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Tissue anoxia has for long been invoked as a cause of venous leg ulcers, and recently it has been suggested that pericapillary fibrin prevents the diffusion of oxygen in the skin. In the present study direct measurements of skin oxygen levels on the lower leg were made using a transcutaneous oxygen monitor. In the recumbent position mean oxygen tensions were higher in patients than in controls, thus disproving the existence of any block to oxygen diffusion. In both groups there was a fall in oxygen tension to low levels on standing as a result of the normal reflex vasoconstrictor response to increased venous pressure. Exercise produced a marked rise in skin oxygen tension in normal legs but not in those affected by venous insufficiency. In normal subjects exercise reduces venous pressure, thus removing the stimulus for reflex vasoconstriction. In patients with defective valves, the venous pressure remains high during exercise and reflex vasoconstriction persists. It is concluded from this study that the sustained low skin oxygen tension in the upright position even during exercise is responsible for leg ulcer formation associated with venous insufficiency. Normal legs are protected by a rise in skin oxygenation during exercise.