Changes in pulmonary and plasma oxidative stress and inflammation following eccentric and concentric cycling in stable COPD patients

Denisse Valladares-Ide, Maria José Bravo, Ana Carvajal, Oscar Florencio Araneda, Marcelo Tuesta, Alvaro Reyes, Reyna Peñailillo, Luis Peñailillo

Research output: Contribution to journalArticlepeer-review

Abstract

Purpose: The purpose of this study was to compare pulmonary and plasma markers of oxidative stress and inflammation after concentric and eccentric cycling bouts in individuals with chronic obstructive pulmonary disease (COPD). Methods: Ten patients with moderate COPD level (68.3 ± 9.1 years; forced expiratory volume in 1 s = 68.6 ± 20.4% of predicted) performed 30 min of moderate-intensity concentric (CONC-M: 50% maximum concentric cycling power output; POmax) and eccentric cycling (ECC-M: 50% POmax), and high-intensity eccentric cycling (ECC-H: 100% POmax) in a randomised order. Cardiometabolic demand was monitored during cycling. Indirect markers of muscle damage were assessed before, immediately after, 24 and 48 h after cycling (muscle strength, muscle soreness and creatine kinase activity). Plasma oxidative stress (malondialdehyde: MDA), antioxidant (glutathione peroxidase activity: GPx) and inflammatory markers (IL-6, TNF-α) were measured before and 5 min after cycling. Exhaled breath condensate (EBC) samples were collected before and 15 min after cycling and analysed for hydrogen peroxide (H2O2), nitrites (NO2−) and pH. Results: Cardiometabolic demand was 40–50% lesser for ECC-M than CONC-M and ECC-H. Greater muscle damage was induced after ECC-H than ECC-M and CONC-M. MDA decreased immediately after CONC-M (− 28%), ECC-M (− 14%), and ECC-H (− 17%), while GPx remained unchanged. IL-6 increased only after ECC-H (28%), while TNF-α remained unchanged after exercise. Pulmonary H2O2, NO2− and pH remained unchanged after exercise. Conclusion: These results suggest that only moderate muscle damage and inflammation were induced after high-intensity eccentric cycling, which did not induce pulmonary or plasmatic increases in markers of oxidative stress. Trial registration number: Trial registration number: DRKS00009755.

Original languageEnglish
JournalEuropean Journal of Applied Physiology
DOIs
StateAccepted/In press - 2021

Bibliographical note

Funding Information:
This work was funded by research grant awarded to L.P. (#11150293) by CONICYT of Chile.

Funding Information:
This work was funded by research grants awarded to L.P. (#11150293) by FONDECYT of Chile.

Publisher Copyright:
© 2021, The Author(s), under exclusive licence to Springer-Verlag GmbH, DE part of Springer Nature.

Keywords

  • COPD
  • Exhaled breath condensate
  • Interleukin-6
  • Lengthening
  • TBARS
  • TNF-α

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