Lower leg blood flow in intermittent claudication

Abstract

Lower leg blood flow was measured at rest and both during and after graduated bicycle exercise in five healthy men and in seventeen patients suffering from various degrees of obliterating arteriosclerosis of the lower limbs. A thermodilution technique was used for flow determinations. The subject exercised in the sitting position and the work load was increased stepwise from a starting load of 100 kpm/min (100 kpm/min load increment every second minute until exhaustion). Three flow phases were depicted during and after the exercise: the aerobic phase, the phase of relative ischaemia and a postexercise phase. During exercise, lower leg blood flow increased approximately twenty times in healthy subjects, while in the arteriosclerotic subjects there was a two-fold to ten-fold increase in flow. In patients with serious distal and proximal stenoses a proximal steal phenomenon was demonstrated during submaximal and maximal exercise. A close correlation was found between maximum individual work load capacity and maximum lower leg blood flow (r = 0.71, P less than 0.001). In the patient group lower leg blood flow at a certain work load was 45% (P less than 0.001) higher in the sitting than in the supine position.

Vasoactive enzymes and blood flow responses to passive and active exercise in peripheral arterial disease

“…Typically, PAD patients who experience intermittent claudication have impaired muscle function and reduced exercise tolerance that limits daily physical activities [2,3]. While alterations in muscle morphology and metabolism are believed to contribute to these functional impairments, it is likely that the limb blood flow limitation is the primary cause of this impairment [4].…”

Skeletal muscle metabolic changes in peripheral arterial disease contribute to exercise intolerance: a point-counterpoint discussion

“…58 There is a large range in leg blood flow responses (200À900 ml min À1 ), and the correlation between maximum leg blood flow and performance is strong and positive. At the average maximum value for a-VO 2 of 0.17 ml ml…”

Chronically ischemic mouse skeletal muscle exhibits myopathy in association with mitochondrial dysfunction and oxidative damage

“…Exercise-induced ischemia-reperfusion is the central problem in PAD patients and in animals with inflow arterial occlusion (2,6,29). The ischemia-reperfusion of every bout of claudication increases oxidative stress, triggers inflammation and oxidative damage to the tissues (4,5,12,13,22,23), and initiates mitochondrial injury and dysfunction (4,5,22,23).…”