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Original article
Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death
  1. Tom Danielsson1,
  2. Hendrik Schreyer2,
  3. Hanna Woksepp3,
  4. Therese Johansson2,
  5. Patrick Bergman1,
  6. Alf Månsson4,
  7. Jörg Carlsson2,5
  1. 1 Department of Sport Sciences, Linnæus University, Kalmar, Sweden
  2. 2 Department of Internal Medicine, Section of Cardiology, Kalmar County Hospital, Kalmar, Sweden
  3. 3 Department of Clinical Microbiology and Research Section Development and Public Health Unit, Kalmar County Hospital, Kalmar, Sweden
  4. 4 Department of Chemistry and Biomedical Sciences, Linnæus University, Kalmar, Sweden
  5. 5 Department of Health and Caring Sciences, Linnæus University, Kalmar, Sweden
  1. Correspondence to Dr Jörg Carlsson; jorg.carlsson{at}ltkalmar.se

Abstract

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.

  • cardiovascular medicine
  • sports and exercise medicine
  • physiology

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/.

https://doi.org/10.1136/bmjsem-2018-000486

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    Footnotes

    • Contributors All authors (TD, HS, HW, TJ, AM, PB and JC) contributed to the conception of the study. JC and PB performed the data analysis. All authors assisted with the interpretation. JC and TD were the principal writers of the manuscript. All authors contributed to the drafting and revision of the final article. All authors approved the final submitted version of the manuscript.

    • Funding The project was funded by Landstinget Kalmar Län through unrestricted funds to a professorship of public health (JC currently holds that position) at the Linnaeus University Kalmar. The study was undertaken as part of the IronWoMan study group.

    • Competing interests None declared.

    • Patient consent for publication Not required.

    • Ethics approval Regional Ethics Review Board in Linköping (EPN, Dnr 2016/86-31).

    • Provenance and peer review Not commissioned; internally peer reviewed.

    • Data sharing statement All measured data separated by sex can be obtained through contact with the corresponding author.