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Biomedical subjects

A Couillard

Publications and source records attributed to A Couillard.

5 recordsLinked to original sources
PubMed2005

From muscle disuse to myopathy in COPD: potential contribution of oxidative stress.

Evidence has been accumulating that chronic inactivity leading to muscle disuse is unlikely to be the only explanation for the peripheral muscle dysfunction of chronic obstructive pulmonary disease (COPD) patients. Although a new concept of myopathy was recently proposed, the question of disuse and/or a form of myopathy is still being debated. This review proposes definitions for the terms used in this debate, discusses the relevant studies and concludes that the evidence points to a myopathy associated with muscle disuse in COPD. COPD myopathy implies pharmacological and/or pathophysiological mechanisms that need to be identified in order to optimally orient therapeutic strategies. The literature indicates that corticosteroids, inflammation, hypoxaemia and oxidative stress are among the factors contributing to COPD muscle dysfunction, but their relative contributions have not been fully elucidated. This review presents the advances in understanding each of these mechanisms, especially the data showing that muscle oxidative stress occurs and contributes to muscle dysfunction in chronic obstructive pulmonary disease. The current review also reports the studies that have elucidated the molecular mechanisms underlying this stress in chronic obstructive pulmonary disease by demonstrating alterations in oxidant and/or antioxidant systems. Finally, the review considers how inflammation and hypoxaemia may trigger oxidative stress in chronic obstructive pulmonary disease muscles and presents the therapeutic modalities that should be proposed to prevent it.

Adrenal Cortex Hormones↗
PubMed2004

Does systemic inflammation trigger local exercise-induced oxidative stress in COPD?

Inflammatory abnormalities may be involved in the inadequate basal oxidant/antioxidant balance and local exercise-induced oxidative stress in chronic obstructive pulmonary disease (COPD) patients. The time course of oxidative stress and inflammation was investigated in 10 COPD patients and seven healthy subjects before and after local dynamic quadriceps endurance exercise at 40% of maximal strength. Venous samples were collected before, immediately after and up to 48 h after exercise. At rest, levels of an oxidant released by stimulated phagocytes, the superoxide anion, were significantly higher in patients, as were plasma levels of C-reactive protein, tumour necrosis factor-alpha and interleukin-6, inflammatory markers. An inverse relationship was found between baseline C-reactive protein levels and endurance time in patients. Six hours after exercise, superoxide anion release and levels of protein oxidation products, an index of oxidative stress, increased similarly in both groups, whereas thiobarbituric acid reactive substance levels, another index of oxidative stress, increased significantly only in patients. Plasma nonenzymatic antioxidant and inflammatory cytokine levels were unchanged by the exercise protocol. The increased baseline systemic inflammation in chronic obstructive pulmonary disease patients could be related to disturbed oxidant/antioxidant balance, and, together, these may have triggered the exercise-induced oxidative stress. The absence, however, of local exercise-induced systemic inflammation suggests that additional mechanisms explain local exercise-induced oxidative stress.

Antioxidants↗
PubMed2002

Evidence of local exercise-induced systemic oxidative stress in chronic obstructive pulmonary disease patients.

Chronic inactivity may not be the sole factor involved in the myopathy of chronic obstructive pulmonary disease (COPD) patients. One hypothesis is that exercise-induced oxidative stress that leads to muscle alterations may also be involved. This study investigated whether exercise localised to a peripheral muscle group would induce oxidative stress in COPD patients. Eleven COPD patients (FEV1 1.15+/-0.4 L (mean+/-SD)) and 12 healthy age-matched subjects with a similar low quantity of physical activity performed endurance exercise localised to a peripheral muscle group, the quadriceps of the dominant leg. The authors measured plasma levels of thiobarbituric reactive substances (TBARs) as an index of oxidative stress, the release in superoxide anion (O2*-) by stimulated phagocytes as an oxidant, and blood vitamin E as one antioxidant. Quadriceps endurance was significantly lower in the COPD patients compared with healthy subjects (136+/-16 s versus 385+/-69 s (mean+/-SEM), respectively). A significant increase in TBARs 6 h after quadriceps exercise was only found in the COPD patients. In addition, significantly higher O2*- release and lower blood vitamin E levels were found in COPD patients than in controls at rest. This blood vitamin E level was significantly correlated with the resting level of plasma TBARs in the COPD patients. This study mainly showed that quadriceps exercise induced systemic oxidative stress in chronic obstructive pulmonary disease patients and that vitamin E levels were decreased in these patients at rest. The exact relevance of these findings to chronic obstructive pulmonary disease myopathy needs to be elucidated.

Aged↗
PubMed2001

[Local exercise and oxidative stress in chronic obstructive broncho-pneumopathies: preliminary results].

UNLABELLED: The role of altered peripheral muscle function in exercise intolerance of chronic obstructive pulmonary disease (COPD) is now well established. However, the mechanisms underlying this phenomen, have not been determined. One hypothesis is that the oxidative stress, that leads to tissue injury may be involved. A recent study has shown that general exercise caused systemic oxidative stress in COPD patients. However, the origin of this stress was not absolutely clear: airways, muscle, both, or other? The aim of this study was first to determine with a systemic approach, whether systemic oxidative stress occur in patients who perform local exercise and then with a muscular needle biopsy approach, to confirm the muscular origin of this oxidative stress. METHODS: In each approach, 7 COPD patients moderate to severe and 7 age-matched subjects performed an endurance test consisting of dynamic strength of the quadriceps against 40% (systemic approach) or 30% (biopsy approach) of maximal voluntary strength at an imposed regular pace until exhaustion. RESULTS: The results showed in each approach, that endurance test duration was significantly decreased in the COPD patients (p < 0.05). In systemic approach, the results showed that blood vitamin E at rest was significantly decreased in the COPD (p < 0.001), with a significant increase in superoxide anion release by stimulated phagocytes (p < 0.001). Local exercise induced, only in COPD, a significant increase in serum MDA (p < 0.05), which is an index of oxidative stress. In the biopsy approach, the results showed that local exercise induced in COPD an increase in muscular levels of MDA. A significant increase in muscular peroxidase glutathion activity (antioxidant) occurred after exercise only in normal subjects (p < 0.05). In conclusion, this study in COPD, confirms the altered peripheral muscle function, reveals a deficit in blood vitamin E and suggest that local muscular exercise causes a muscular oxidative stress in these patients. Further studies are needed to confirm these results and evaluate the implication of this oxidative stress in the myopathy of COPD.

Aged↗