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2019 (Engelska)Ingår i: BMJ Open Sport & Exercise Medicine, E-ISSN 2055-7647, Vol. 5, artikel-id e000486Artikel i tidskrift (Refereegranskat) Published
Abstract [en]
Objective It has been suggested that the mechanism behind cardiac troponin elevation after strenuous exercise is passage through a cell membrane with changed permeability rather than myocardial cell death. We hypothesised that an increase of cardiac specific myosin heavy chain-alpha (MHC-α; 224 kDa compared with cardiac troponin T’s (cTnT) 37 kDa) could hardly be explained by passage through a cell membrane.
Methods Blood samples were collected from 56 athletes (15 female, age 42.5±9.7, range 24–70 years) before, directly after and on days 1–8 after an Ironman. Biomarkers (C reactive protein (CRP), cTnT, creatinekinase (CK), MHC-α, myoglobin (MG), creatinine (C) and N-terminal prohormone of brain natriuretic peptide (NTproBNP) were measured.
Results The course of MHC-α concentration (μg/L) was 1.33±0.53 (before), 2.57±0.78 (directly after), 1.51±0.53 (day 1), 2.74±0.55 (day 4) and 1.83±0.76 (day 6). Other biomarkers showed a one-peaked increase with maximal values either directly after the race or at day 1: cTnT 76 ±80 ng/L (12–440; reference<15), NT-proBNP 776±684 ng/L (92–4700; ref.<300), CK 68±55 μkat/L (5–280; ref.<1.9), MG 2088±2350 μg/L (130–17 000; ref.<72) and creatinine 100±20 μmol/L (74–161; ref.<100), CRP 49±23 mg/L(15–119; ref.<5).
Conclusion MHC-α exhibited a two-peaked increase which could represent a first release from the cytosolic pool and later from cell necrosis. This is the first investigation of MHC-α plasma concentration afterexercise.
Ort, förlag, år, upplaga, sidor
BMJ Publishing Group Ltd, 2019
Nyckelord
cardiovascular medicine, physiology, sports and exercise medicine
Nationell ämneskategori
Idrottsvetenskap och fitness Kardiologi och kardiovaskulära sjukdomar
Forskningsämne
Samhällsvetenskap, Idrottsvetenskap
Identifikatorer
urn:nbn:se:lnu:diva-79922 (URN)10.1136/bmjsem-2018-000486 (DOI)000596810500018 ()30740234 (PubMedID)2-s2.0-85060492223 (Scopus ID)
2019-01-252019-01-252025-08-28Bibliografiskt granskad