Impaired muscle oxygen use at onset of exercise in peripheral arterial disease

Objectives. In patients with peripheral arterial disease (PAD), abnormal muscle metabolism and impaired oxygen delivery distal to the arterial occlusions may contribute to the exercise limitation observed in this population. Muscle tissue hemoglobin saturation (StO(2)) measured with near-infrared spectroscopy, reflects the relative contributions of oxygen delivery and oxygen use. Thus differences in the kinetics Of StO(2) in response to exercise may yield important insight into the potential mechanisms associated with the PAD exercise impairment. The purposes of this study were to characterize the muscle oxygenation responses in patients with PAD and in healthy control subjects at the onset of exercise, and to compare the kinetics of StO(2) desaturation. We hypothesized that at the onset of exercise the kinetics of StO(2) desaturation would be slowed in PAD compared with control responses. Material and methods: Six patients with PAD and 6 healthy control subjects from a university center were examined in a prospective cross-sectional analysis that evaluated the desaturation kinetics of StO(2) at the onset of walking exercise. On separate visits subjects performed graded treadmill exercise and 3 constant work rate treadmill tests equivalent to similar to60% (low), similar to80% (medium), and 100% (peak) of their peak exercise work rate. Gastrocnernious muscle StO(2) response profiles (InSpectra tissue spectrometer) were measured at rest and across the rest to exercise transition. Muscle StO(2) responses were characterized by an exponential mathematical model. The end point value was taken as the time constant of StO(2) desaturation after onset of exercise (ie, equivalent to time to reach approximately 63% of StO(2) decrease). Results: The patients with PAD and the control subjects were of similar age and activity level. The qualitative patterns of StO(2) responses at onset of exercise were also similar between patients and control subjects at all work rates. However, the kinetic time constants of StO(2) desaturation were prolonged in patients with PAD versus control subjects (averaged time constant across all work rates, 21.9 +/- 9.4 seconds vs 4.9 +/- 2.2 seconds; P <.01). Conclusions. The slowed muscle StO(2) kinetics in PAD are consistent with an impairment in muscle oxygen use at the onset of walking exercise. Impaired muscle metabolism may contribute to the altered physiologic responses to exercise and to exercise impairment in patients with PAD.