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Updated: Jul 15, 2026
05:51
Measuring Diaphragm Thickness and Function Using Point-of-Care Ultrasound
Published on: November 3, 2023
Diaphragm muscle fiber dysfunction in chronic obstructive pulmonary disease: toward a pathophysiological concept
Coen A C Ottenheijm1, Leo M A Heunks, P N Richard Dekhuijzen
1Department of Pulmonary Diseases, 454 Radboud University, Nijmegen Medical Centre, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands. c.ottenheijm@long.umcn.nl
Summary
Inspiratory muscle weakness in chronic obstructive pulmonary disease (COPD) stems from cellular damage and protein loss in the diaphragm. Early-stage COPD patients may have these changes before symptoms appear, warranting further research.
Area of Science:
- Pulmonary Medicine
- Respiratory Physiology
- Muscle Biology
Background:
- Inspiratory muscle weakness, particularly in the diaphragm, is clinically significant in chronic obstructive pulmonary disease (COPD).
- Traditionally attributed to hyperinflation, recent studies reveal underlying cellular and molecular pathology in the COPD diaphragm.
Purpose of the Study:
- To explore the cellular and molecular mechanisms contributing to diaphragm weakness in COPD.
- To investigate the presence of these pathological alterations in early-stage COPD.
- To highlight the need for in vivo diaphragm function studies in mild to moderate COPD.
Main Methods:
- Invasive evaluation of diaphragm contractile function, structure, and biochemistry.
- Analysis of myosin content and fiber-type shifts.
- Postulation of oxidative stress and proteolytic machinery activation.
Main Results:
- COPD diaphragms exhibit cellular and molecular alterations, including loss of myosin content and sarcomeric injury.
- Oxidative stress and injury activate proteolytic pathways, leading to contractile protein wasting.
- Pathological changes are present even in early GOLD I/II stages of COPD, despite lack of daily activity limitation.
Conclusions:
- Diaphragm weakness in COPD is linked to contractile protein loss due to oxidative stress and proteolytic activity.
- Early-stage COPD diaphragms show pathological changes, suggesting potential for early intervention.
- Future research should focus on in vivo diaphragm function in mild to moderate COPD, with proteasome inhibitors showing therapeutic promise.
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