Walking performance, oxygen uptake kinetics and resting muscle pyruvate dehydrogenase complex activity in peripheral arterial disease

In the present study, we tested the hypothesis that walking intolerance in intermittent claudication (IC) is related to both slowed whole body oxygen uptake (VO₂) kinetics and altered activity of the active fraction of the pyruvate dehydrogenase complex (PDCa) in skeletal muscle. Ten patients with IC and peripheral arterial disease [ankle/brachial index (ABI)=0.73±0.13] and eight healthy controls (ABI=1.17±0.13) completed three maximal walking tests. From these tests, averaged estimates of walking time, peak VO₂ and the time constant of VO₂ (τ) during submaximal walking were obtained. A muscle sample was taken from the gastrocnemius medialis muscle at rest and analysed for PDCa and several other biochemical variables. Walking time and peak VO₂ were approx. 50% lower in patients with IC than controls, and τ was 2-fold higher (P<0.05). τ was significantly correlated with walking time (r=-0.72) and peak VO₂ (r=-0.66) in patients with IC, but not in controls. PDCa was not significantly lower in patients with IC than controls; however, PDCa tended to be correlated with τ (r=-0.56, P=0.09) in patients with IC, but not in controls (r=-0.14). A similar correlation was observed between resting ABI and τ (r=-0.63, P=0.05) in patients with IC. These data suggest that the impaired VO₂ kinetics contributes to walking intolerance in IC and that, within a group of patients with IC, differences in VO₂ kinetics might be partly linked to differences in muscle carbohydrate oxidation.