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Biological markers of cardiac damage are not related to measures of cardiac systolic and diastolic function using cardiovascular magnetic resonance and echocardiography after an acute bout of prolonged endurance exercise
  1. M Wilson1,2,
  2. R O'Hanlon3,
  3. S Prasad3,
  4. D Oxborough4,
  5. R Godfrey5,
  6. F Alpendurada3,
  7. G Smith3,
  8. J Wong3,
  9. S Basavarajaiah6,
  10. S Sharma6,
  11. A Nevill1,
  12. David Gaze7,
  13. K George8,
  14. G Whyte2,8
  1. 1Research Centre of Sport and Exercise Performance, University of Wolverhampton, Walsall, UK
  2. 2Centre for Sports Cardiology, Centre for Health and Human Performance, 76 Harley Street, London, UK
  3. 3Department of Cardiac Magnetic Resonance Imaging, Royal Brompton and Harefield NHS Trust, London, UK
  4. 4University of Leeds, Leeds, UK
  5. 5Department of Sport and Exercise Science, Brunel University, London, UK
  6. 6Department of Heart Muscle Disorders, Kings College London, London, UK
  7. 7Department of Clinical Biochemistry, St Georges Hospital Medical School, London, UK
  8. 8Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, UK
  1. Correspondence to Mathew Wilson, Research Centre for Sport and Exercise Performance, School of Sport, Performing Arts and Leisure, University of Wolverhampton, Walsall WS1 3BD, UK; mat.wilson{at}wlv.ac.uk

Abstract

Objectives Seventeen male participants (mean (SD) (range): age 33.5 (6.5) years (46–26 years), body mass 80 (9.2) kg (100–63 kg), height 1.81 (0.06) m (1.93– 1.70 m)) ran a marathon to investigate the relationship between systolic function (using cardiac magnetic resonance (CMR)) and diastolic function (using echocardiography) against biomarkers of cardiac damage.

Methods Echocardiographic and cardiac troponin I (cTnI)/N-terminal pro-B-type natriuretic peptide (NTproBNP) data were collected 24 h premarathon, immediately postmarathon and 6 h postmarathon. CMR data were collected 24 h premarathon and at 6 h postmarathon.

Results Body mass was significantly reduced postmarathon (80 (9.2) vs 78.8 (8.6) kg; p<0.001). There was a significant E/A reduction postmarathon (1.11 (0.34) vs 1.72 (0.44); p<0.05) that remained depressed 6 h postmarathon (1.49 (0.43); p<0.05). CMR demonstrated left ventricular end-diastolic and end-systolic volumes were reduced postmarathon, with a preserved stroke volume. Left ventricular ejection fraction 6 h postmarathon significantly increased (64.4% (4.2%) vs 67.4% (5%); p<0.05). There were significant elevations in cTnI (0.00 vs 0.04 (0.03) μg/l; p<0.05) and NTproBNP (37.4 (24.15) ng/l vs 59.34 (43.3) ng/l; p<0.05) immediately postmarathon. Eight runners had cTnI elevations immediately postmarathon above acute myocardial infarction cutoff levels (≥0.03 μg/l). No correlations between cTnI/NTproBNP and measures of diastolic function (E, A, E/A, isovolumic relaxation time, E deceleration time and E/E′) or measures of systolic function (stroke volume or ejection fraction) were observed immediately postmarathon or 6 h postmarathon.

Conclusions Biomarkers of cardiac damage after prolonged exercise are not associated with either systolic or diastolic functional measures.

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Footnotes

  • Competing interests None.

  • Ethical approval Brompton, Harefield and NHLI research ethics committee.

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

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