# Effects of swimming on bone loss and mechanisms in ovariectomized osteoporotic rats **Authors:** Yingying Zhao, Yinyu Chen, Xinyan Yang, Yilin Wang, Yangyang Zhang, Lin Li, Peng Zhang PMC · DOI: 10.1515/med-2026-1382 · Open Medicine · 2026-02-23 ## TL;DR Swimming helps reduce bone loss in rats with osteoporosis by affecting a key bone regulation pathway. ## Contribution This study shows swimming reduces bone loss in ovariectomized rats by modulating the OPG/RANKL/RANK pathway. ## Key findings - Swimming increased bone volume and density while decreasing bone resorption markers in osteoporotic rats. - Swimming upregulated OPG and downregulated RANKL and RANK, shifting the pathway toward bone protection. - The results suggest swimming could be a beneficial exercise for preventing osteoporosis. ## Abstract To investigate the effects of swimming on bone loss and the OPG/RANKL/RANK pathway in ovariectomized (OVX) osteoporotic rats. Twenty female SD rats were randomly divided into a sham-operated group, a ovariectomized osteoporosis group, a short-duration exercise group, and a long-duration exercise group. Bone volume fraction (BV/TV), trabecular thickness (Tb.Th), bone mineral density (BMD), trabecular separation (Tb.Sp), and trabecular number (Tb.N) of bone tissue were measured by Micro-CT. The expression of human C-terminal peptide collagen type I (CTX-Ⅰ), tartrate-resistant acid phosphatase 5b (TRAP-5b), bone-specific alkaline phosphatase (BALP) and serum bone glycoprotein (BGP) were measured by ELISA. The mRNA and protein expression of OPG, RANKL, and RANK in bone tissue were detected by qRT-PCR and Western bolt, respectively. After swimming treatment, compared with the ovariectomized osteoporosis group, BV/TV, BMD, Tb.Th, and Tb.N increased, while Tb.Sp decreased; CTX-Ⅰ, TRAP-5b, BGP, and BALP levels decreased. OPG mRNA and protein expression increased, while RANKL and RANK decreased. Swimming training alleviated ovariectomy-induced bone loss and was accompanied by a shift of the OPG/RANKL/RANK axis toward an anti-resorptive profile, suggesting that modulation of this pathway may contribute to the bone-protective effects of swimming. Further functional studies are warranted to test causality. ## Linked entities - **Genes:** BTF3P11 (basic transcription factor 3 pseudogene 11) [NCBI Gene 690], TNFSF11 (TNF superfamily member 11) [NCBI Gene 8600], TNFRSF11A (TNF receptor superfamily member 11a) [NCBI Gene 8792] - **Proteins:** acp5.S (acid phosphatase 5, tartrate resistant S homeolog), BGLAP (bone gamma-carboxyglutamate protein), BTF3P11 (basic transcription factor 3 pseudogene 11), TNFSF11 (TNF superfamily member 11), TNFRSF11A (TNF receptor superfamily member 11a) - **Diseases:** osteoporosis (MONDO:0005298) - **Species:** Rattus norvegicus (taxon 10116) ## Full-text entities - **Genes:** Bglap (bone gamma-carboxyglutamate protein) [NCBI Gene 25295] {aka Bglap2, Bgp, Bgpr, Bgpra}, Tff2 (trefoil factor 2) [NCBI Gene 116592], ACP5 (acid phosphatase 5, tartrate resistant) [NCBI Gene 54] {aka HPAP, TRACP5a, TRACP5b, TRAP, TRAcP, TrATPase}, TNFRSF11B (TNF receptor superfamily member 11b) [NCBI Gene 4982] {aka OCIF, OPG, PDB5, TR1}, TNFSF11 (TNF superfamily member 11) [NCBI Gene 8600] {aka CD254, ODF, OPGL, OPTB2, RANKL, TNLG6B}, Tnfrsf11b (TNF receptor superfamily member 11B) [NCBI Gene 25341] {aka Opg}, Alb (albumin) [NCBI Gene 24186] {aka Alb1, Albza}, Tnfsf11 (TNF superfamily member 11) [NCBI Gene 117516] {aka ODF, OPGL, RANKL, TRANCE}, Actb (actin, beta) [NCBI Gene 81822] {aka Actx}, CYP27A1 (cytochrome P450 family 27 subfamily A member 1) [NCBI Gene 1593] {aka CP27, CTX, CYP27}, BGLAP (bone gamma-carboxyglutamate protein) [NCBI Gene 632] {aka BGP, OC, OCN}, Ceacam1 (CEA cell adhesion molecule 1) [NCBI Gene 81613] {aka BGPR, Bgp, CD66a, Ccam1}, ESR1 (estrogen receptor 1) [NCBI Gene 2099] {aka ER, ESR, ESRA, ESTRR, Era, NR3A1} - **Diseases:** diabetes (MESH:D003920), osteoporotic (MESH:D058866), diseases (MESH:D004194), inflammatory (MESH:D007249), fracture (MESH:D050723), respiratory diseases (MESH:D012140), bone fragility (MESH:C536063), systemic diseases (MESH:D034721), bone metabolic disorders (MESH:D001851), obesity (MESH:D009765), Accelerated bone resorption (MESH:D001862), cardiovascular diseases (MESH:D002318), bone loss (MESH:D001847), toxicity (MESH:D064420), neurasthenia (MESH:D009440), Osteoporosis (MESH:D010024), Estrogen (E) deficiency (MESH:D014811), arthritis (MESH:D001168), endometrial cancer (MESH:D016889), hyperplasia (MESH:D006965), ovarian dysfunction (MESH:D010049), estrogen deficiency (MESH:D056828), type 2 diabetic (MESH:D003924), skeletal deformities (MESH:D009140), breast cancer (MESH:D001943), pathological fractures (MESH:D005598) - **Chemicals:** N (MESH:D009584), polyacrylamide (MESH:C016679), pentobarbital sodium (MESH:D010424), paraffin (MESH:D010232), carbonate (MESH:D002254), vitamin D (MESH:D014807), saline (MESH:D012965), TMAO (MESH:C005855), SDS (MESH:D012967), Sp (MESH:C000604007), water (MESH:D014867), TRIzol (MESH:C411644), fluoride (MESH:D005459), HE (-), denosumab (MESH:D000069448), teriparatide (MESH:D019379), Hematoxylin (MESH:D006416), eosin (MESH:D004801), Tween-20 (MESH:D011136), PVDF (MESH:C024865), formalin (MESH:D005557), bisphosphonates (MESH:D004164), calcium (MESH:D002118), Th (MESH:D013910), alendronate (MESH:D019386) - **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606] - **Mutations:** rs3102735, T950C, rs2073618 ## Full text _Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12922758/full.md ## Figures 7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12922758/full.md ## References 50 references — full list in the complete paper: https://tomesphere.com/paper/PMC12922758/full.md --- Source: https://tomesphere.com/paper/PMC12922758