Motor cortex alteration and maximal voluntary strength in COPD: Impact of non-rapid eye movement sleep desaturation

Abstract

Brain impairment is a major extrapulmonary effect of COPD and is involved in locomotor muscle weakness by reducing cortical motor output. Cerebrovascular O 2 reactivity (i.e. an increase in cerebral blood flow) protects the brain against the effects of chronic hypoxemia by preventing brain hypoxia. However, during non-rapid eye movement (NREM) sleep stages, patients are highly exposed to brain damage as this reactivity is abolished [1] . This study assessed the involvement of NREM sleep desaturation in decreasing cortical motor output and muscle strength in COPD. Twenty-nine patients with COPD were enrolled. On the basis of a polysomnography, they were divided in 2 groups: NREM desaturators (NREM Des ) if they spent more than 10% of NREM sleep time with SpO 2 < 90%, otherwise non desaturators (NREM NoDes ). Serum S100b concentration was measured on awakening as a marker of cerebral lesions. Quadriceps peak twitch (TwQ) was measured by femoral nerve stimulation and voluntary quadriceps strength during isometric maximal voluntary contractions (QMVC), respectively. Level of voluntary activation (LOA) and cortical motor output (VA cortical ) were assessed by interpolated twitches and magnetic stimulation of motor cortex, respectively. Serum S100b was higher in NREM Des ( p < 0.05). In addition, LOA and VA cortical were both reduced in NREM Des ( p < 0.05). However, there were no differences in TwQ and QMVC between the two groups of patients. Higher serum S100b was consistent with higher cerebral lesions in patients with NREM sleep desaturation, which may explain the reduced voluntary activation and cortical output. Surprisingly, QMVC was not different between the NREM Des and NREM NoDes groups, suggesting compensatory mechanism(s) to ensure comparable muscle strength despite motor cortex alteration.