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Published online before print December 20, 2006
Eur Respir J 2006, doi:10.1183/09031936.00086306
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ORIGINAL ARTICLE

Mitochondrial dysfunction in copd patients with low body mass index

R.A. Rabinovich 1*, R. Bastos 1, E. Ardite 1, L. Llinàs 1, M. Orozco-Levi 2, J. Gea 2, J. Vilaró 3, J.A. Barberà 1, R. Rodriguez-Roisin 1, J.C. Fernandez-Checa 4, J. Roca 1

1 Servei de Pneumologia (ICT), Hospital Clínic, IDIBAPS, Universitat de Barcelona, Barcelona
2 Muscle and Respiratory System Research Unit, IMIM, CEXS, Universitat Pompeu Fabra; and Respiratory Medicine Department, Hospital del Mar, Barcelona
3 EUIF Blanquerna. Universitat Ramon Llull, Barcelona
4 Liver Unit (IMD)-CSIC, IDIBAPS, Universitat de Barcelona, Barcelona, Spain

* To whom correspondence should be addressed. E-mail: roberto.rabinovich{at}ed.ac.uk.


  Abstract

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. This study explores the association between body composition and mitochondrial respiration in seven patients with low body mass index (BMIL), eight COPD patients with normal BMI (BMIN), 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, isolated mitochondria and whole muscle glutathione levels were determined. Mitochondrial respiratory function (ACR, acceptor control ratio) was impaired in BMIL (2.2±0.6) compared to both BMIN (5.3±1.3) and controls (8.2±1.3) (ANOVA, p<0.01). ACR significantly correlated with PaO2 (r=0.70, p<0.01) and with muscle endurance (r=0.44, p<0.05); but, it showed a negative association with exercise-induced increase in blood lactate levels (r= -0.60, p=0.01). UCP3 mRNA expression was reduced in BMIL patients (p=0.07). We conclude that COPD patients with low BMI show electron transport chain dysfunction that may contribute to low muscle endurance in this subgroup of patients.

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




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