Key result
Acute marathon running raises galectin-3, linked to reduced left atrial contractile function in trained athletes.
Why the study?
It was unclear whether acute marathon running engages circulating fibrosis-related biomarkers and whether these biomarkers track with atrial function in a training volume-dependent manner.
Does marathon running acutely alter plasma galectin-3 and PIIINP levels, and are these changes associated with left atrial contractile function in long-distance runners?
Observational (n=54)
Echocardiography and biomarker analysis performed by blinded operators
No
Does marathon running acutely alter plasma galectin-3 and PIIINP levels, and are these changes associated with left atrial contractile function in long-distance runners?
Effect estimate: r = 0.413
p-value: p=0.015
Acute marathon running significantly increases plasma galectin-3 and PIIINP levels, with the galectin-3 rise correlating with reduced left atrial contractile function particularly in highly trained athletes, suggesting a potential link between cumulative endurance training and adverse atrial remodeling.
No immediate practice change for athletes; hypothesis-generating for galectin-3 as endurance-related atrial remodeling marker.
High‐intensity endurance exercise induces myocardial remodelling as an adaptive response to sustained volume overload, but excessive cumulative training might also favour deleterious cardiac remodelling, including atrial fibrosis. Whether acute marathon running engages circulating fibrosis‐related biomarkers and whether these biomarkers track with atrial function in a training volume‐dependent manner remains unclear. This study, with within‐subject pre‐ and post‐marathon comparisons, evaluated plasma galectin‐3 and amino‐terminal type III procollagen propeptide (PIIINP) in 36 male long‐distance runners before and immediately after completion of a marathon and examined their relationship to atrial function assessed by speckle‐tracking echocardiography. Participants were stratified into high‐training (HT; ≥100 km week −1 ; n = 18) and low‐training (LT; <100 km week −1 ; n = 18) groups, with 18 age‐matched non‐active control subjects. At baseline, galectin‐3, PIIINP, left atrial strain a wave (LASa) and right atrial strain a wave (RASa) were comparable across groups. Marathon completion significantly increased galectin‐3 [mean (SD): LT, from 5.2 (2.3) to 23.1 (8.2) ng mL −1 ; HT, from 7.2 (3.8) to 26.5 (11.0) ng mL −1 ; both P < 0.001] and PIIINP in both runner groups. The pre‐to‐post fractional changes in galectin‐3 and PIIINP were moderately correlated when all runners were considered together ( r = 0.569, P = 0.006). In exploratory correlation analyses, the post‐marathon galectin‐3 fractional change was positively correlated with the post‐marathon LASa across all runners ( r = 0.413, P = 0.015), indicating that larger increases in galectin‐3 were associated with less negative atrial strain values; subgroup analysis indicated that this association was driven by the highly trained athletes (HT, r = 0.476, P = 0.045); the corresponding correlation did not reach significance in the LT group ( r = 0.378, P = 0.148). No such association was observed for PIIINP or for the RASa in any group. These findings suggest that the acute galectin‐3 response to marathon running might be linked to left atrial contractile function selectively in highly trained athletes.
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Contreras–Briceño et al. (2026) conducted an observational in Healthy male long-distance runners and non-active controls (n=54). Marathon running vs. Pre-marathon baseline (within-subject) and non-active controls was evaluated on Correlation between post-marathon galectin-3 fractional change and post-marathon left atrial strain a wave (LASa) across all runners (r = 0.413, p=0.015). Acute marathon running significantly increased plasma galectin-3 levels, and the magnitude of this increase correlated with reduced left atrial contractile function selectively in highly trained athletes.
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