RT Journal Article SR Electronic T1 Increased tumour necrosis factor‐α plasma levels during moderate-intensity exercise in COPD patients JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP 789 OP 794 DO 10.1183/09031936.03.00042702 VO 21 IS 5 A1 R.A. Rabinovich A1 M. Figueras A1 E. Ardite A1 N. Carbó A1 T. Troosters A1 X. Filella A1 J.A. Barberà A1 J.C. Fernandez-Checa A1 J.M. Argilés A1 J. Roca YR 2003 UL http://erj.ersjournals.com/content/21/5/789.abstract AB Post-training downregulation of muscle tumour necrosis factor (TNF)‐α messenger ribonucleic acid (mRNA) expression and decrease in cellular TNF‐α levels have been reported in the elderly. It is hypothesised that chronic obstructive pulmonary disease (COPD) patients may not show these adaptations due to their reduced ability to increase muscle antioxidant capacity with training. Eleven COPD patients (forced expiratory volume in one second 40±4.4% of the predicted value) and six age-matched controls were studied. Pre- and post-training levels of TNF‐α, soluble TNF receptors (sTNFRs: sTNFR55 and sTNFR75) and interleukin (IL)‐6 in plasma at rest and during exercise and vastus lateralis TNF‐α mRNA were examined. Moderate-intensity constant-work-rate exercise (11 min at 40% of pretraining peak work-rate) increased pretraining plasma TNF‐α levels in COPD patients (from 17±3.2 to 23±2.7 pg·mL−1; p<0.005) but not in controls (from 19±4.6 to 19±3.2 pg·mL−1). No changes were observed in sTNFRs or IL‐6 levels. After 8 weeks' endurance training, moderate-intensity exercise increased plasma TNF‐α levels similarly to pretraining (from 16±3 to 21±4 pg·mL−1; p<0.01). Pretraining muscle TNF‐α mRNA expression was significantly higher in COPD patients than in controls (29.3±13.9 versus 5.0±1.5 TNF‐α/18S ribonucleic acid, respectively), but no changes were observed after exercise or training. It is concluded that moderate-intensity exercise abnormally increases plasma tumour necrosis factor‐α levels in chronic obstructive pulmonary disease patients without exercise-induced upregulation of the tumour necrosis factor‐α gene in skeletal muscle. This study was supported by grants FIS 99/0029 and 00/0281 from the Spanish Fund for Health Research, e‐Remedy (IST-2000-25146) from the European Union (FP5) and Comissionat per a Universitats i Recerca de la Generalitat de Catalunya (1999 SGR 00228). R.A. Rabinovich and T. Troosters were research fellows supported by the European Respiratory Society (2000). M. Figueras is the recipient of a predoctoral scholarship from the Ministry of Education and Culture of the Spanish Government. Support was also received from E. Jaeger GmbH, Würzburg, Germany.