Background: Peripheral muscle weakness can be caused by both peripheral muscle and neural alterations. Although peripheral alterations cannot totally explain peripheral muscle weakness in COPD, the existence of an activation deficit remains controversial. The heterogeneity of muscle weakness (between 32 and 57% of COPD patients) is generally not controlled in studies and could explain this discrepancy. This study aimed to specifically compare voluntary and stimulated activation levels in COPD patients with and without muscle weakness. Methods: Twenty-two patients with quadriceps weakness (COPD MW), 18 patients with preserved quadriceps strength (COPD NoMW) and 20 controls were recruited. Voluntary activation was measured through peripheral nerve (VA peripheral) and transcranial magnetic (VA cortical) stimulation. Corticospinal and spinal excitability (MEP/Mmax and Hmax/Mmax) and corticospinal inhibition (silent period duration) were assessed during maximal voluntary quadriceps contractions. Results: COPD MW exhibited lower VA cortical and lower MEP/Mmax compared with COPD NoMW (p < 0.05). Hmax/Mmax was not significantly different between groups (p = 0.25). Silent period duration was longer in the two groups of COPD patients compared with controls (p < 0.01). Interestingly, there were no significant differences between all COPD patients taken together and controls regarding VA cortical and MEP/Mmax. Conclusions: COPD patients with muscle weakness have reduced voluntary activation without altered spinal excitability. Corticospinal inhibition is higher in COPD regardless of muscle weakness. Therefore, reduced cortical excitability and a voluntary activation deficit from the motor cortex are the most likely cortical mechanisms implicated in COPD muscle weakness. The mechanisms responsible for cortical impairment and possible therapeutic interventions need to be addressed.

Background. Skeletal muscle dysfunction in patients with chronic obstructive pulmonary disease (COPD) is not fully reversed by exercise training. Antioxidants are critical for muscle homeostasis and adaptation to training. However, COPD patients experience antioxidant deficits that worsen after training and might impact their muscle response to training. Nutritional antioxidant supplementation in combination with pulmonary rehabilitation (PR) would further improve muscle function, oxidative stress, and PR outcomes in COPD patients. Methods. Sixty-four COPD patients admitted to inpatient PR were randomized to receive 28 days of oral antioxidant supplementation targeting the previously observed deficits (PR antioxidant group; α-tocopherol: 30 mg/day, ascorbate: 180 mg/day, zinc gluconate: 15 mg/day, selenomethionine: 50 μg/day) or placebo (PR placebo group). PR consisted of 24 sessions of moderate-intensity exercise training. Changes in muscle endurance (primary outcome), oxidative stress, and PR outcomes were assessed. Results. Eighty-one percent of the patients (FEV1=58.9±20.0%pred) showed at least one nutritional antioxidant deficit. Training improved muscle endurance in the PR placebo group (+37.4±45.1%, p<0.001), without additional increase in the PR antioxidant group (-6.6±11.3%; p=0.56). Nevertheless, supplementation increased the α-tocopherol/γ-tocopherol ratio and selenium (+58±20%, p<0.001, and +16±5%, p<0.01, respectively), muscle strength (+11±3%, p<0.001), and serum total proteins (+7±2%, p<0.001), and it tended to increase the type I fiber proportion (+32±17%, p=0.07). The prevalence of muscle weakness decreased in the PR antioxidant group only, from 30.0 to 10.7% (p<0.05). Conclusions. While the primary outcome was not significantly improved, COPD patients demonstrate significant improvements of secondary outcomes (muscle strength and other training-refractory outcomes), suggesting a potential “add-on” effect of the nutritional antioxidant supplementation (vitamins C and E, zinc, and selenium) during PR. This trial is registered with NCT01942889.

Oxidative stress (OS) plays a key role in the muscle impairment and exercise capacity of COPD patients. However, the literature reveals that systemic OS markers show great heterogeneity, which may hinder the prescription of effective antioxidant supplementation. This study therefore aimed to identify OS markers imbalance of COPD patients, relative to validated normal reference values, and to investigate the possibility of systemic OS profiles. We measured systemic enzymatic/nonenzymatic antioxidant and lipid peroxidation (LP) levels in 54 stable COPD patients referred for a rehabilitation program. The main systemic antioxidant deficits in these patients concerned vitamins and trace elements. Fully 89% of the COPD patients showed a systemic antioxidant imbalance which may have caused the elevated systemic LP levels in 69% of them. Interestingly, two patient profiles (clusters 3 and 4) had a more elevated increase in LP combined with increased copper and/or decreased vitamin C, GSH, and GPx. Further analysis revealed that the systemic LP level was higher in COPD women and associated with exercise capacity. Our present data therefore support future supplementations with antioxidant vitamins and trace elements to improve exercise capacity, but COPD patients will probably show different positive responses.

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When two tasks are performed simultaneously, they compete for attentional resources, resulting in a performance decrement in one or both tasks. Patients with attention disorders have a reduced ability to perform several tasks simultaneously (e.g., talking while walking), which increases the fall risk and frailty. This study assessed the cognitive and motor performances of patients with COPD and healthy controls within a dual-task walking paradigm. A subobjective was to assess the impact of a pulmonary rehabilitation program on the dual-task performances in COPD. Twenty-five patients with COPD and 20 controls performed a cognitive task (subtraction) and a 15-m walking test separately (single-task; ST) and jointly (dual-task; DT). In addition, a subsample of 10 patients performed the same evaluations 5 weeks later after a pulmonary rehabilitation program following current recommendations. Cognitive and gait performances in ST showed no differences between patients with COPD and controls (all p > 0.05). However, COPD patients exhibited a greater increase in gait variability than controls in DT (4.07 ± 1.46% vs. 2.17 ± 0.7%, p < 0.001). The pulmonary rehabilitation program had no effect on the dual-task impairment for the subsample of patients (p = 0.87). This study provides evidence of insufficient attentional resources to successfully deal with DT in patients with COPD, and this was expressed through an exaggerated increase in gait variability in DT walking. Given the high risk of falls and disability associated with altered gait variability, dual-task training interventions should be considered in pulmonary rehabilitation programs.