TY - JOUR
T1 - Reduced muscle redox capacity after endurance training in patients with chronic obstructive pulmonary disease
AU - Rabinovich, Roberto A.
AU - Ardite, Esther
AU - Troosters, Thierry
AU - Carbó, Neus
AU - Alonso, Juli
AU - Gonzalez De Suso, José Manuel
AU - Vilaró, Jordi
AU - Barberà, Joan Albert
AU - Polo, Maite Figueras
AU - Argilés, Josep M.
AU - Fernandez-Checa, José C.
AU - Roca, Josep
PY - 2001/10/1
Y1 - 2001/10/1
N2 - The present study was undertaken to test whether endurance training in patients with COPD, along with enhancement of muscle bioenergetics, decreases muscle redox capacity as a result of recurrent episodes of cell hypoxia induced by high intensity exercise sessions. Seventeen patients with COPD (FEV1, 38 ± 4% pred; Pao2, 69 ± 2.7 mm Hg; Paco2,42 ± 1.7 mm Hg) and five age-matched control subjects (C) were studied pretraining and post-training. Reduced (GSH) and oxidized (GSSG) glutathione, lipid peroxidation, and gamma-glutamyl cysteine synthase heavy subunit chain mRNA expression (γGCS-HS mRNA) were measured in the vastus lateralis. Pretraining redox status at rest and after moderate (40% Wpeak) constant-work rate exercise were similar between groups. After training (ΔWpeak, 27 ± 7% and 37 ± 18%, COPD and C, respectively) (p < 0.05 each), GSSG levels increased only in patients with COPD (from 0.7 ± 0.08 to 1.0 ± 0.15 nmol/mg protein, p < 0.05) with maintenance of GSH levels, whereas GSH markedly increased in C (from 4.6 ± 1.03 to 8.7 ± 0.41 nmol/mg protein, p < 0.01). Post-training γGCS-HS mRNA levels increased after submaximal exercise in patients with COPD. No evidence of lipid peroxidation was observed. We conclude that although endurance training increased muscle redox potential in healthy subjects, patients with COPD showed a reduced ability to adapt to endurance training reflected in lower capacity to synthesize GSH.
AB - The present study was undertaken to test whether endurance training in patients with COPD, along with enhancement of muscle bioenergetics, decreases muscle redox capacity as a result of recurrent episodes of cell hypoxia induced by high intensity exercise sessions. Seventeen patients with COPD (FEV1, 38 ± 4% pred; Pao2, 69 ± 2.7 mm Hg; Paco2,42 ± 1.7 mm Hg) and five age-matched control subjects (C) were studied pretraining and post-training. Reduced (GSH) and oxidized (GSSG) glutathione, lipid peroxidation, and gamma-glutamyl cysteine synthase heavy subunit chain mRNA expression (γGCS-HS mRNA) were measured in the vastus lateralis. Pretraining redox status at rest and after moderate (40% Wpeak) constant-work rate exercise were similar between groups. After training (ΔWpeak, 27 ± 7% and 37 ± 18%, COPD and C, respectively) (p < 0.05 each), GSSG levels increased only in patients with COPD (from 0.7 ± 0.08 to 1.0 ± 0.15 nmol/mg protein, p < 0.05) with maintenance of GSH levels, whereas GSH markedly increased in C (from 4.6 ± 1.03 to 8.7 ± 0.41 nmol/mg protein, p < 0.01). Post-training γGCS-HS mRNA levels increased after submaximal exercise in patients with COPD. No evidence of lipid peroxidation was observed. We conclude that although endurance training increased muscle redox potential in healthy subjects, patients with COPD showed a reduced ability to adapt to endurance training reflected in lower capacity to synthesize GSH.
KW - COPD
KW - Endurance training
KW - Glutathione
KW - Muscle dysfunction
KW - Oxidative stress
UR - http://www.scopus.com/inward/record.url?scp=0035481989&partnerID=8YFLogxK
U2 - 10.1164/ajrccm.164.7.2103065
DO - 10.1164/ajrccm.164.7.2103065
M3 - Article
C2 - 11673195
AN - SCOPUS:0035481989
SN - 1073-449X
VL - 164
SP - 1114
EP - 1118
JO - American Journal of Respiratory and Critical Care Medicine
JF - American Journal of Respiratory and Critical Care Medicine
IS - 7
ER -