Specific motor cortex hypoexcitability and hypoactivation in COPD patients with peripheral muscle weakness

Abstract

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.