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1 Department of Respiratory Medicine, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, The Netherlands
2 Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, The Netherlands
3 Movement Sciences, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, The Netherlands
* To whom correspondence should be addressed. E-mail: h.gosker{at}pul.unimaas.nl.
Oxidative capacity and uncoupling protein-3 (UCP3) content are reduced in limb muscles of patients with chronic obstructive pulmonary disease (COPD). It has been hypothesized that the physiological role of UCP3 is to protect mitochondria against lipotoxicity in case where fatty acid influx exceeds the capacity to oxidize them. Exercise training improves oxidative capacity and reduces UCP3 protein content in healthy subjects, but the response of UCP3 to training in COPD is unknown. We studied the effect of exercise training on UCP3 content in limb muscles of COPD patients. For this, seven healthy age-matched subjects and thirteen patients with COPD were studied. All patients were admitted to an eight-week exercise training intervention. Exercise capacity was assessed by means of an incremental cycle ergometry test. Biopsies were taken from the vastus lateralis in which UCP3 and lipid peroxidation levels were determined by Western Blotting. Citrate synthase and 3-hydroxyacyl-CoA dehydrogenase (HAD; an enzyme involved in fatty acid oxidation) were measured as indices of muscle oxidative capacity. UCP3 in COPD was ~50% lower compared to healthy age-matched controls. In COPD, training induced upregulation of UCP3 (from 67.7 ± 41.8 to 113.8 ± 104.2 AU, p=0.062), especially in the patients who showed no increase in HAD activity (from 80.9 ± 52.6 to 167.9 ± 109.1 AU, p=0.028), whereas lipid peroxidation levels remained unaltered. We conclude that exercise-training can restore muscle UCP3 protein level in COPD and the nature of this response complies with the hypothesis that UCP3 may protect against lipotoxicity.
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