Chronic obstructive pulmonary disease (COPD) patients exhibit not only respiratory symptoms but also a peripheral muscular weakness. This weakness is characterized by a loss in strength, harmful for the patients' life quality and vital prognosis (Swallow et al., 2007). Even if many studies have enlightened damages at a peripheral level, the muscular atrophy itself cannot totally explain the loss in force (Menon et al., 2012). Furthermore, the contractile properties of COPD muscles fibres are preserved (Debigare et al., 2003). Consequently, peripheral muscle weakness cannot only be explained by peripheral factors and central structures must be investigated.~At the central level, it is admitted that force production is controlled by the activation of contralateral motor areas. In COPD, these areas were found to be less activated than in controls during force production (Alexandre et al., 2014). However, recent studies bring the evidence that ipsilateral motor areas are also mobilized to cope demand during such task. The activation of ipsilateral areas is possible through inter hemispheric pathways, as the corpus callosum. Recently, the integrity of the corpus callosum have been linked to the capability of activating the ipsilateral motor cortex (Chiou et al., 2014) during force production. This is of concern knowing that several studies reported white matter lesions in the brain of COPD patients (Dodd et al, 2012) and more precisely in regions containing the corpus callosum (Lahousse et al., 2013).~Therefore, we hypothesize that COPD patients have a lower capability of activating their ipsilateral motor cortex during force production compared to controls.
Patients with COPD have lower capability of activating their muscles. At the cortical level, force production is not only controlled by contralateral primary motor cortex but also by ipsilateral motor cortex. The aim of this study is to determine whether ipsilateral areas are functionally impaired in COPD.