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Background: Patients with chronic obstructive pulmonary disease (COPD) have difficulties inhaling as the diaphragm becomes flattened and weakened due to lung hyperinflation. This weakened respiratory function is compensated for by the increased activity of the accessory respiratory muscles, such as the sternocleidomastoid muscle (SCM). Objectives: This study aimed to evaluate the difference in the SCM thickening fraction (SCM TF) of each respiratory phase (end-expiration, resting inspiration, and end-inspiration), as measured using ultrasonography (US), between patients with COPD and control subjects. We also evaluate the correlation between the SCM TF of each respiratory phase and exercise tolerance in patients with COPD. Methods: Patients with COPD (n = 44) and age-matched controls (n = 20) underwent US for determination of the SCM TF. Ventilation parameters, including the peak oxygen uptake (peak VO2) and the change in the inspiratory capacity, were measured during cardiopulmonary exercise testing. The SCM thickness and TF was measured during end-expiration, resting breathing, and end-inspiration. Results: The SCM was significantly thinner in patients with COPD than in controls at end-expiration. The increase in the SCM TF from end-expiration to end-inspiration in patients with COPD did not differ significantly from that in control subjects. In contrast, the SCM TF from end-expiration to resting inspiration was significantly greater in patients with COPD than in control subjects. The peak VO2 was strongly positively correlated with the SCM TF from end-expiration to end-inspiration in patients with COPD (r = 0.71, p < 0.01). Conclusions: The SCM may be thinner in patients with COPD than in controls. The SCM TF may also be associated with exercise tolerance.

Background In patients with chronic obstructive pulmonary disease (COPD), the maximum level of diaphragm excursion (DEmax) is correlated with dynamic lung hyperinflation and exercise tolerance. This study aimed to elucidate the utility of DEmax to predict the improvement in exercise tolerance after pulmonary rehabilitation (PR) in patients with COPD. Methods This was a prospective cohort study. Of the 62 patients with stable COPD who participated in the outpatient PR programme from April 2018 to February 2021, 50 completed the programme. Six-minute walk distance (6MWD) was performed to evaluate exercise tolerance, and ultrasonography was performed to measure DEmax. Responders to PR in exercise capacity were defined as patients who demonstrated an increase of > 30 m in 6MWD. The receiver operating characteristic (ROC) curve was used to determine the cut-off point of DEmax to predict responses to PR. Results Baseline levels of forced expiratory volume in 1 s, 6MWD, maximum inspiratory pressure, DEmax and quadriceps muscle strength were significantly higher, and peak dyspnoea of modified Borg (mBorg) scale score was lower in responders (n = 30) than in non-responders (n = 20) to PR (p max was significantly correlated with an increase of > 30 m in 6MWD. The area under the ROC curve of DEmax to predict responders was 0.915, with a sensitivity and specificity of 83% and 95%, respectively, at a cut-off value of 44.9 mm of DEmax. Conclusion DEmax could adequately predict the improvement in exercise tolerance after PR in patients with COPD.

BACKGROUND: A recent paper reported that low muscle mass in the erector spinae muscles (ESM) was strongly associated with poor prognosis and declining muscle mass over time in subjects with COPD. However, effects of pulmonary rehabilitation (PR), if any, on ESM mass have not been reported. We hypothesized that PR reduces the annual decline in ESM mass. METHODS: This was a retrospective cohort study. Thirty-nine subjects with COPD who received PR and underwent chest computed tomography before and after PR were evaluated (rehabilitation group). We also evaluated 39 age-matched subjects with COPD who did not receive PR (nonrehabilitation group). Data were collected from August 2010 until March 2020 in both groups. The ESM cross-sectional area (ESM(CSA)) was measured using axial computed tomography images, and annual changes were calculated. The 6-min walk distance (6MWD) was measured before and after PR; the minimum clinically important difference was defined as 30 m. RESULTS: ESM(CSA) declined in the nonrehabilitation group over time (−116.0 ± 141.2 mm(2)/y) but increased in the PR group (51.0 ± 95.3 mm(2)/y; P < .001). The annual increase in ESM(CSA) was significantly higher among subjects with an increase in 6MWD that exceeded the minimum clinically important difference compared with nonresponders in the rehabilitation group. The annual change in ESM(CSA) was negatively correlated with comorbidity index, and triple therapy (long-acting β(2)-agonist/long-acting muscarinic antagonist/inhaled corticosteroid) had a favorable effect on annual change in ESM(CSA). Multiple regression analysis revealed that only PR was an independent factor for annual change in ESM(CSA). CONCLUSIONS: ESM mass was shown to decline yearly in subjects with COPD. The annual decline in muscle mass was reduced by PR.

Background Although the pathophysiological mechanisms involved in the development of dyspnoea and poor exercise tolerance in patients with COPD are complex, dynamic lung hyperinflation (DLH) plays a central role. Diaphragmatic excursions can be measured by ultrasonography (US) with high intra- and interobserver reliability. The objective of this study was to evaluate the effect of diaphragmatic excursions as assessed by US on exercise tolerance and DLH in patients with COPD. Methods Patients with COPD (n=20) and age-matched control subjects (n=20) underwent US, which was used to determine the maximum level of diaphragmatic excursion (DEmax). Ventilation parameters, including the change in inspiratory capacity (ΔIC), were measured in the subjects during cardiopulmonary exercise testing (CPET). We examined the correlations between DEmax and the ventilation parameters. Results The DEmax of patients with COPD was significantly lower than that of the controls (45.0±12.8 mm versus 64.6±6.3 mm, respectively; p, Reduced diaphragmatic excursion, as measured on ultrasound images, might predict decreased exercise capacity and increased dyspnoea due to dynamic lung hyperinflation in COPD patients https://bit.ly/3jkERxZ

The purpose of this study was to elucidate whether the anticipatory postural adjustment (APA) and focal step movement of gait initiation are produced as a single process or different processes and whether the APA receives an inhibitory drive from the ongoing stop process of gait initiation. Healthy humans initiated gait in response to a first visual cue that instructed the initial swing leg. In some trials, a switch or stop cue was also provided after the first cue. When the stop cue was provided, participants withheld gait initiation. When the switch cue was provided, participants immediately switched the initial swing leg. In both the stop and switch tasks, the APA in response to the first cue, represented by the S1 period of the displacement of the center of pressure, appeared in more than half of the trials in which the withholding of gait initiation or switching of the initial swing leg was successfully completed. These findings indicate that the APA and focal step movement of gait initiation are produced as a dual process. In trials in which the APA in response to the first cue appeared, the amplitude and duration of the APA were decreased when the participants switched the initial swing leg or withheld gait initiation. This finding indicates that the ongoing stop process of gait initiation produces an inhibitory drive over the APA. The decreases in the amplitude and duration of the APA during the switching of the initial swing leg were similar to those during the withholding of gait initiation; moreover, the decreases during the switching of the initial swing leg were positively correlated with the decreases during the withholding of gait initiation. Thus, the stop processes during switching the initial swing leg and withholding gait initiation likely share a common inhibitory mechanism over the APA.

The present study examined whether the excitability of the corticospinal pathway and the GABA-mediated inhibitory circuits of the primary motor cortex that project onto the corticospinal neurons in the tonically contracting hand muscle are changed by tonic contraction of the adjacent hand muscle. The motor evoked potential (MEP) and cortical silent period (CSP) in the tonically contracting hand muscle were obtained while the adjacent hand muscle was either tonically contracting or at rest. The MEP and CSP of the first dorsal interosseous (FDI) muscle elicited across the scalp sites where the MEP is predominantly elicited in the FDI muscle were decreased by tonic contraction of the abductor digiti minimi (ADM) muscle. The centers of the area of the MEP and the duration of the CSP in the FDI muscle elicited across the sites where the MEP is predominantly elicited in the FDI muscle were lateral to those in the FDI muscle elicited across the sites where the MEP is elicited in both the FDI and ADM muscles. They were also lateral to those in the ADM muscle elicited either across the sites where the MEP is predominantly elicited in the ADM muscle, or across the sites where the MEP is elicited in both the FDI and ADM muscles. The decrease in the corticospinal excitability and the excitability of the GABA-mediated inhibitory circuits of the primary motor cortex that project onto the corticospinal neurons in the FDI muscle may be due either to (1) the interaction between the activity of the lateral area of the FDI representation and the descending drive to the ADM muscle, or (2) the decreased susceptibility of the primary motor area that predominantly projects onto the corticospinal neurons in the FDI muscle, which also plays a role in independent finger movement when both the FDI and ADM muscles act together as synergists.

The present study investigated whether the long-interval interhemispheric inhibition (LIHI) is induced by the transcranial magnetic stimulation over the primary sensory area (S1-TMS) without activation of the conditioning side of the primary motor area (M1) contributing to the contralateral motor evoked potential (MEP), whether the S1-TMS-induced LIHI is dependent on the status of the S1 modulated by the tactile input, and whether the pathways mediating the LIHI are different from those mediating the M1-TMS-induced LIHI. In order to give the TMS over the S1 without eliciting the MEP, the intensity of the S1-TMS was adjusted to be the sub-motor-threshold level and the trials with the MEP response elicited by the S1-TMS were discarded online. The LIHI was induced by the S1-TMS given 40 ms before the test TMS in the participants with the attenuation of the tactile perception of the digit stimulation (TPDS) induced by the S1-TMS, indicating that the LIHI is induced by the S1-TMS without activation of the conditioning side of the M1 contributing to the contralateral MEP in the participants in which the pathways mediating the TPDS is sensitive to the S1-TMS. The S1-TMS-induced LIHI was positively correlated with the attenuation of the TPDS induced by the S1-TMS, indicating that the S1-TMS-induced LIHI is dependent on the effect of the S1-TMS on the pathways mediating the TPDS at the S1. In another experiment, the effect of the digit stimulation given before the conditioning TMS on the S1- or M1-TMS-induced LIHI was examined. The digit stimulation produces tactile input to the S1 causing change in the status of the S1. The S1-TMS-induced LIHI was enhanced when the S1-TMS was given in the period in which the tactile afferent volley produced by the digit stimulation just arrived at the S1, while the LIHI induced by above-motor-threshold TMS over the contralateral M1 was not enhanced by the tactile input. Thus, the S1-TMS-induced LIHI is dependent on the status of the S1 modulated by the tactile input, and the pathways mediating the sub-motor-threshold S1-TMS-induced LIHI are not the same as the pathways mediating the above-motor-threshold M1-TMS-induced LIHI.