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Inflammatory and Metabolic Responses to Different Resistance Training on Chronic Obstructive Pulmonary Disease: A Randomized Control Trial.

ABSTRACT: Background: Low-grade inflammation can be present in chronic obstructive pulmonary disease (COPD), which may affect the regulation of muscle protein and body metabolism. Regular exercise show improvement in muscle strength and dyspnea in patients with COPD, however, the response to training on inflammatory and metabolic disorders is unclear. In this study, we compared the effects of resistance training using weight machines and elastic resistance (bands and tubes) on the inflammatory and metabolic responses in patients with COPD. Methods: Patients with COPD were randomized into three groups: elastic band group (EBG), elastic tube group (ETG), and weight machines equipment group (MG). EBG and ETG were analyzed together [elastic group (EG)]. The participants were evaluated for pulmonary function (spirometry), peripheral muscle strength (digital dynamometry), IL-6, TNF-?, IL-10, IL-15 (Immunoassay), glucose, triacylglycerol, total cholesterol, HDL-c, and albumin levels (Enzymatic colorimetric). Blood samples were collected to assess the acute and chronic exercise responses after 12 weeks of training protocol. Results: The patient's mean age was 71.53 ± 6.97 years old. FEV1 (percent predicted) was 50.69 ± 16.67 and 45.40 ± 15.15% for EG and MG, respectively (p = 0.28). All groups increased muscle strength (p < 0.05) with no differences between groups. The acute response to exercise after 12 weeks of training showed improvement of inflammation when compared to baseline. Regarding the chronic effects, it was observed a decrease of all cytokines, except IL-10 (p < 0.05). After 12 weeks of training, the analysis of the metabolic profile presented a reduction in glucose concentration (p < 0.01), with no differences between groups (p = 0.30) and a decrease in triacylglycerol for the EG (p > 0.01). Conclusions: Training with elastic resistances or conventional weight machines showed improvement of inflammation response after 12 weeks of training. Chronically, both training groups showed anti-inflammatory effects, with the EG showing a strong tendency to improve IL-10/TNF-? ratio and IL-10 levels. TRIAL REGISTRATION:RBR-6V9SJJ.

SUBMITTER: Silva BSA

PROVIDER: S-EPMC5877487 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Inflammatory and Metabolic Responses to Different Resistance Training on Chronic Obstructive Pulmonary Disease: A Randomized Control Trial.

Silva Bruna S de Alencar BSA Lira Fábio S FS Rossi Fabrício E FE Ramos Dionei D Uzeloto Juliana S JS Freire Ana P C F APCF de Lima Fabiano F FF Gobbo Luís A LA Ramos Ercy M C EMC

Frontiers in physiology 20180323

<b>Background:</b> Low-grade inflammation can be present in chronic obstructive pulmonary disease (COPD), which may affect the regulation of muscle protein and body metabolism. Regular exercise show improvement in muscle strength and dyspnea in patients with COPD, however, the response to training on inflammatory and metabolic disorders is unclear. In this study, we compared the effects of resistance training using weight machines and elastic resistance (bands and tubes) on the inflammatory and ...[more]

PMID: 29628896

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Project description:BackgroundSubjects with chronic obstructive pulmonary disease (COPD) are prone to accelerated decay of muscle strength and mass with advancing age. This is believed to be driven by disease-inherent systemic pathophysiologies, which are also assumed to drive muscle cells into a state of anabolic resistance, leading to impaired abilities to adapt to resistance exercise training. Currently, this phenomenon remains largely unstudied. In this study, we aimed to investigate the assumed negative effects of COPD for health- and muscle-related responsiveness to resistance training using a healthy control-based translational approach.MethodsSubjects with COPD (n = 20, GOLD II-III, FEV1predicted 57 ± 11%, age 69 ± 5) and healthy controls (Healthy, n = 58, FEV1predicted 112 ± 16%, age 67 ± 4) conducted identical whole-body resistance training interventions for 13 weeks, consisting of two weekly supervised training sessions. Leg exercises were performed unilaterally, with one leg conducting high-load training (10RM) and the contralateral leg conducting low-load training (30RM). Measurements included muscle strength (nvariables = 7), endurance performance (nvariables = 6), muscle mass (nvariables = 3), muscle quality, muscle biology (m. vastus lateralis; muscle fiber characteristics, RNA content including transcriptome) and health variables (body composition, blood). For core outcome domains, weighted combined factors were calculated from the range of singular assessments.ResultsCOPD displayed well-known pathophysiologies at baseline, including elevated levels of systemic low-grade inflammation ([c-reactive protein]serum), reduced muscle mass and functionality, and muscle biological aberrancies. Despite this, resistance training led to improved lower-limb muscle strength (15 ± 8%), muscle mass (7 ± 5%), muscle quality (8 ± 8%) and lower-limb/whole-body endurance performance (26 ± 12%/8 ± 9%) in COPD, resembling or exceeding responses in Healthy, measured in both relative and numeric change terms. Within the COPD cluster, lower FEV1predicted was associated with larger numeric and relative increases in muscle mass and superior relative improvements in maximal muscle strength. This was accompanied by similar changes in hallmarks of muscle biology such as rRNA-content↑, muscle fiber cross-sectional area↑, type IIX proportions↓, and changes in mRNA transcriptomics. Neither of the core outcome domains were differentially affected by resistance training load.ConclusionsCOPD showed hitherto largely unrecognized responsiveness to resistance training, rejecting the notion of disease-related impairments and rather advocating such training as a potent measure to relieve pathophysiologies.Trial registrationClinicalTrials.gov ID: NCT02598830. Registered November 6th 2015, https://clinicaltrials.gov/ct2/show/NCT02598830.

Project description:Antimicrobial resistance is a global concern in chronic respiratory diseases, including chronic obstructive pulmonary disease (COPD). The collection of antibiotic resistance genes or resistome in human airways may underlie the resistance. COPD is heterogeneous, and understanding the airway resistome in relation to patient phenotype and endotype may inform precision antibiotic therapy. Here, we characterized the airway resistome for 94 COPD participants at stable disease. Among all demographic and clinical factors, patient inflammatory endotype was associated with the airway resistome. There were distinct resistome profiles between patients with neutrophilic or eosinophilic inflammation, two primary inflammatory endotypes in COPD. For neutrophil-predominant COPD, the resistome was dominated by multidrug resistance genes. For eosinophil-predominant COPD, the resistome was diverse, with an increased portion of patients showing a macrolide-high resistome. The differential antimicrobial resistance pattern was validated by sputum culture and in vitro antimicrobial susceptibility testing. Ralstonia and Pseudomonas were the top contributors to the neutrophil-associated resistome, whereas Campylobacter and Aggregatibacter contributed most to the eosinophil-associated resistome. Multiomic analyses revealed specific host pathways and inflammatory mediators associated with the resistome. The arachidonic acid metabolic pathway and matrix metallopeptidase 8 (MMP-8) exhibited the strongest associations with the neutrophil-associated resistome, whereas the eosinophil chemotaxis pathway and interleukin-13 (IL-13) showed the greatest associations with the eosinophil-associated resistome. These results highlight a previously unrecognized link between inflammation and the airway resistome and suggest the need for considering patient inflammatory subtype in decision-making about antibiotic use in COPD and broader chronic respiratory diseases. IMPORTANCE Antibiotics are commonly prescribed for both acute and long-term prophylactic treatment in chronic airway disorders, such as chronic obstructive pulmonary disease (COPD), and the rapid growth of antibiotic resistance is alarming globally. The airway harbors a diverse collection of microorganisms known as microbiota, which serve as a reservoir for antibiotic resistance genes or the resistome. A comprehensive understanding of the airway resistome in relation to patient clinical and biological factors may help inform decisions to select appropriate antibiotics for clinical therapies. By deep multiomic profiling and in vitro phenotypic testing, we showed that inflammatory endotype, the underlying pattern of airway inflammation, was most strongly associated with the airway resistome in COPD patients. There were distinct resistome profiles between neutrophil-predominant and eosinophil-predominant COPD that were associated with different bacterial species, host pathways, and inflammatory markers, highlighting the need of considering patient inflammatory status in COPD antibiotic management.

Project description:BackgroundMetabolic adaptation in immune cells is necessary to modulate immune cell function as it is intricately coupled with intracellular metabolism. We aimed to characterize the metabolic state of human peripheral blood mononuclear cells (PBMCs) after long-term exposure to tobacco smoke in smokers with preserved lung function and COPD subjects.MethodsPBMCs were isolated from healthy non-smokers (HNS), healthy smokers (HS) and COPD subjects, cultured and the mitochondrial respiration while utilizing glucose (glycolysis), fatty acids (β-oxidation) or pyruvate (direct Krebs' cycle substrate) was measured using the XFp Extracellular Flux Analyzer. Plasma levels of inflammatory cytokines IFN-γ, IL-17, TNF-α, IL-5, IL-9 and IFN-α were measured using flow cytometry. RAW264.7 cells were exposed to cigarette smoke condensate (CSC) for 1 h and its effect on cell viability, cellular metabolism and phagocytosis ability were also studied. Patient's data was analyzed using the Mann Whitney U test, whereas Student's t test was performed to analyze the in-vitro data.ResultsPBMCs from COPD subjects showed a significant decrease in extracellular acidification rate (ECAR) while utilizing glucose as compared to HNS (151.9 Vs 215%). Mitochondrial oxygen consumption rate (OCR) on palmitate or pyruvate was also found to be significantly lower in COPD subjects as compared to HS and a strong positive correlation between palmitate OCR in PBMCs and FEV1 (r = 0.74, p < 0.05) and FVC (r = 0.79, p < 0.05) values in HS was observed. The metabolic shift towards fatty acid metabolism in healthy smokers promoted an inflammatory cytokine response with a greater increase in the levels of IL-5, IL-9 and IFN-α as compared to IFN-γ, IL-17 and TNF-α. In-vitro experiments with RAW 264.7 cells showed similar metabolic alterations and a reduced ability to phagocytose Streptococcus pneumonia and Haemophilus influenza after cigarette smoke exposure in the presence of glucose or palmitate.ConclusionsThese findings indicate a metabolic basis for the inflammatory response in COPD and could suggest a new therapeutic target for controlling the immune response and delaying the onset of disease.Trial registrationThis observational study was retrospectively registered in the Clinical Trails Registry - India (ICMR - NIMS) on 19th January 2018 with the registration number CTRI/2018/01/011441 .

Project description:IntroductionIn activities involving upper limbs, patients with chronic obstructive pulmonary disease (COPD) report an increase in dyspnea. For this reason, the authors of the recommendations about pulmonary rehabilitation propose to perform upper limbs muscle strengthening in patients with COPD. However, the modalities of strengthening are not clearly established.The aim of this study is to compare the effects of upper limbs endurance strengthening versus upper limbs force strengthening, in patients with COPD during a pulmonary rehabilitation program.MethodsThis study is a randomized, open-label, bi-center controlled trial in parallel groups distributed in a ratio (1:1) comparing upper limbs force strengthening (group F) to the upper limbs endurance strengthening (group E) during a pulmonary rehabilitation program in patients with COPD stages 2 to 4 (A-D).After randomization, patients will be allocated to follow: A 4 weeks pulmonary rehabilitation program with upper limbs resistance strengthening (group F). A 4 weeks pulmonary rehabilitation program with upper limbs endurance strengthening (group E).The primary outcome is dyspnea measured with the London Chest Activity of daily Living questionnaire. The secondary outcomes are dyspnea (using Modified Medical Research Council dyspnea Scale, dyspnea-12 questionnaire, multidimensional dyspnea profile questionnaire), upper limb exercise capacity (using the 6-minute Peg Board and Ring Test), Maximal voluntary strength of deltoid, biceps, and brachial triceps.The sample size calculated is 140 patients per group, or 280 in total.DiscussionThe modalities of upper limb strengthening are not very well known, and evidence based is lacking to recommend endurance or resistance upper limb strengthening.We anticipate that the results of this study will be of relevance to clinical practice. They will bring information about the best modality of upper limb strengthening to use during a pulmonary rehabilitation program.Trial registrationIdRCB n°2018-A00955-50; V1.1 du 11/07/2018; REHABSUP, clinical trial.gov (NCT03611036), registered August 02, 2018, https://clinicaltrials.gov/ct2/show/NCT03611036.

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Inflammatory and Metabolic Responses to Different Resistance Training on Chronic Obstructive Pulmonary Disease: A Randomized Control Trial.

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Inflammatory and Metabolic Responses to Different Resistance Training on Chronic Obstructive Pulmonary Disease: A Randomized Control Trial.

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