ReviewJournal of applied physiology (Bethesda, Md. : 1985)2009
Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?
Review in Journal of applied physiology (Bethesda, Md. : 1985), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 69 citations in OpenAlex.
- Inspiratory muscle training, with or without concomitant pulmonary rehabilitation, for chronic obstructive pulmonary disease (COPD).The Cochrane database of systematic reviews · 2023Pooled it
- Inspiratory muscle training for asthma.The Cochrane database of systematic reviews · 2013Pooled it
- Effects of pulmonary rehabilitation on diaphragm thickness and contractility in patients with chronic obstructive pulmonary disease.Turkish journal of medical sciences · 2022Article
- The role of muscle-specific MicroRNAs in patients with chronic obstructive pulmonary disease and skeletal muscle dysfunction.Frontiers in physiology · 2022Review
- Effects of Altitude on Chronic Obstructive Pulmonary Disease Patients: Risks and Care.Life (Basel, Switzerland) · 2021Review
- Obesity modulates diaphragm curvature in subjects with and without COPD.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Medium term effects of including manual therapy in a pulmonary rehabilitation program for chronic obstructive pulmonary disease (COPD): a randomized controlled pilot trial.The Journal of manual & manipulative therapy · 2016Article
- Muscle dysfunction in chronic obstructive pulmonary disease: update on causes and biological findings.Journal of thoracic disease · 2015Review
- Increased inspiratory esophagogastric junction pressure in systemic sclerosis: an add-on to antireflux barrier.World journal of gastroenterology · 2015Article
- Diaphragm remodeling and compensatory respiratory mechanics in a canine model of Duchenne muscular dystrophy.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
- COPD elicits remodeling of the diaphragm and vastus lateralis muscles in humans.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Review
- Exposure to neonatal cigarette smoke causes durable lung changes but does not potentiate cigarette smoke-induced chronic obstructive pulmonary disease in adult mice.Experimental lung research · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The diaphragm and other respiratory muscles undergo extensive remodeling in both animal models of emphysema and in human chronic obstructive pulmonary disease, but the nature of the remodeling is different in many respects. One common feature is a shift toward improved endurance characteristics and increased oxidative capacity. Furthermore, both animals and humans respond to chronic hyperinflation by diaphragm shortening. Although in rodent models this clearly arises by deletion of sarcomeres in series, the mechanism has not been proven conclusively in human chronic obstructive pulmonary disease. Unique characteristics of the adaptation in human diaphragms include shifts to more predominant slow, type I fibers, expressing slower myosin heavy chain isoforms, and type I and type II fiber atrophy. Although some laboratories report reductions in specific force, this may be accounted for by decreases in myosin heavy chain content as the muscles become more oxidative and more efficient. More recent findings have reported reductions in Ca(2+) sensitivity and reduced myofibrillar elastic recoil. In contrast, in rodent models of disease, there is no consistent evidence for loss of specific force, no consistent shift in fiber populations, and atrophy is predominantly seen only in fast, type IIX fibers. This review challenges the hypothesis that the adaptations in human diaphragm represent a form of dysfunction, secondary to systemic disease, and suggest that most findings can as well be attributed to adaptive processes of a complex muscle responding to unique alterations in its working environment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.