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      Motor Pathophysiology Related to Dyspnea in COPD Evaluated by Cardiopulmonary Exercise Testing

      review-article
      Diagnostics
      MDPI
      acidosis, breathing, cardiopulmonary exercise testing, dynamic hyperinflation, muscle, ventilation

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          Abstract

          In chronic obstructive pulmonary disease (COPD), exertional dyspnea, which increases with the disease’s progression, reduces exercise tolerance and limits physical activity, leading to a worsening prognosis. It is necessary to understand the diverse mechanisms of dyspnea and take appropriate measures to reduce exertional dyspnea, as COPD is a systemic disease with various comorbidities. A treatment focusing on the motor pathophysiology related to dyspnea may lead to improvements such as reducing dynamic lung hyperinflation, respiratory and metabolic acidosis, and eventually exertional dyspnea. However, without cardiopulmonary exercise testing (CPET), it may be difficult to understand the pathophysiological conditions during exercise. CPET facilitates understanding of the gas exchange and transport associated with respiration-circulation and even crosstalk with muscles, which is sometimes challenging, and provides information on COPD treatment strategies. For respiratory medicine department staff, CPET can play a significant role when treating patients with diseases that cause exertional dyspnea. This article outlines the advantages of using CPET to evaluate exertional dyspnea in patients with COPD.

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          Most cited references85

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          The FNIH Sarcopenia Project: Rationale, Study Description, Conference Recommendations, and Final Estimates

          Background. Low muscle mass and weakness are common and potentially disabling in older adults, but in order to become recognized as a clinical condition, criteria for diagnosis should be based on clinically relevant thresholds and independently validated. The Foundation for the National Institutes of Health Biomarkers Consortium Sarcopenia Project used an evidence-based approach to develop these criteria. Initial findings were presented at a conference in May 2012, which generated recommendations that guided additional analyses to determine final recommended criteria. Details of the Project and its findings are presented in four accompanying manuscripts. Methods. The Foundation for the National Institutes of Health Sarcopenia Project used data from nine sources of community-dwelling older persons: Age, Gene/Environment Susceptibility-Reykjavik Study, Boston Puerto Rican Health Study, a series of six clinical trials, Framingham Heart Study, Health, Aging, and Body Composition, Invecchiare in Chianti, Osteoporotic Fractures in Men Study, Rancho Bernardo Study, and Study of Osteoporotic Fractures. Feedback from conference attendees was obtained via surveys and breakout groups. Results. The pooled sample included 26,625 participants (57% women, mean age in men 75.2 [±6.1 SD] and in women 78.6 [±5.9] years). Conference attendees emphasized the importance of evaluating the influence of body mass on cutpoints. Based on the analyses presented in this series, the final recommended cutpoints for weakness are grip strength <26kg for men and <16kg for women, and for low lean mass, appendicular lean mass adjusted for body mass index <0.789 for men and <0.512 for women. Conclusions. These evidence-based cutpoints, based on a large and diverse population, may help identify participants for clinical trials and should be evaluated among populations with high rates of functional limitations.
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            Ghrelin is a growth-hormone-releasing acylated peptide from stomach.

            Small synthetic molecules called growth-hormone secretagogues (GHSs) stimulate the release of growth hormone (GH) from the pituitary. They act through GHS-R, a G-protein-coupled receptor for which the ligand is unknown. Recent cloning of GHS-R strongly suggests that an endogenous ligand for the receptor does exist and that there is a mechanism for regulating GH release that is distinct from its regulation by hypothalamic growth-hormone-releasing hormone (GHRH). We now report the purification and identification in rat stomach of an endogenous ligand specific for GHS-R. The purified ligand is a peptide of 28 amino acids, in which the serine 3 residue is n-octanoylated. The acylated peptide specifically releases GH both in vivo and in vitro, and O-n-octanoylation at serine 3 is essential for the activity. We designate the GH-releasing peptide 'ghrelin' (ghre is the Proto-Indo-European root of the word 'grow'). Human ghrelin is homologous to rat ghrelin apart from two amino acids. The occurrence of ghrelin in both rat and human indicates that GH release from the pituitary may be regulated not only by hypothalamic GHRH, but also by ghrelin.
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              Association between chronic obstructive pulmonary disease and systemic inflammation: a systematic review and a meta-analysis.

              Individuals with chronic obstructive pulmonary disease (COPD) are at increased risk of cardiovascular diseases, osteoporosis, and muscle wasting. Systemic inflammation may be involved in the pathogenesis of these disorders. A study was undertaken to determine whether systemic inflammation is present in stable COPD. A systematic review was conducted of studies which reported on the relationship between COPD, forced expiratory volume in 1 second (FEV(1)) or forced vital capacity (FVC), and levels of various systemic inflammatory markers: C-reactive protein (CRP), fibrinogen, leucocytes, tumour necrosis factor-alpha (TNF-alpha), and interleukins 6 and 8. Where possible the results were pooled together to produce a summary estimate using a random or fixed effects model. Fourteen original studies were identified. Overall, the standardised mean difference in the CRP level between COPD and control subjects was 0.53 units (95% confidence interval (CI) 0.34 to 0.72). The standardised mean difference in the fibrinogen level was 0.47 units (95% CI 0.29 to 0.65). Circulating leucocytes were also higher in COPD than in control subjects (standardised mean difference 0.44 units (95% CI 0.20 to 0.67)), as were serum TNF-alpha levels (standardised mean difference 0.59 units (95% CI 0.29 to 0.89)). Reduced lung function is associated with increased levels of systemic inflammatory markers which may have important pathophysiological and therapeutic implications for subjects with stable COPD.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Diagnostics (Basel)
                Diagnostics (Basel)
                diagnostics
                Diagnostics
                MDPI
                2075-4418
                21 February 2021
                February 2021
                : 11
                : 2
                : 364
                Affiliations
                Department of Respiratory Medicine, National Hospital Organization Osaka Toneyama Medical Center, 5-1-1 Toneyama, Toyonaka, Osaka 560-8552, Japan; miki.keisuke.pu@ 123456mail.hosp.go.jp
                Author information
                https://orcid.org/0000-0002-3600-8595
                Article
                diagnostics-11-00364
                10.3390/diagnostics11020364
                7926713
                ff9f54dc-cdf1-4492-ba17-15f72eec8125
                © 2021 by the author.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 14 January 2021
                : 19 February 2021
                Categories
                Review

                acidosis,breathing,cardiopulmonary exercise testing,dynamic hyperinflation,muscle,ventilation

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