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O2 dynamics during treadmill and arm exercise in peripheral arterial disease
1Section of Vascular Medicine, 2Division of Geriatrics, and 3Department of Surgery, Section of Vascular Surgery, University of Colorado Health Sciences Center, Denver, Colorado 80262; Departments of 4Anatomy and Physiology, and 5Kinesiology, Kansas State University, Manhattan, Kansas 66506;6Center for Clinical Pharmacology, Harbor-University of California–Los Angeles Medical Center, Torrance, California 90502
Submitted 16 June 2003 ; accepted in final form 8 April 2004
Slowed pulmonary O2 uptake (
O2) kinetics in peripheral arterial disease (PAD) have been attributed to impaired limb blood flow and/or peripheral muscle metabolic abnormalities. Although PAD results from atherosclerotic occlusive disease in the arteries to the lower extremities, systemic abnormalities affecting whole body O2 delivery or vascular function in PAD could also partially explain the exercise impairment. To date, the effects of these systemic abnormalities have not been evaluated. To test the hypothesis that the slowed pulmonary O2 kinetics in PAD reflects local and not systemic abnormalities, O2 kinetics were evaluated after the onset of constant-load exercise of the upper and lower limbs in PAD patients and healthy controls (Con). Ten PAD patients and 10 Con without significant cardiopulmonary dysfunction performed multiple transitions from rest to moderate-intensity arm ergometry and treadmill exercise to assess their O2 kinetic responses. Reactive hyperemic (RH) blood flow was assessed in the arms and legs as a measure of endothelial function. Compared with Con, PAD O2 kinetic phase 2 time constants were prolonged during treadmill exercise (PAD 34.3 ± 9.2 s vs. Con 19.6 ± 3.5 s; P < 0.01) but not arm exercise (PAD 38.5 ± 7.5 s vs. Con 32.5 ± 9.0 s; P > 0.05). RH blood flow was significantly reduced in the legs (PAD 20.7 ± 8.3 vs. Con 46.1 ± 17.1 ml·100 ml–1·min–1; P < 0.01) and arms of PAD subjects (PAD 34.0 ± 8.6 vs. Con 50.8 ± 12.2 ml·100 ml–1·min–1; P < 0.01) compared with Con, but RH limb flow was not correlated with arm or treadmill O2 kinetic responses in either group. In summary, slowed pulmonary O2 kinetics in PAD patients occur only with exercise of the lower limbs affected by the arterial occlusive disease process and are not slowed with exercise of the unaffected upper extremities compared with controls. Furthermore, the slowed pulmonaryO2 kinetics of the lower extremity could not be explained by any abnormalities in resting cardiac or pulmonary function and were not related to the magnitude of reduction in limb vascular reactivity.
oxygen consumption; vascular disease; reactive hyperemia
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