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1 Section of Vascular Medicine, University of Colorado Health Sciences Center, Denver, CO, USA; Departments of Anatomy and Physiology, Kansas State University, Manhattan, KS, USA
2 Center for Clinical Pharmacology, Harbor-UCLA Medical Center, Torrance, CA, USA
3 Department of Surgery, Section of Vascular Surgery, University of Colorado Health Sciences Center, Denver, CO, USA
4 Department of Kinesiology, Kansas State University, Manhattan, KS, USA
5 Section of Vascular Medicine, University of Colorado Health Sciences Center, Denver, CO, USA; Division of Geriatrics, University of Colorado Health Sciences Center, Denver, CO, USA
* To whom correspondence should be addressed. E-mail: will.hiatt{at}uchsc.edu.
Slowed pulmonary oxygen uptake kinetics (VO2 kinetics) in peripheral arterial disease (PAD) have been attributed to impaired limb blood flow and/or peripheral muscle metabolic abnormalities. While PAD results from atherosclerotic occlusive disease in the arteries to the lower extremities, systemic abnormalities affecting whole body oxygen 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. In order to test the hypothesis that the slowed pulmonary VO2 kinetics in PAD reflect local and not systemic abnormalities, VO2 kinetics were evaluated following the onset of constant load exercise of the upper and lower limbs in PAD patients and healthy controls. Ten PAD patients and 10 control subjects (CON) without significant cardiopulmonary dysfunction performed multiple transitions from rest to moderate intensity arm ergometry and treadmill exercise to assess their VO2 kinetic responses. Reactive hyperemic (RH) blood flow was also assessed in the arms and legs as a measure of endothelial function. As compared to controls, PAD VO2 kinetic phase 2 time constants were prolonged during treadmill exercise (PAD 34.3+9.2 sec. vs. CON 19.6+3.5 sec., p<0.01) but not arm exercise (PAD 38.5+7.5 sec. vs. CON 32.5+9.0 sec. p>0.05). RH blood flow was significantly reduced in the legs (PAD 20.7+8.3 vs. CON 46.1+17.1 ml/100ml/min, p<0.01) and arms of PAD subjects (PAD 34.0+8.6 vs. CON 50.8+12.2 ml/100ml/min, p<0.01) compared with controls, but RH limb flow was not correlated with arm or treadmill VO2 kinetic responses in either group. In summary, slowed pulmonary VO2 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 as compared with controls. Further, the slowed pulmonary VO2 kinetics of the lower extremity could not be explained by any abnormalities in resting cardiac function, pulmonary function, and were not related to the magnitude of reduction in limb vascular reactivity.
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