Serum heart-type fatty acid-binding protein decreases and soluble isoform of suppression of tumorigenicity 2 increases significantly by long-term physical activity.


Journal

Journal of investigative medicine : the official publication of the American Federation for Clinical Research
ISSN: 1708-8267
Titre abrégé: J Investig Med
Pays: England
ID NLM: 9501229

Informations de publication

Date de publication:
06 2019
Historique:
accepted: 02 12 2018
pubmed: 30 12 2018
medline: 11 7 2020
entrez: 30 12 2018
Statut: ppublish

Résumé

The aim of this prospective study was to investigate the influence of long-term physical activity on biomarkers for myocyte ischemia (heart-type fatty acid-binding protein, H-FABP), matrix remodelling/vascular stress (soluble isoform of suppression of tumorigenicity 2, sST2) and inflammation (soluble urokinase-type plasminogen activator receptor, suPAR). In this prospective observational study 109 subjects were recruited, 98 completed the study. Subjects were asked to perform exercise within the calculated training pulse for 8 months. The performance gain was measured/quantified by bicycle stress tests at the beginning and end of the observation period. Twenty-seven subjects with a performance gain <2.9% were excluded. suPAR, H-FABP and sST2 were measured in serum at baseline and after 2, 4 and 8 months by ELISA. We found a significant decrease in H-FABP (1.86 (0.86) to 1.29 (0.98) ng/mL; p<0.01) and a significant increase in sST2 levels (6126 (2759) to 6919 (3720) pg/mL; p=0.045) during the observation period of 8 months while there was no remarkable change in suPAR levels. We interpret the activity-induced decrease in H-FABP as sign of lower subclinical myocardial ischemia and better perfusion, probably due to a more economic metabolization and electrolyte balance. The increase in sST2 might reflect physiological sports-induced vascular stress. As H-FABP and sST2 play an important role in the pathomechanism of ischemic cardiomyopathy (iCMP) further studies should investigate the influence of regular physical activity on these biomarkers in a population of patients with iCMP. TRIAL REGISTRATION NUMBER: NCT02097199.

Identifiants

pubmed: 30593542
pii: jim-2018-000913
doi: 10.1136/jim-2018-000913
doi:

Substances chimiques

FABP3 protein, human 0
Fatty Acid Binding Protein 3 0
IL1RL1 protein, human 0
Interleukin-1 Receptor-Like 1 Protein 0
Protein Isoforms 0
Receptors, Urokinase Plasminogen Activator 0

Banques de données

ClinicalTrials.gov
['NCT02097199']

Types de publication

Clinical Trial Journal Article Observational Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

833-840

Informations de copyright

© American Federation for Medical Research 2019. No commercial re-use. See rights and permissions. Published by BMJ.

Déclaration de conflit d'intérêts

Competing interests: None declared.

Auteurs

Michael Sponder (M)

Department of Cardiology, Medical University of Vienna, Vienna, Vienna, Austria.

Michael Lichtenauer (M)

Department of Cardiology, Clinic of Internal Medicine II, Paracelsus Medical University of Salzburg, Salzburg, Austria.

Bernhard Wernly (B)

Department of Cardiology, Clinic of Internal Medicine II, Paracelsus Medical University of Salzburg, Salzburg, Austria.

Vera Paar (V)

Department of Cardiology, Clinic of Internal Medicine II, Paracelsus Medical University of Salzburg, Salzburg, Austria.

Uta Hoppe (U)

Department of Cardiology, Clinic of Internal Medicine II, Paracelsus Medical University of Salzburg, Salzburg, Austria.

Michael Emich (M)

Austrian Federal Ministry of Defence and Sports, Austrian Armed Forces, Vienna, Austria.

Monika Fritzer-Szekeres (M)

Department of Medical-Chemical Laboratory Analysis, Medical University of Vienna, Vienna, Austria.

Brigitte Litschauer (B)

Department of Pharmacology, Medical University of Vienna, Vienna, Austria.

Jeanette Strametz-Juranek (J)

SKA-RZ Bad Tatzmannsdorf, Bad Tatzmannsdorf, Austria.

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Classifications MeSH