Evaluation of the Metabolic Compensation After Treadmill Test in Patients with Peripheral Occlusive Arterial Disease

Abstract

Patterns of release of lactate, hypoxanthine, and arginine into the bloodstream after a standardized treadmill test (twelve minutes, 1.6-2.8 mph, inclination 0,5,10,15%) were recorded in 21 consecutive patients with stage II peripheral arterial occlusive disease. Heart rate, systolic blood pressure, ankle blood pres sure, and ankle/brachial systolic blood pressure ratio (A/B ratio), as well as plas ma lactate, plasma hypoxanthine and serum arginine were recorded before and at fifteen to thirty-minute intervals for up to two hours after the treadmill test.

Immediately after the treadmill test, lactate levels (36.6 ± 3.7 mg/L) and hypoxanthine levels (2.73 ± 0.19 mmol/L) were significantly (p < 0.001) increased but returned to preexercise levels after thirty and sixty minutes, respectively. Ar ginine levels did not change significantly. Ankle blood pressure (57 ± 5 mm Hg) and A/B ratio (0.40 ± 0.04) were significantly (p < 0.001) decreased after exercise, while heart rate and systolic blood pressure were increased. These parameters returned to normal as well within a half hour after exercise. Abso lute walking distance correlated significantly (p < 0.01) with the postexercise sys tolic blood pressure (r = - 0.62), ankle pressure (r = 0.63) and A/B ratio (r = 0.72). Induced hypoxanthine and lactate production intercorrelated signifi cantly positively (r = 0.57, p = 0.007) but were independent of the absolute walking distance. In contrast with lactate, hypoxanthine production correlated significantly with postexercise ankle pressure (r = 0.49, p = 0.02) and exercise- induced fall in A/B ratio (r = 0.66, p = 0.001). Initial preexercise venous hypox anthine, but not lactate levels were correlated with postexercise A/B ratio (r = - 0.49, p = 0.02) but not with the patients' walking distance.

These results indicate that hypoxanthine determination may reflect more close ly than lactate the degree of metabolic compensation after exercise in peripheral arterial occlusive disease.