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To test the hypothesis of a myofascial component in intermittent claudication, 56 male patients were studied. Calf blood flow, at rest and during postischemic and postexercise hyperemia, presence of trigger areas, and exercise tolerance were evaluated and compared. The results can be summarized as follows: The exercise tolerance is reduced when trigger areas are present in the calf muscles, and the more severe the trigger areas, the lower is the exercise tolerance. Trigger areas are more severe when the hyperemic flow is more reduced. The peak flow of reactive hyperemia is also correlated to work load. Pain in intermittent claudication is a complex phenomenon. According to the aforesaid results, the severity of limb ischemia and the presence of trigger areas in the calf appear to be the major factors. Besides the two reasons already known, a third is suggested to explain calf claudication: the elective location of trigger points in the gastrocnemius muscle.

Blood flow in the calf was measured during postexercise hyperemia in normal subjects and in PAD patients by means of a foot ergometer that gives direct reading of the work performed. In normals, first and peak flow increased with the rise of work load up to 100 KGM. The duration of hyperemia increased with a work load of 30 to 200 KGM. In PAD patients, first flow did not coincide with peak flow. Peak flow was lower and delayed, and the duration of hyperemia was more prolonged than in normal subjects. In patients with intermittent claudication, first flow, peak flow, and work load were higher than in patients with rest pain or impending gangrene. Exercise hyperemia appears as a useful test for screening normal limbs from those with arterial obstruction. Since in PAD patients exercise is interrupted when muscular pain appears, it is evident that the earlier the arrest of work and the appearance of pain, the greater is the involvement in the arterial tree of the leg. Therefore the exercise hyperemia test can be used also as a means of evaluating the different stages of PAD.

Calf basal resting and reactive hypercemia blood flow were measured at 4-h intervals during a day in fifteen healthy subjects and in fifteen patients with intermittent claudication by means of a venous occlusion plethysmograph. Mathematical-statistical analysis of the data failed to demonstrate circadian periodicity of calf blood flow in healthy subjects, but proved the existence of a 24-h rhythm of calf basal resting and reactive hyperemia blood flow in patients with intermittent claudication. This different behavior of calf blood flow can be understood if one considers that in healthy subjects the voluntary muscles in the extremities have a blood supply which can be instantaneously adjusted over a large area. In patients with peripheral arterial disease, on the other hand, the vascular responses in voluntary muscles of the limbs to various endogenous or exogenous stimuli are impaired and reduced. The circadian rhythm observed in patients with intermittent claudication has early evening peaks and a nocturnal trough with a nadir occurring after midnight and before 0400. This rhythm displays marked similarities with those of all other circulatory values. As to the mechanism of rhythm, it is hard to decide whether or not it has an independent endogenous origin. It is known that many of the circulatory variables are interrelated and that some are clearly related to other circadian rhythms. Perhaps the rhythmic reduction of limb blood flow which occurs during the night is the mechanism underlying the nocturnal pain of subjects with limb ischemia by peripheral arterial disease.