PurposeThis study was designed to investigate the effects of long-term home-based Liuzijue exercise combined with clinical guidance in elderly patients with chronic obstructive pulmonary disease (COPD).MethodsForty patients with COPD at stages II–III of the Global Initiative for Chronic Obstructive Lung Disease were enrolled. The subjects were randomly allocated to the Liuzijue exercise group (LG) or control group (CG) in a 1:1 ratio. Participants in the LG performed six Liuzijue training sessions, including 4 days at home and 2 days in the hospital with clinical guidance for 60 minutes/day for 6 months. Participants in the CG conducted no exercise intervention. In addition, lung function test, 6-minute walking test (6MWT), 30-second sit-to-stand test (30 s SST), and the St George’s Respiratory Questionnaire (SGRQ) were conducted at the baseline and at the end of the intervention.ResultsThirty-six patients completed the study. The patients’ lung function improved significantly (p < 0.05) in the LG as well as the 6MWT, 30 s SST, and SGRQ score (p < 0.01). While the SGRQ total score, activity, and impact scores increased significantly (p < 0.05) in the CG. In addition, there were significant differences between the groups (p < 0.01) in regard to the values of forced expiratory volume in 1 second as a percentage of the predicted volume, 6MWT, 30 s SST, and SGRQ.ConclusionsLong-term home-based Liuzijue exercise combined with clinical guidance can effectively improve the pulmonary function, exercise capacity, and quality of life of elderly patients with moderate to severe COPD.

BACKGROUND: We sought to investigate the effects of home-based breathing exercises on pulmonary function, respiratory muscle strength, exercise capacity, dyspnea, and health-related quality of life in patients with COPD. METHODS: All randomized, controlled trials involving the use of home-based breathing exercises as an intervention in patients with COPD were searched on

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BackgroundUpper limb muscle strength plays an important role in respiratory and pulmonary function, and limited research focuses on the role of strength and endurance of the elbow extensor and flexor. This study was conducted to accurately assess upper limb muscle function and quantified associations with pulmonary function and respiratory muscle strength in patients with stable chronic obstructive pulmonary disease (COPD).MethodsIn this cross-sectional study, patients with stable COPD treated in Yue-Yang Integrative Medicine Hospital from March 2014 to March 2016 were recruited. All participants underwent a pulmonary function test (forced expiratory volume in first second/forced vital capacity, FEV1/FVC; percentage value of predicted FEV1, FEV1%pred), a respiratory muscle strength test (maximal inspiratory pressure, MIP; maximal expiratory pressure, MEP), and an isokinetic test of dominant upper limb after a 24-hr interval (peak torque, PT; PT/body weight, PT/BW; total work, TW; endurance ratio, ER).ResultsA total of 88 patients with stable COPD (age: 65.5±8.7 years) were recruited, of which 73% (64 patients) were male. In the multiple stepwise regression analysis, sex remained as significant impactors in the final model for FEV1%pred (adjusted R2=0.243, P<0.001). Elbow flexor PT/BW and ER, sex, and BMI remained as significant impactors in the final model for FEV1/FVC (adjusted R2=0.255, P<0.01). Elbow flexor TW remained as significant impactors for MIP (adjusted R2=0.112, P=0.001), while elbow extensor PT and PT/BW and sex remained as significant impactors for MEP (adjusted R =0.385, P<0.01).ConclusionIn stable COPD, pulmonary function and respiratory muscle strength are associated with upper limb muscle strength. In particular, elbow flexor endurance is likely an important impactor for pulmonary function and inspiratory muscle strength, while elbow extensor strength is of importance for expiratory muscle strength.

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decreased diaphragm function is a crucial factor leading to reduced ventilatory efficiency and worsening of quality of life in chronic obstructive pulmonary disease (cOPd). Exercise training has been demonstrated to effectively improve the function of the diaphragm. However, the mechanism of this process has not been identified. The emergence of metabolomics has allowed the exploration of new ideas. The present study aimed to analyze the potential biomarkers of exercise-dependent enhancement of diaphragm function in COPD using metabolomics. Sprague Dawley rats were divided into three groups: COPD + exercise group (CEG); COPD model group (CMG); and control group (CG). The first two groups were exposed to cigarette smoke for 16 weeks to establish a COPD model. Then, the rats in the CEG underwent aerobic exercise training for 9 weeks. Following confirmation that exercise effectively improved the diaphragm function, a gas chromatography tandem time-of-flight mass spectrometry analysis system was used to detect the differential metabolites and associated pathways in the diaphragm muscles of the different groups. Following exercise intervention, the pulmonary function and diaphragm contractility of the CEG rats were significantly improved compared with those of the CMG rats. A total of 36 different metabolites were identified in the comparison between the CMG and the CG. Pathway enrichment analysis indicated that these different metabolites were involved in 17 pathways. A total of 29 different metabolites were identified in the comparison between the CMG and the CEG, which are involved in 14 pathways. Candidate biomarkers were selected, and the pathways analysis of these metabolites demonstrated that 2 types of metabolic pathways, the nicotinic acid and nicotinamide metabolism and arginine and proline metabolism pathways, were associated with exercise-induced pulmonary rehabilitation.

Chronic obstructive pulmonary disease (COPD) features chronic inflammatory reactions of both intra- and extrapulmonary nature. Moreover, COPD is associated with abnormal glucose and lipid metabolism in patients, which influences the prognosis and chronicity of this disease. Abnormal glucose and lipid metabolism are also closely related to inflammation processes. Further insights into the interactions of inflammation and glucose and lipid metabolism might therefore inspire novel therapeutic interventions to promote lung rehabilitation. Chemerin, as a recently discovered adipokine, has been shown to play a role in inflammatory response and glucose and lipid metabolism in many diseases (including COPD). Chemerin recruits inflammatory cells to sites of inflammation during the early stages of COPD, leading to endothelial barrier dysfunction, early vascular remodeling, and angiogenesis. Moreover, it supports the recruitment of antigen-presenting cells that guide immune cells as part of the body’s inflammatory responses. Chemerin also regulates metabolism via activation of its cognate receptors. Glucose homeostasis is affected via effects on insulin secretion and sensitivity, and lipid metabolism is changed by increased transformation of preadipocytes to mature adipocytes through chemerin-binding receptors. Controlling chemerin signaling may be a promising approach to improve various aspects of COPD-related dysfunction. Importantly, several studies indicate that chemerin expression in vivo is influenced by exercise. Although available evidence is still limited, therapeutic alterations of chemerin activity may be a promising target of therapeutic approaches aimed at the rehabilitation of COPD patients based on exercises. In conclusion, chemerin plays an essential role in COPD, especially in the inflammatory responses and metabolism, and has a potential to become a target for, and a biomarker of, curative mechanisms underlying exercise-mediated lung rehabilitation.

Background: Chronic obstructive pulmonary disease (COPD) skeletal muscle dysfunction is a prevalent malady that significantly affects patients' prognosis and quality of life. Although the study of this disease has attracted considerable attention, a definite animal model is yet to be established. This study investigates whether smoke exposure could lead to the development of a COPD skeletal muscle dysfunction model in rats. Methods: Sprague Dawley rats were randomly divided into model (MG, n = 8) and control groups (CG, n = 6). The MG was exposed to cigarette smoke for 16 weeks while the CG was not. The body weight and forelimb grip strength of rats were monitored monthly. The pulmonary function and the strength of tibialis anterior muscle were assessed in vitro and compared after establishing the model. The histological changes in lung and gastrocnemius muscles were observed. The expressions of interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α were detected by ELISA, while the expressions of Atrogin-1 and MuRF1 in the gastrocnemius muscle were determined by Western blotting. Results: Smoke exposure slowly increases the body weight and forelimb grip strength of MG rats, compared to CG rats. However, it significantly decreases the pulmonary ventilation function and the skeletal muscle contractility of the MG in vitro. Histologically, the lung tissues of MG show typical pathological manifestations of emphysema, while the skeletal muscles present muscular atrophy. The expressions of IL-6, IL-8, and TNF-α in MG rats are significantly higher than those measured in CG rats. Increased levels of Atrogin-1 and MuRF1 were also detected in the gastrocnemius muscle tissue of MG. Conclusion: Progressive smoking exposure decreases the contractile function of skeletal muscles, leading to muscular atrophy. It also increases the expressions of inflammatory and muscle protein degradation factors in COPD rats. This indicates that smoke exposure could be used to establish a COPD skeletal muscle dysfunction model in rats.