External compression of limbs to below-diastolic pressure (venous compression) has been shown to produce a short-lived hyperaemia in supply arteries. Intermittent pneumatic compression is currently under investigation therefore as a treatment for peripheral arterial disease. The optimal timing of the compression will depend on the duration of hyperaemia produced by a particular duration of compression, and the purpose of this work was to test that link. Nineteen healthy volunteers underwent intermittent compression of one leg with two compression cycles – one compressing for 10 s each time, the other for 1 min. Blood flow velocities in the common femoral artery was shown to increase on release of the compression by 38% (inter-quartile range 27–56%) for the sequence with short duration compression, and by 57% (inter-quartile range 37–87%) for the longer sequence (difference, P = 0·005, Wilcoxon). The hyperaemia duration above the baseline level was 37 s (inter-quartile range 32–49 s) for the short sequence, and 54 s (inter-quartile range 37–76 s) for the longer sequence (difference, P = 0·001, Wilcoxon). The magnitude of the change in the compression duration was not equalled by the difference in hyperaemia duration, suggesting that the physiological mechanism behind the hyperaemia is unlikely to be due solely to simple accumulation of metabolites, and a myogenic mechanism remains possible. Therapies for peripheral arterial disease need not employ long duration compression, as a greater percentage of time will be spent in hyperaemia with short duration intermittent compression.