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Mitochondrial dysfunction in COPD patients with low body mass index

¹ Pneumology Service (ICT), Hospital Clinic, and ⁶ Liver Unit (IMD)-CSIC, IDIBAPS, Barcelona University, ³ Muscle and Respiratory System Research Unit, IMIM, CEXS, Pompeu Fabra University, ⁴ Respiratory Medicine Department, Hospital del Mar, and ⁵ EUIF Blanquerna, Ramon Llull University, Barcelona, Spain., and ² R.A. Rabinovich and R. Bastos contributed equally to the study.

CORRESPONDENCE: R. A. Rabinovich, ELEGI Laboratory, Centre for Inflammation Research MRC/University of Edinburgh 47 Little France Crescent, Edinburgh EH16 4TJ, UK. Fax: 44 1312426582. E-mail: roberto.rabinovich{at}ed.ac.uk

Keywords: Endurance training, glutathione, mitochondrial respiration, muscle dysfunction

Received: June 30, 2006
Accepted December 10, 2006

Patients with chronic obstructive pulmonary disease (COPD) show abnormal adaptations of skeletal muscle redox status after exercise training. Increased skeletal muscle oxidative stress in COPD patients may prompt mitochondrial dysfunction.

The present study explores the association between body composition and mitochondrial respiration in seven COPD patients with low body mass index (BMI_L), eight COPD patients with normal body mass index (BMI_N) and seven healthy controls. All of them underwent a vastus lateralis biopsy in which muscle structure, in vitro mitochondrial respiratory function, uncoupling protein 3 (UCP3) mRNA expression and glutathione levels in both isolated mitochondria and the whole muscle were determined.

Mitochondrial respiratory function (assessed by acceptor control ratio (ACR)) was impaired in BMI_L (2.2±0.6) compared with both BMI_N (5.3±1.3) and controls (8.2±1.3). ACR significantly correlated with arterial oxygen tension and with muscle endurance but it showed a negative association with exercise-induced increase in blood lactate levels. UCP3 mRNA expression was reduced in BMI_L patients.

In conclusion, chronic obstructive pulmonary disease patients with low body mass index show electron transport chain dysfunction, which may contribute to low muscle endurance in the current subgroup of patients.

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