Cortical Implication in Lower Voluntary Muscle Force Production in Non-Hypoxemic COPD Patients

Abstract

Recent studies have shown that muscle alterations cannot totally explain peripheral muscle weakness in COPD. Cerebral abnormalities in COPD are well documented but have never been implicated in muscle torque production. The purpose of this study was to assess the neural correlates of quadriceps torque control in COPD patients. Fifteen patients (FEV1 54.1±3.6% predicted) and 15 age- and sex-matched healthy controls performed maximal (MVCs) and submaximal (SVCs) voluntary contractions at 10, 30 and 50% of the maximal voluntary torque of the knee extensors. Neural activity was quantified with changes in functional near-infrared spectroscopy oxyhemoglobin (fNIRS-HbO) over the contralateral primary motor (M1), primary somatosensory (S1), premotor (PMC) and prefrontal (PFC) cortical areas. In parallel to the lower muscle torque, the COPD patients showed lower increase in HbO than healthy controls over the M1 (p<0.05), PMC (p<0.05) and PFC areas (p<0.01) during MVCs. In addition, they exhibited lower HbO changes over the M1 (p<0.01), S1 (p<0.05) and PMC (p<0.01) areas during SVCs at 50% of maximal torque and altered motor control characterized by higher torque fluctuations around the target. The results show that low muscle force production is found in a context of reduced motor cortex activity, which is consistent with central nervous system involvement in COPD muscle weakness.

Exertional dyspnoea and cortical oxygenation in patients with COPD

“…However, both BOLD-fMRI and PET require complete immobilisation of the head and are therefore unsuitable for the assessment of exercising COPD patients. NIRS is a more practical method and has been used to assess the brain activity of patients performing exercise [14,31]. NIRS oxy-Hb and deoxy-Hb signals are strongly correlated with BOLD-fMRI signals [32].…”

“…NIRS oxy-Hb and deoxy-Hb signals are strongly correlated with BOLD-fMRI signals [32]. As patients with COPD usually perceive dyspnoea during exercise, but not at rest, NIRS is better for identifying the cortical activation associated with the exertional dyspnoea of these patients [31].…”

“…The exercise load by itself possibly led to a change in cortical hemodynamics and induced the activation of PMA, although we chose to use constant low-intensity exercise to minimise the effect of exercise on cortical activation. Using NIRS assessment, ALEXANDRE et al [31] reported that there was cortical activation of the PMA, MI and S1 regions of COPD patients performing submaximal exercise of their knee extensors. GOSWAMI et al [33] reported that electrical stimulation of the wrist flexors at a submotor threshold increased neural activity in the bilateral posterior insula, ventral medial pre-frontal cortex, subgenualanterior cingulate cortex, mid-cingulate cortex and posterior cingulate cortex.…”

Brain Damage and Motor Cortex Impairment in Chronic Obstructive Pulmonary Disease: Implication of Nonrapid Eye Movement Sleep Desaturation

“…2 By using the neuroimaging technique, it was not possible to infer that the lower cortical activity resulted in lower cortical output. 2 In the current study, we assessed the cortical motor output with a more direct approach by stimulating the motor cortex. Our results confirm that cortical output is impaired in COPD but that it mainly concerns those patients with NREM sleep desaturation, as the values of voluntary activation reached by the NREMnoDes patients (around 95%) were substantially similar to those of healthy subjects reported in other studies.…”

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

“…By using the twitch interpolation method, most studies have failed to observe an activation deficit in COPD during maximal voluntary contractions [11][12][13], while others have clearly shown this deficit during submaximal voluntary contractions [14]. By using a different method and applying sensors directly to the scalp, lower neural drive from the motor cortex was reported during maximal and submaximal voluntary contractions in COPD [15]. Both methodological concerns and the heterogeneity of muscle weakness in COPD could explain these discrepancies.…”