Key result
Elevated cTnI affects ~10% of elite endurance athletes, largely driven by autoantibodies rather than injury.
Why the study?
Elevations in cTnI are frequently observed in athletes after exercise, and cTnI autoantibodies or macrotroponin complexes were hypothesised to explain these repeated elevations.
Does high-intensity endurance training increase the prevalence of cTnI elevations and cTnI autoantibodies compared to non-athletes?
Cross-Sectional (n=456)
Yes
Does high-intensity endurance training increase the prevalence of cTnI elevations and cTnI autoantibodies compared to non-athletes?
Absolute Event Rate: 10.1% vs 0%
p-value: p=0.002
Elevated troponin I in healthy endurance athletes is common and largely driven by benign autoantibodies rather than true myocardial injury, highlighting the need to test for macrotroponin to avoid misdiagnosis.
May confound post-exercise cTnI interpretation in athletes; leaves open whether autoantibodies or macrotroponin explain repeated elevations.
Background and Aims Elevations in cardiac troponin I (cTnI), a marker of myocardial injury, have been frequently observed in athletes after intense exercise. cTnI autoantibodies (cTnI Ab) and macrotroponin complexes can confound assessment, and we hypothesised that they may explain the paradox of repeated cTnI elevations in athletes. Methods Athletes and non-athlete controls underwent high-sensitivity cTnI testing, cardiac magnetic resonance imaging (CMR), 24-hour ambulatory electrocardiographic monitoring and VO 2 peak assessment. Athletes with cTnI values >99 th percentile sex-specific upper reference limit were assessed for cTnI Ab using polyethylene glycol (PEG) precipitation and troponin T (TnT)/TnI discordance. Results Overall, 456 participants were evaluated (387 athletes and 69 non-athletes). cTnI elevations were observed in 39 (10.1%) athletes and no (0%) control participants (p=0.002). Athletes with cTnI elevation demonstrated higher VO 2 peak and larger biventricular dimensions compared to athletes without cTnI elevations (p<0.001). Of the athletes with cTnI elevations, 31 of 39 (79%) had evidence of cTnI Ab; 26 (66.7%) met both criteria for cTnI Ab (low PEG recovery and normal cTnT), a further 5 (12.8%) met one criteria (low PEG recovery but slightly elevated cTnT out of keeping with cTnI elevation [median TnT/TnI=3.7%]) and the remaining 8 athletes met neither (high PEG recovery and cTnT elevation [median TnT/TnI=81.2%]). Four of these 8 athletes with TnI elevation but without cTnI Ab had evidence of possible myocardial injury on CMR. Conclusions cTnI elevations are commonly found in highly-trained endurance athletes, especially the fittest athletes with greatest cardiac remodelling, but are due to antibodies in a majority. Graphic Abstract Key Question What is the prevalence of cardiac troponin I (cTnI) elevation in highly-trained endurance athletes outside of competition and what proportion are due to cTnI antibodies? How do elevated cTnI measures relate to exercise-induced cardiac remodelling and VO 2 peak? Key Finding 1 in 10 endurance athletes had elevated cTnI with 80% due to cTnI antibodies as opposed to ‘true’ cTnI elevations. cTnI elevation and antibodies were found in the fittest athletes with the greatest cardiac remodelling on cardiac magnetic resonance imaging. Take-home message cTnI antibodies are highly prevalent in endurance athletes and are not associated with myocardial damage. Awareness of cTnI antibodies and appropriate testing will help avoid intensive investigation and misdiagnoses. Non-standard abbreviations/acronyms cTnI = cardiac troponin I cTnT = cardiac troponin T PEG = polyethylene glycol precipitation Ab = antibody LGE = late gadolinium enhancement NSVT = non-sustained ventricular tachycardia
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Rowe et al. (2026) conducted a cross-sectional in Cardiac troponin I elevation (n=456). Elite endurance athletic training vs. Non-athlete controls was evaluated on Cardiac troponin I (cTnI) elevation (>99th percentile sex-specific upper reference limit) (p=0.002). Cardiac troponin I elevations were found in 10.1% of elite endurance athletes compared to 0% of controls, with 79% of these elevations attributable to troponin I autoantibodies rather than true myocardial injury.
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