the leg. The prognosis for the claudicating limb is reasonably good, but patients have excess cardiovascular morbidity and mortality rates compared with a control population. Increasing evidence suggests that the calf pain experienced when walking followed by rest generates a low-grade inflammatory response. The cumulative effects of these individual events may have an adverse effect on the progression of atherosclerosis. A review of the literature was performed to identify studies measuring the exercise-induced inflammatory response in claudicants and to try to identify the role of cumulative inflammatory changes in the progression of atherosclerosis. The effect of exercise training on these markers is briefly explored. Walking until the onset of calf pain (ischaemia) followed by rest (reperfusion) results in the generation of oxygen-derived free radicals, neutrophil activation and a generalized increase in vascular permeability. Baseline levels of chronic inflammatory markers such as acute-phase proteins are elevated in claudicants compared with controls, suggesting that the transient acute inflammatory response has longer-term consequences. Therapeutic exercise training appears to lead to an attenuation of these inflammatory markers. Intermittent claudication can be considered as part of an inflammatory disease process. However, the concerns that exercise training might potentiate the vascular inflammatory response appear to be unjustified, although further work is needed to clarify this. Exercise training should therefore be considered as an important treatment option for claudication.