The distribution between
carnitine and the acyl derivatives of
carnitine reflects changes in the metabolic state of a variety of tissues. Patients with
peripheral vascular disease (PVD) develop skeletal muscle
ischemia with exertion. This impairment in oxidative metabolism during exercise may result in the generation of acylcarnitines. To test this hypothesis, 11 patients with PVD and 7 age-matched control subjects were evaluated with graded treadmill exercise. Subjects with PVD walked to maximal claudication
pain at a peak O2 consumption (VO2) of 19.9 +/- 1.3 ml X kg-1 X min-1 (mean +/- SE). Control subjects were taken to a near-maximal work load at a VO2 of 31.3 +/- 1.0 ml X kg-1 X min-1. In patients with PVD, the plasma concentration of total
acid-soluble, long-chain
acylcarnitine and total
carnitine was increased at peak exercise compared with resting values. Four minutes postexercise, the plasma short-chain
acylcarnitine concentration was also increased. In control subjects taken to the higher work load, only the long-chain
acylcarnitine concentration was increased at peak exercise. In patients with PVD, plasma short-chain
acylcarnitine concentration at rest was negatively correlated with subsequent maximal walking time (r = -0.51, P less than 0.05). In conclusion, acylcarnitines increased in patients with PVD who walked to maximal claudication
pain, whereas control subjects did not show equivalent changes even when taken to a higher work load. The relationship between short-chain
acylcarnitine concentration at rest and subsequent exercise performance suggests that repeated episodes of
ischemia may cause chronic accumulation of short-chain
acylcarnitine in plasma in proportion to the severity of disease.(ABSTRACT TRUNCATED AT 250 WORDS)