Muscle sodium content in patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.

Chronic Fatigue Syndrome Exercise Magnetic Resonance Imaging Muscle, skeletal Myalgia Sodium Sodium–hydrogen exchangers Sodium–potassium-exchanging ATPase

Journal

Journal of translational medicine
ISSN: 1479-5876
Titre abrégé: J Transl Med
Pays: England
ID NLM: 101190741

Informations de publication

Date de publication:
09 12 2022
Historique:
received: 13 05 2022
accepted: 25 08 2022
entrez: 9 12 2022
pubmed: 10 12 2022
medline: 15 12 2022
Statut: epublish

Résumé

Muscle fatigue and pain are key symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). Although the pathophysiology is not yet fully understood, there is ample evidence for hypoperfusion which may result in electrolyte imbalance and sodium overload in muscles. Therefore, the aim of this study was to assess levels of sodium content in muscles of patients with ME/CFS and to compare these to healthy controls. Six female patients with ME/CFS and six age, BMI and sex matched controls underwent Baseline tissue sodium content was higher in all 5 lower leg muscle compartments in ME/CFS compared to controls. Within the anterior extensor muscle compartment, the highest difference in baseline muscle sodium content between ME/CFS and controls was found (mean ± SD; 12.20 ± 1.66 mM in ME/CFS versus 9.38 ± 0.71 mM in controls, p = 0.0034). Directly after exercise, tissue sodium content increased in gastrocnemius and triceps surae muscles with + 30% in ME/CFS (p = 0.0005) and + 24% in controls (p = 0.0007) in the medial gastrocnemius muscle but not in the extensor muscles which were not exercised. Compared to baseline, the increase of sodium content in medial gastrocnemius muscle was stronger in ME/CFS than in controls with + 30% versus + 17% to baseline at 12 min (p = 0.0326) and + 29% versus + 16% to baseline at 15 min (p = 0.0265). Patients had reduced average handgrip strength which was associated with increased average muscle tissue sodium content (p = 0.0319, R Muscle sodium content before and after exercise was higher in ME/CFS than in healthy controls. Furthermore, our findings indicate an inverse correlation between muscle sodium content and handgrip strength. These findings provide evidence that sodium overload may play a role in the pathophysiology of ME/CFS and may allow for potential therapeutic targeting.

Sections du résumé

BACKGROUND
Muscle fatigue and pain are key symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). Although the pathophysiology is not yet fully understood, there is ample evidence for hypoperfusion which may result in electrolyte imbalance and sodium overload in muscles. Therefore, the aim of this study was to assess levels of sodium content in muscles of patients with ME/CFS and to compare these to healthy controls.
METHODS
Six female patients with ME/CFS and six age, BMI and sex matched controls underwent
RESULTS
Baseline tissue sodium content was higher in all 5 lower leg muscle compartments in ME/CFS compared to controls. Within the anterior extensor muscle compartment, the highest difference in baseline muscle sodium content between ME/CFS and controls was found (mean ± SD; 12.20 ± 1.66 mM in ME/CFS versus 9.38 ± 0.71 mM in controls, p = 0.0034). Directly after exercise, tissue sodium content increased in gastrocnemius and triceps surae muscles with + 30% in ME/CFS (p = 0.0005) and + 24% in controls (p = 0.0007) in the medial gastrocnemius muscle but not in the extensor muscles which were not exercised. Compared to baseline, the increase of sodium content in medial gastrocnemius muscle was stronger in ME/CFS than in controls with + 30% versus + 17% to baseline at 12 min (p = 0.0326) and + 29% versus + 16% to baseline at 15 min (p = 0.0265). Patients had reduced average handgrip strength which was associated with increased average muscle tissue sodium content (p = 0.0319, R
CONCLUSION
Muscle sodium content before and after exercise was higher in ME/CFS than in healthy controls. Furthermore, our findings indicate an inverse correlation between muscle sodium content and handgrip strength. These findings provide evidence that sodium overload may play a role in the pathophysiology of ME/CFS and may allow for potential therapeutic targeting.

Identifiants

pubmed: 36494667
doi: 10.1186/s12967-022-03616-z
pii: 10.1186/s12967-022-03616-z
pmc: PMC9733289
doi:

Substances chimiques

Sodium 9NEZ333N27

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

580

Commentaires et corrections

Type : ErratumIn

Informations de copyright

© 2022. The Author(s).

Références

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Auteurs

Elisabeth Petter (E)

Institute of Medical Immunology, Charité Universitätsmedizin Berlin, Campus Virchow, Berlin, Germany.
Institute of Computer-Assisted Cardiovascular Medicine, Charité Universitätsmedizin Berlin, Berlin, Germany.
Department of Congenital Heart Disease, German Heart Center Berlin, Berlin, Germany.

Carmen Scheibenbogen (C)

Institute of Medical Immunology, Charité Universitätsmedizin Berlin, Campus Virchow, Berlin, Germany.

Peter Linz (P)

Institute of Radiology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), University Hospital Erlangen, Erlangen, Germany.

Christian Stehning (C)

Philips Healthcare, Hamburg, Germany.

Klaus Wirth (K)

Institute of General Pharmacology and Toxicology, University Hospital Frankfurt am Main, Goethe-University, Theodor-Stern Kai 7, Frankfurt am Main, Germany.

Titus Kuehne (T)

Institute of Computer-Assisted Cardiovascular Medicine, Charité Universitätsmedizin Berlin, Berlin, Germany.
Department of Congenital Heart Disease, German Heart Center Berlin, Berlin, Germany.

Marcus Kelm (M)

Institute of Computer-Assisted Cardiovascular Medicine, Charité Universitätsmedizin Berlin, Berlin, Germany. mkelm@dhzb.de.
Department of Congenital Heart Disease, German Heart Center Berlin, Berlin, Germany. mkelm@dhzb.de.
Berlin Institute of Health (BIH), Berlin, Germany. mkelm@dhzb.de.
German Centre for Cardiovascular Research (DZHK), Partner Site, Berlin, Germany. mkelm@dhzb.de.

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