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The weak regenerative ability of adult hearts originates from limited cell proliferation and polyploidization of postnatal cardiomyocytes, which severely hinders tissue repair after myocardial injury. Fetal development represents a critical window during which maternal physiological and metabolic status can shape long-term offspring cardiac structure and function. Maternal exercise represents a safe nonpharmacological prenatal intervention that confers long-term benefits to offspring health. Available evidence indicates that maternal exercise enhances placental apelin secretion and elevates \u03b1-ketoglutarate (\u03b1-KG) levels in fetal brown adipose tissue, liver, and skeletal muscle. The apelin and \u03b1-KG signaling cascade participates in epigenetic regulation and confers protective effects on offspring metabolic health. Independent animal experiments have further validated that supplementation with either apelin or \u03b1-KG alleviates myocardial infarction (MI)-induced cardiac injury in adult mice, with \u03b1-KG showing direct evidence of reactivating cardiomyocyte proliferation. Nevertheless, it remains poorly elucidated whether maternal exercise could modulate fetal cardiomyocyte proliferative capacity in offspring through apelin- or \u03b1-KG-associated signaling. This narrative review integrates current evidence and proposes a testable framework in which maternal exercise influences fetal cardiac growth and regenerative potential through placental, metabolic, and epigenetic signaling. Because direct evidence remains limited, this model should be regarded as a hypothesis that requires further experimental validation.<\/jats:p>","DOI":"10.3390\/biology15161422","type":"journal-article","created":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T13:11:57Z","timestamp":1787058717000},"page":"1422","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Maternal Exercise and Offspring Cardiac Regenerative Potential: Roles of Apelin and \u03b1-Ketoglutarate"],"prefix":"10.3390","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-6158-6049","authenticated-orcid":false,"given":"Guanfeng","family":"Qin","sequence":"first","affiliation":[{"name":"Laboratory of Regenerative Medicine in Sports Science, School of Physical Education and Sports Science, South China Normal University, Guangzhou 510006, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4073-4493","authenticated-orcid":false,"given":"Fan","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Physiology and Biomedical Engineering, Center for Regenerative Biotherapeutics, Mayo Clinic Arizona, Scottsdale, AZ 85259, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haiwang","family":"Shi","sequence":"additional","affiliation":[{"name":"Laboratory of Regenerative Medicine in Sports Science, School of Physical Education and Sports Science, South China Normal University, Guangzhou 510006, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2026,8,18]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1001","DOI":"10.1093\/eurjpc\/zwae281","article-title":"Global burden of cardiovascular diseases: Projections from 2025 to 2050","volume":"32","author":"Chong","year":"2025","journal-title":"Eur. 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