Motor cortex alteration and maximal voluntary strength in COPD: impact of non-rapid eye movement sleep desaturation.
Mr Francois ALEXANDREa, Dr Nelly HERAUDb, Dr Anthony Mj SANCHEZc, Dr Emilie TREMEYb, Dr Nicolas OLIVERb, Dr Philippe GUERINd, Prof Alain VARRAYe
a Laboratoire Movement To Health, Euromov, Université de Montpellier AND Clinique du souffle La Vallonie, Fontalvie, b Clinique du souffle La Vallonie, Fontalvie, c UMR866 Dynamique Musculaire et Métabolisme, INRA, Université de Montpellier, d Clinique du souffle Les Clarines, Fontalvie, e Laboratoire Movement To Health, Euromov, Université de Montpellier
Introduction : Brain impairment is a major extrapulmonary effect of COPD and is involved in locomotor muscle weakness by reducing cortical motor output .Cerebrovascular O2 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 (Meadows et al., 2004).
Objective : This study assessed the involvement of NREM sleep desaturation in decreasing cortical motor output and muscle strength in COPD.
Method : 29 patients with COPD were enrolled. On the basis of a polysomnography, they were divided in 2 groups: NREM desaturators (NREMDes) if they spent more than 10% of NREM sleep time with SpO2<90%, otherwise non desaturators (NREMNoDes). 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 ( VAcortical) were assessed by interpolated twitches and magnetic stimulation of motor cortex, respectively.
Results :Serum S100b was higher in NREMDes (p<0.05). In addition, LOA and VAcortical were both reduced in NREMDes (p<0.05). However, there were no differences in TwQ and QMVC between the two groups of patients.
Discussion : 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 NREMDes and NREMNoDes groups, suggesting compensatory mechanism(s) to ensure comparable muscle strength despite motor cortex alteration.
Alexandre, F., Heraud, N., Oliver, N. & Varray, A. 2014. Cortical Implication in Lower Voluntary Muscle Force Production in Non-Hypoxemic COPD Patients. PLoS One, 9, e100961.
Meadows, G. E., O'Driscoll, D. M., Simonds, et al. 2004. Cerebral blood flow response to isocapnic hypoxia during slow-wave sleep and wakefulness. J Appl Physiol, 97, 1343-8.
Vogiatzis, I., Louvaris, Z., Habazettl, et al. 2013. Cerebral cortex oxygen delivery and exercise limitation in patients with COPD. Eur Respir J, 41, 295-301.
Keywords : Voluntary activation, electromyography, muscle weakness, cerebral cortex, central nervous system.