The clinical model of exercise inducing an ischaemia-reperfusion type injury has been substantiated by evidence of markers of inflammation. Neutrophils are the first cells to begin accumulating in the tissue at the injury site, destroying necrotic tissue through phagocytosis while working in conjunction with resident macrophages from the muscle tissue itself. Neutrophil presence has been documented in muscle after various types of eccentric exercise. A study looking at neutrophil function in exercising claudicants showed increased neutrophil activation manifest by increased expression of the neutrophil adhesion receptor cluster of differentiation antigen IIb (CD11b) and degranulation manifest by an increase in plasma neutrophil elastase. This occurred immediately after exercise in these patients with intermittent claudication. Whether this equates to a trend to predict outcomes is still not clear.