This study systematically elucidates the regulatory mechanisms and potential therapeutic value of the exercise-induced hormone Irisin in the pathological progression of cardiac fibrosis. Through comprehensive analysis and multidimensional data integration, we constructed a complete regulatory network of Irisin within the cardiovascular system, spanning its secretion, signal transduction, and precise regulatory control. Our findings demonstrate that exercise intervention significantly elevates circulating Irisin levels via the skeletal muscle–peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)–fibronectin type III domain-containing protein 5 (FNDC5) signaling axis. Irisin establishes a multidimensional molecular barrier against cardiac fibrosis by targeting Sirtuin 1 (Sirt1) activation, inhibiting the transforming growth factor-beta (TGF-β)/Smad3 signaling pathway, and modulating the transcriptional activity of the mitochondrial biogenesis core factors PGC-1α and nuclear respiratory factor 1 (NRF-1). Moreover, the dual regulatory mechanism of the exercise–skeletal muscle–heart axis not only effectively suppresses the aberrant activation of cardiac fibroblasts but also significantly reduces collagen deposition, oxidative stress, and inflammatory infiltration by restoring mitochondrial dynamics balance. Taken together, this study reveals a novel exercise-mediated cardioprotective mechanism at the molecular interaction network level, thereby providing a theoretical basis for the development of non-pharmacological bio-intervention strategies targeting the Irisin signaling pathway and laying a translational foundation for precise exercise prescriptions in cardiovascular diseases.

Elite boxing induces rapid metabolic changes that are not fully captured by conventional physiological measurements. A standardized untargeted serum metabolomics workflow based on liquid chromatography-quadrupole time-of-flight tandem mass spectrometry (LC-QTOF-MS/MS) was applied to samples collected before sparring, immediately after sparring, and 24 h after sparring in seven elite male boxers. The workflow included standardized sample collection, pooled quality-control monitoring, metabolite profiling, multivariate statistical analysis, and pathway interpretation. Acute sparring was associated with changes in metabolites related to glycolysis and gluconeogenesis, whereas the 24-h timepoint was associated with sulfur metabolism. Phosphatidylinositol PI(16:0/18:2(9Z,12Z)) showed strong discrimination of the immediate post-sparring state, and thiosulfate was associated with the 24-h recovery state. These findings support the use of this workflow for reproducible profiling of exercise-related metabolic changes in this cohort of seven elite male boxers. The protocol is intended for controlled small-cohort studies of acute exercise and short-term recovery and emphasizes reproducible sample handling, pooled quality-control monitoring, and interpretable downstream analysis.