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Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death

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...

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Autores principales: Danielsson, Tom, Schreyer, Hendrik, Woksepp, Hanna, Johansson, Therese, Bergman, Patrick, Månsson, Alf, Carlsson, Jörg
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BMJ Publishing Group 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6347893/
https://www.ncbi.nlm.nih.gov/pubmed/30740234
http://dx.doi.org/10.1136/bmjsem-2018-000486
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author Danielsson, Tom
Schreyer, Hendrik
Woksepp, Hanna
Johansson, Therese
Bergman, Patrick
Månsson, Alf
Carlsson, Jörg
author_facet Danielsson, Tom
Schreyer, Hendrik
Woksepp, Hanna
Johansson, Therese
Bergman, Patrick
Månsson, Alf
Carlsson, Jörg
author_sort Danielsson, Tom
collection PubMed
description 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, creatine kinase (CK), MHC-α, myoglobin (MG), creatinine (C) and N-terminal prohormone of brain natriuretic peptide (NT-proBNP) 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 after exercise.
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spelling pubmed-63478932019-02-08 Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death Danielsson, Tom Schreyer, Hendrik Woksepp, Hanna Johansson, Therese Bergman, Patrick Månsson, Alf Carlsson, Jörg BMJ Open Sport Exerc Med Original Article 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, creatine kinase (CK), MHC-α, myoglobin (MG), creatinine (C) and N-terminal prohormone of brain natriuretic peptide (NT-proBNP) 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 after exercise. BMJ Publishing Group 2019-01-21 /pmc/articles/PMC6347893/ /pubmed/30740234 http://dx.doi.org/10.1136/bmjsem-2018-000486 Text en © Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.
spellingShingle Original Article
Danielsson, Tom
Schreyer, Hendrik
Woksepp, Hanna
Johansson, Therese
Bergman, Patrick
Månsson, Alf
Carlsson, Jörg
Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death
title Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death
title_full Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death
title_fullStr Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death
title_full_unstemmed Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death
title_short Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death
title_sort two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6347893/
https://www.ncbi.nlm.nih.gov/pubmed/30740234
http://dx.doi.org/10.1136/bmjsem-2018-000486
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