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      Clinical Effects Of Acupuncture On The Pathophysiological Mechanism Of Chronic Obstructive Pulmonary Disease During Exercise

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          Pharmacological therapy and pulmonary rehabilitation are useful for exertional dyspnoea in patients with chronic obstructive pulmonary disease (COPD); however, several patients have no meaningful improvements. Although acupuncture significantly improves exercise intolerance and dyspnoea, the pathophysiological mechanism of these effects is unknown; therefore, we evaluated this mechanism using cardiopulmonary exercise testing in a single-arm, open experimental study.

          Patients and methods

          Sixteen patients with COPD underwent acupuncture once a week for 12 weeks. Primary outcomes were exercise performance parameters, including peak oxygen uptake in the incremental exercise tests (IETs) and the time to the limit of tolerance measured in constant work rate exercise tests (CWRETs) at 70% peak work-rate of the IET. IETs and CWRETs were performed at baseline and at weeks 12, 16, and 24.


          During the time course, there were significant increases in peak oxygen uptake (p = 0.018) and minute ventilation (V̇ E, p = 0.04) in the IETs. At 12 weeks, the endurance time significantly increased (810 ± 470 vs 1125 ± 657 s, p < 0.001) and oxygen uptakes at terminated exercise were significantly lower (771 ± 149 mL/min, p < 0.05) than those at baseline (822 ± 176 mL/min) in CWRETs. The significant decreases in oxygen uptake and minute ventilation and improvements in Borg scale scores were also observed during CWRETs after acupuncture. The decreases at isotime in the Borg scale (r = −0.789, p = 0.0007) and V̇ E (r = −0.6736, p = 0.0042) were significantly correlated with the improvement of endurance time.


          The positive effects of acupuncture on exertional dyspnoea were associated with increased endurance time influenced by improved oxygen utilisation and reduced ventilation during exercise. Acupuncture may be a new intervention for COPD in addition to conventional maintenance therapies.

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          Most cited references 20

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          Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin.

          Follistatin (FS) inhibits several members of the TGF-beta superfamily, including myostatin (Mstn), a negative regulator of muscle growth. Mstn inhibition by FS represents a potential therapeutic approach of muscle atrophy. The aim of our study was to investigate the mechanisms of the FS-induced muscle hypertrophy. To test the role of satellite cells in the FS effect, we used irradiation to destroy their proliferative capacity. FS overexpression increased the muscle weight by about 37% in control animals, but the increase reached only 20% in irradiated muscle, supporting the role of cell proliferation in the FS-induced hypertrophy. Surprisingly, the muscle hypertrophy caused by FS reached the same magnitude in Mstn-KO as in WT mice, suggesting that Mstn might not be the only ligand of FS involved in the regulation of muscle mass. To assess the role of activin (Act), another FS ligand, in the FS-induced hypertrophy, we electroporated FSI-I, a FS mutant that does not bind Act with high affinity. Whereas FS electroporation increased muscle weight by 32%, the muscle weight gain induced by FSI-I reached only 14%. Furthermore, in Mstn-KO mice, FSI-I overexpression failed to induce hypertrophy, in contrast to FS. Therefore, these results suggest that Act inhibition may contribute to FS-induced hypertrophy. Finally, the role of Act as a regulator of muscle mass was supported by the observation that ActA overexpression induced muscle weight loss (-15%). In conclusion, our results show that satellite cell proliferation and both Mstn and Act inhibition are involved in the FS-induced muscle hypertrophy.
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            Differential response to pulmonary rehabilitation in COPD: multidimensional profiling.

            The aim of the present study was to profile a multidimensional response to pulmonary rehabilitation in patients with chronic obstructive pulmonary disease (COPD).Dyspnoea, exercise performance, health status, mood status and problematic activities of daily life were assessed before and after a 40-session pulmonary rehabilitation programme in 2068 patients with COPD (mean forced expiratory volume in 1 s of 49% predicted). Patients were ordered by their overall similarity concerning their multidimensional response profile, which comprises the overall response on MRC dyspnoea grade, 6MWD, cycle endurance time, Canadian Occupational Performance Measure performance and satisfaction scores, Hospital Anxiety and Depression Scale anxiety and depression, and St George's Respiratory Questionnaire total score, using a novel non-parametric regression technique.Patients were clustered into four groups with distinct multidimensional response profiles: n=378 (18.3%; "very good responder"), n=742 (35.9%; "good responder"), n=731 (35.4%; "moderate responder"), and n=217 (10.5%; "poor responder"). Patients in the "very good responder" cluster had higher symptoms of dyspnoea, number of hospitalisations <12 months, worse exercise performance, worse performance and satisfaction scores for problematic activities of daily life, more symptoms of anxiety and depression, worse health status, and a higher proportion of patients following an inpatient PR programme compared to the other three clusters.A multidimensional response outcome needs to be considered to study the efficacy of pulmonary rehabilitation services in patients with COPD, as responses to regular outcomes are differential within patients with COPD.
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              Dyspnoea: a multidimensional and multidisciplinary approach.

              Dyspnoea is a debilitating symptom that affects quality of life, exercise tolerance and mortality in various disease conditions/states. In patients with chronic obstructive pulmonary disease (COPD), it has been shown to be a better predictor of mortality than forced expiratory volume in 1 s. In patients with heart disease it is a better predictor of mortality than angina. Dyspnoea is also associated with decreased functional status and worse psychological health in older individuals living at home. It also contributes to the low adherence to exercise training programmes in sedentary adults and in COPD patients. The mechanisms of dyspnoea are still unclear. Recent studies have emphasised the multidimensional nature of dyspnoea in the sensory-perceptual (intensity and quality), affective distress and impact domains. The perception of dyspnoea involves a complex chain of events that depend on varying cortical integration of several afferent/efferent signals and coloured by affective processing. This review, which stems from the European Respiratory Society research symposium held in Paris, France in November 2012, aims to provide state-of-the-art advances on the multidimensional and multidisciplinary aspects of dyspnoea, by addressing three different themes: 1) the neurophysiology of dyspnoea, 2) exercise and dyspnoea, and 3) the clinical impact and management of dyspnoea.

                Author and article information

                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of Chronic Obstructive Pulmonary Disease
                05 December 2019
                : 14
                : 2787-2798
                [1 ]Department of Respiratory Medicine, National Hospital Organization Osaka Toneyama Medical Center , Toyonaka, Japan
                [2 ]Course of Safety Management in Health Care Sciences, Graduate School of Health Care Sciences, Jikei Institute , Osaka, Japan
                Author notes
                Correspondence: Ryoji Maekura Course of Safety Management in Health Care Sciences, Graduate School of Health Care Sciences, Jikei Institute , 1-2-8 Miyahara, Yodogawa-Ku, Osaka532-0003, JapanTel +81 6 6150 1336Fax +81 6 6150 1337 Email
                © 2019 Maekura et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (

                Page count
                Figures: 4, Tables: 5, References: 33, Pages: 12
                Original Research


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