Physiological rather than pathological cardiac remodeling in olympic-style elite weightlifters: an imaging and biomarker study.

High-intensity resistance training causes intermittent extreme afterload, but its potential to induce maladaptive myocardial fibrosis remains unclear. This study investigated the molecular and tissue-level cardiac consequences of long-term resistance training. A cross-sectional study of 13 elite male weightlifters (≥ 5 years experience) and 13 age-matched healthy controls. Participants underwent transthoracic echocardiography (longitudinal strain) and cardiac magnetic resonance imaging (native T1, extracellular volume [ECV], and late gadolinium enhancement [LGE]). Serum biomarkers (galectin-3, soluble ST2, TNF-α, endothelin-1, TGF-β, and cardiac troponin) were measured at rest and, for athletes, immediately post-training. Weightlifters showed higher native T1 values than controls (1003.39 vs. 974.06 ms, p<0.05), but ECV was identical (25%) and LGE prevalence was equal (15.40%), indicating no structural fibrosis. Global strain was slightly lower in athletes but remained within physiological limits. At rest, biomarkers did not differ between groups. Post-exercise, galectin-3 increased significantly (2.04 ± 0.80 to 3.01 ± 0.92 ng/mL, p=0.001), while TGF-β decreased (3.08 ± 0.41 to 2.84 ± 0.37 ng/mL, p=0.046). No significant changes occurred in other biomarkers or troponin. Despite repeated peak pressure loads, elite weightlifters exhibited physiological rather than maladaptive remodeling. The absence of structural fibrosis (normal ECV/LGE) suggests that long-term resistance training remains within an adaptive range. The post-exercise galectin-3 spike likely reflects transient extracellular matrix turnover rather than sustained profibrotic signaling.