The relationship between workload and exercise‐induced cardiac troponin elevations is influenced by non‐obstructive coronary atherosclerosis

Author:

Bjorkavoll‐Bergseth Magnus12ORCID,Erevik Christine1,Kleiven Øyunn1ORCID,Wiktorski Tomasz3,Auestad Bjørn34,Skadberg Øyvind5,Aakre Kristin M.6,Eijsvogels Thijs M. H.7,Ørn Stein18

Affiliation:

1. Department of Cardiology Stavanger University Hospital Stavanger Norway

2. Clinical Institute II University of Bergen Bergen Norway

3. Department of Mathematics and Physics The University of Stavanger Stavanger Norway

4. Research Department Stavanger University Hospital Stavanger Norway

5. Departement of Biochemistry Stavanger University Hospital Stavanger Norway

6. Department of Biochemistry Haukeland University Hospital Bergen Norway

7. Department of Medical Biosciences, Exercise Physiology Research Group Radboud University Medical Center Nijmegen the Netherlands

8. Department of Electrical Engineering and Computer Science University of Stavanger Stavanger Norway

Abstract

AbstractThe relationship between exercise‐induced troponin elevation and non‐obstructive coronary artery disease (CAD) is unclear. This observational study assessed non‐obstructive CAD's impact on exercise‐induced cardiac Troponin I (cTnI) elevation in middle‐aged recreational athletes. cTnI levels of 40 well‐trained recreational athletes (73% males, 50 ± 9 years old) were assessed by a high‐sensitive cTnI assay 24 h before, and at 3 and 24 h following two high‐intensity exercises of different durations; a cardiopulmonary exercise test (CPET), and a 91‐km mountain bike race. Workload was measured with power meters. Coronary computed tomography angiography was used to determine the presence or absence of non‐obstructive (<50% obstruction) CAD. A total of 15 individuals had non‐obstructive CAD (Atherosclerotic group), whereas 25 had no atherosclerosis (normal). There were higher post‐exercise cTnI levels following the race compared with CPET, both at 3 h (77.0 (35.3–112.4) ng/L vs. 11.6 (6.4–22.5) ng/L, p < 0.001) and at 24 h (14.7 (6.7–16.3) vs. 5.0 (2.6–8.9) ng/L, p < 0.001). Absolute cTnI values did not differ among groups. Still, the association of cTnI response to power output was significantly stronger in the CAD versus Normal group both at 3 h post‐exercise (Rho = 0.80, p < 0.001 vs. Rho = −0.20, p = 0.33) and 24‐h post‐exercise (Rho = 0.87, p < 0.001 vs. Rho = −0.13, p = 0.55). Exercise‐induced cTnI elevation was strongly correlated with exercise workload in middle‐aged athletes with non‐obstructive CAD but not in individuals without CAD. This finding suggests that CAD influences the relationship between exercise workload and the cTnI response even without coronary artery obstruction.

Funder

Simon Fougner Hartmanns Familiefond

Helse Vest

ConocoPhillips

Publisher

Wiley

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