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From the authors

¹ Pulmonary Dept (ICT), Hospital Clinic, IDIBAPS, and ⁵ Liver Unit (IMD)-CSIC, IDIBAPS, Universitat de Barcelona, ² Muscle and Respiratory System Research Unit, IMIM, CEXS, Universitat Pompeu Fabra, ³ Respiratory Medicine Dept, Hospital del Mar, and ⁴ EUIF Blanquerna, Universitat Ramon Llull, Barcelona, Spain.

We would like to thank D-J. Slebos and co-workers for their interesting and assertive contribution to the present issue of the European Respiratory Journal. Following their arguments, one can reasonably state that because tobacco smoking is the main cause of chronic obstructive pulmonary disease (COPD), it might also play a role in a mechanism leading to the extra-pulmonary effects of the disease. In their recently published work 1, it was shown that cigarette smoke condensate can induce mitochondrial dysfunction in an in vitro model. This makes it more tempting to embrace their hypothesis. Nevertheless, one should be cautious in transferring in vitro results to the real situation in patients. We should bear in mind that muscle dysfunction, as one of the so-called systemic effects of COPD, is a complex phenomenon caused by multiple factors, such as oxidative stress, systemic inflammation, muscle disuse and hypoxaemia, among others. Our report on mitochondrial dysfunction at the peripheral muscle level in patients with COPD and low body mass index (and significantly reduced fat-free mass index) 2 should be added to the list of pathological findings at the muscle level in these patients. With regard to the smoking status, there were no differences among the three subpopulations included in our study. None of the subjects smoked at the time of their inclusion in the study. Unfortunately, we do not have data on the accumulative smoking history in this population, which may have helped to shed light on this issue. It should be added that, although causality cannot be established, the significant association between acceptor control ratio and arterial oxygen tension may indicate an abnormal mitochondrial adaptation to long-term repeated episodes of cell hypoxia.

D-J. Slebos and co-workers were also interested in mitochondrial adenosine triphosphate production in our population. Although we did not specifically assess the rate of adenosine triphosphate production, the lower State 3 of respiration in energised mitochondria by succinate in the subpopulation of chronic obstructive pulmonary disease patients with low body mass index reflects a lower oxidative phosphorylation in this subset of patients.

REFERENCES

1. van der Toorn M, Slebos DJ, de Bruin HG, et al. Cigarette smoke-induced blockade of the mitochondrial respiratory chain switches lung epithelial cell apoptosis into necrosis. Am J Physiol Lung Cell Mol Physiol 2007;292:L1211–L1218.[Abstract/Free Full Text]
2. Rabinovich RA, Bastos R, Ardite E, et al. Mitochondrial dysfunction in COPD patients with low body mass index. Eur Respir J 2007;29:643–650.[Abstract/Free Full Text]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Permissions Request Permissions Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Rabinovich, R. A. Articles by Roca, J. Search for Related Content PubMed Articles by Rabinovich, R. A. Articles by Roca, J.