Marathon Running Triggers Acute Cardiac Biomarker Spikes and Structural Changes, but Long-Term Clinical Significance Remains Unclear
核心洞察
A systematic review and meta-analysis of 69 studies confirms marathon running consistently elevates cardiac troponins and NT-proBNP beyond clinical thresholds within the first hour post-race.
Echocardiography reveals modest reductions in left ventricular dimensions and increases in right ventricular volume, though these changes fall outside clinically meaningful ranges.
Observed cardiac biomarker elevations and structural shifts likely represent physiological responses to extreme endurance demands, but pathological consequences in susceptible individuals cannot be excluded.
A comprehensive systematic review and meta-analysis published in BMJ Open Sport & Exercise Medicine has found that marathon running consistently triggers measurable spikes in cardiac biomarkers and subtle alterations in heart structure and function among healthy adults. However, researchers caution that the clinical significance of these acute changes remains uncertain, and the evidence does not yet demonstrate that these responses translate into lasting heart damage.
The analysis, which screened 7,377 records from electronic databases, included 69 studies in the systematic review and 49 in the pooled data analysis, encompassing 3,274 predominantly male (73%) participants aged between 27 and 63.
Cardiac Biomarkers Surge Beyond Clinical Thresholds
The meta-analysis revealed that all three key cardiac biomarkers—cardiac troponin T (搜索) (cTnT), cardiac troponin I (搜索) (cTnI), and N-terminal pro-B-type natriuretic peptide (搜索) (NT-proBNP)—were consistently elevated within the first hour after marathon completion. Reported levels exceeded commonly used clinical thresholds for myocardial injury, ischemia, or heart failure.
Troponins, regulatory proteins involved in cardiac muscle contraction, increased markedly after racing. While elevated troponin concentrations are routinely used in clinical medicine as markers of myocardial injury, the researchers note that exercise-induced increases may occur through several physiological mechanisms and do not necessarily indicate permanent cardiac damage. Existing evidence suggests that prolonged endurance exercise can increase cardiac cell membrane permeability, allowing troponins to enter the bloodstream.
NT-proBNP, released by cardiac cells in response to myocardial stretch caused by pressure overload or left ventricular expansion, also showed significant post-race elevations. Several studies reported concentrations above thresholds commonly used in heart failure assessment. The prolonged cardiovascular demands of marathon running may promote cardiac cell stretching, endocrine activation, and myocardial hypoxia, all of which could contribute to increased NT-proBNP release. Whether repeated elevations in this biomarker are associated with adverse long-term cardiac outcomes remains unknown.
Structural and Functional Cardiac Changes Are Modest
Regarding structural changes, the meta-analysis demonstrated marathon-induced reductions in left ventricular dimensions alongside increases in right ventricular volume and diameter. The magnitude of these changes was modest and did not reflect significant clinical relevance.
Modest changes in systolic function were also observed, including a 3% increase in left ventricular fractional shortening and a 3.5% reduction in right ventricular ejection fraction. These changes fell outside the ranges commonly accepted as indicating clinically relevant ventricular function impairment in healthy individuals.
Diastolic function analysis revealed a 16% reduction in early ventricular filling velocity and a 26% increase in late ventricular filling velocity—changes that also remained within physiological ranges.
Notably, fewer studies employed cardiac Magnetic Resonance Imaging (MRI), and these findings did not replicate the structural changes observed with echocardiography. The discrepancy may be explained by differences in assessment timing: MRI scans were typically performed around seven hours after marathon completion, whereas echocardiographic measurements were obtained immediately post-race. Transient factors such as hydration status and pulmonary pressure may therefore have influenced echocardiographic findings.
Individual Variability and Unanswered Questions
The findings suggest that the magnitude of these cardiac changes varies according to age, sex, training status, marathon performance, and overall exercise load, highlighting substantial differences in how individuals respond to endurance exercise.
The researchers acknowledge several limitations. Most study participants were men, and women might have different cardiovascular responses to marathon running, both in the short and long term. Training status, a potentially influential factor, was not consistently reported across included studies. Additionally, many studies scored high on the risk of bias, indicating room for methodological improvement.
"The potential for pathological consequences in susceptible individuals or with repeated participation in extreme endurance events remains," the researchers state. They conclude that well-designed long-term studies in diverse groups, including sex and ethnicity, are needed to determine "whether these effects represent physiological responses to extreme levels of exercise or reflect early markers of pathological cardiac remodeling."
Overall, the observed biomarker elevations and cardiac changes are likely to represent predominantly physiological responses to the intense cardiovascular demands of marathon running, although the possibility of adverse effects in susceptible individuals cannot yet be excluded.