Abstract

BackgroundPeripheral 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.MethodsTwenty-two patients with quadriceps weakness (COPDMW), 18 patients with preserved quadriceps strength (COPDNoMW) and 20 controls were recruited. Voluntary activation was measured through peripheral nerve (VAperipheral) and transcranial magnetic (VAcortical) stimulation. Corticospinal and spinal excitability (MEP/Mmax and Hmax/Mmax) and corticospinal inhibition (silent period duration) were assessed during maximal voluntary quadriceps contractions.ResultsCOPDMW exhibited lower VAcortical and lower MEP/Mmax compared with COPDNoMW (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 VAcortical and MEP/Mmax.ConclusionsCOPD 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.

Highlights

  • Peripheral muscle weakness can be caused by both peripheral muscle and neural alterations

  • Patients with Isometric maximal quadriceps torque (QMVC) below 80% of predicted values were assigned to the muscle weakness group (COPDMW) and the others to the non-muscle weakness group (COPDNoMW) [34]

  • When Quadriceps Peak twitch (QPt) was included as a covariate in Analysis of covariance (ANCOVA) analysis, the maximal voluntary contraction (QMVC) remained significantly lower in COPD patients with quadriceps muscle weakness (COPDMW)

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Summary

Introduction

Peripheral muscle weakness can be caused by both peripheral muscle and neural alterations. Central (respiratory) and peripheral (limb) muscle weakness is one of the main systemic effects of chronic obstructive pulmonary disease (COPD) [1]. It primarily affects the lower limb muscles [2], contributes to exercise intolerance [3] and is associated with increasing disability and mortality [4, 5]. Lower quadriceps strength is not observed in some patients when peripheral nerve stimulation is used instead of voluntary contraction [9, 10] This raises the hypothesis of altered neural drive to the muscle in COPD

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