Denisse Valladares-Ide1, Maria José Bravo2, Ana Carvajal2, Oscar F Araneda3, Marcelo Tuesta4, Alvaro Reyes4, Reyna Peñailillo5, Luis Peñailillo6. 1. Instituto de Ciencias de la Salud, Universidad de O'Higgins, Rancagua, Chile. 2. Exercise Science Laboratory, Faculty of Medicine, School of Kinesiology, Universidad Finis Terrae, 1509 Pedro de Valdivia Av., Providencia, Santiago, Chile. 3. Laboratorio Integrativo de Biomecánica y Fisiologia del Esfuerzo (LIBFE), Escuela de Kinesiologia, Facultad de Medicina, Universidad de los Andes, Santiago, Chile. 4. Escuela de Kinesiologia, Facultad de Ciencias de la Rehabilitación, Universidad Andres Bello, Vina del Mar, Chile. 5. Laboratory of Reproductive Biology, Faculty of Medicine, Centre for Biomedical Research, Universidad de los Andes, Santiago, Chile. 6. Exercise Science Laboratory, Faculty of Medicine, School of Kinesiology, Universidad Finis Terrae, 1509 Pedro de Valdivia Av., Providencia, Santiago, Chile. lpenailillo@uft.cl.
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.
RCT Entities:
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.
Authors: O F Araneda; R Urbina-Stagno; M Tuesta; D Haichelis; M Alvear; M P Salazar; C García Journal: J Physiol Biochem Date: 2013-08-27 Impact factor: 4.158
Authors: C Berzosa; I Cebrián; L Fuentes-Broto; E Gómez-Trullén; E Piedrafita; E Martínez-Ballarín; L López-Pingarrón; R J Reiter; J J García Journal: J Biomed Biotechnol Date: 2011-03-09