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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.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.The results showed in each approach, that endurance test duration was significantly decreased in the COPD patients (p0.05). In systemic approach, the results showed that blood vitamin E at rest was significantly decreased in the COPD (p0.001), with a significant increase in superoxide anion release by stimulated phagocytes (p0.001). Local exercise induced, only in COPD, a significant increase in serum MDA (p0.05), 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 (p0.05). 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.

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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 (FEV 1 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 (O 2 · − ) 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 O 2 · − 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.

In order to study the efficiency of individual training programs at the ventilatory threshold level, twenty COPD patients were randomized into two groups and studied over a two-month period. At the start, during, and at the end of the study all subjects performed incremental exercise tests. The trained group (59.60 SEM +/- 2.75 years) walked four times a week at the heart rate corresponding to the metabolic level of ventilatory threshold. The other group served as controls (58.2 +/- 1.80 years). A marked increase in the symptom-limited oxygen consumption (+/- 25%) (p0.01), the maximal ventilation (+20%) (p0.01), and the ventilatory threshold (+19%) (p0.05) was found in the trained group. No modification was recorded in the control group. The ventilatory pattern at submaximal intensities expressed in percentage of the initial oxygen consumption showed significant differences between groups, the trained-group ventilation decreased at 50% and 75% VO2 sl (p0.05). The breathing frequency also decreased at 50% and 75% VO2 sl (p0.05). Moreover, we observed an increase in the oxygen pulse at 50% VO2 sl (p0.05). In conclusion, this study demonstrates that individualized training at the ventilatory threshold level increases exercise tolerance and produces better ventilatory comfort in COPD patients.

The occurrence of a late reaction following exercise induced asthma is questionable and its relationship with the non specific bronchial hyperreactivity is poorly known. In this study, nine patients (age 15-21 years) underwent an exercise challenge in order to (a) determine the incidence of immediate and late phase reaction and (b) analyse the modifications of non specific bronchial hyperreactivity. Study design was a follow; day-3: determination of bronchial responsiveness to metacholine; day 0: control day with FEV1 measurements every hour for 11 hours; day 1: exercise challenge followed by a careful observation of change in FEV1; day 2: new determination of bronchial responsiveness to metacholine. An immediate exercise induced bronchial obstruction was observed in 5 patients. A late phase reaction (6th hour) with a fall of FEV1 equal to or more than 20% has been demonstrated in two patients. For the former, the change in FEV1 did not differ from the value of the control day. For the second, the FEV1 changed spontaneously during the control day so that decreases of FEV1 during control and challenge days were parallel. Thus, no late phase reaction were observed (F = 0.46; ns). There was no modification of bronchial responsiveness to metacholine (pre-exercise: 1,784 +/- 1,970 [SD]; post-exercise 1,827 +/- 2,231 micrograms [SD]). The lack of true late phase reaction when the post-exercise change in FEV1 is compared to the one of a control day and the absence of modification of non specific bronchial hyperreactivity weaken the hypothesis of an inflammatory mechanism of exercise induced asthma.