# How Swimming Modulates Inflammatory Pathways in Pain, Neurodegenerative, and Metabolic Disorders

**Authors:** Mahdiyeh Kooshki, Rozhin Rezeai-Farimani, Amirmohammad Moradpour, Vafa Baradaran Rahimi, Vahid Reza Askari

PMC · DOI: 10.3390/brainsci15101121 · Brain Sciences · 2025-10-18

## TL;DR

Swimming reduces inflammation by modulating key immune pathways, offering potential benefits for conditions like heart disease, diabetes, and neurological disorders.

## Contribution

This study systematically reviews how swimming modulates inflammatory pathways in various disorders, highlighting its therapeutic potential.

## Key findings

- Swimming reduces neuroinflammation by enhancing BDNF, CREB, and PI3K/Akt while suppressing NF-κB, TNF-α, and IL-6.
- Swimming activates SIRT1 and PGC-1α in metabolic tissues, improving mitochondrial function and antioxidant defenses.
- Swimming reduces vascular inflammation and oxidative stress by upregulating PPAR-α and eNOS while downregulating iNOS.

## Abstract

Background: As a non-weight-bearing full-body exercise, swimming may reduce inflammation and boost anti-inflammatory agents to decrease the risk of cardiovascular, neurological, and rheumatological disorders. This systematic review examines the current evidence on the role of swimming exercise in modulating immune responses through inflammatory pathways. Methods: First, the PubMed and Scopus databases were searched through December 2024 for studies on swimming and inflammation. The initial search using keywords yielded 509 articles; 102 met the inclusion criteria after screening for relevance, language, and full-text availability. Results: This study suggests that regular swimming reduces neuroinflammation by enhancing BDNF, CREB, and PI3K/Akt signaling while suppressing both mRNA and protein levels of NF-κB, TNF-α, and IL-6 in the brain. In metabolic tissues, it activates SIRT1 and PGC-1α, improving mitochondrial biogenesis and antioxidant defense. Swimming also upregulates PPAR-α and eNOS while downregulating iNOS, leading to reduced vascular inflammation, oxidative stress, and fibrosis in renal and cardiac tissues. Moreover, the enhanced production of IL-10 and the decreasing levels of IL-1β and CRP contribute to systemic anti-inflammatory effects. Conclusions: Consequently, the available evidence suggests that swimming can be a low-impact, full-body exercise with potential therapeutic options in managing inflammation-related conditions such as cardiovascular disease, diabetes, and obesity. Future studies should focus on human clinical trials, investigate mechanisms, and assess longer time frames.

## Linked entities

- **Genes:** BDNF (brain derived neurotrophic factor) [NCBI Gene 627], CREB1 (cAMP responsive element binding protein 1) [NCBI Gene 1385], PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) [NCBI Gene 5290], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790], TNF (tumor necrosis factor) [NCBI Gene 7124], IL6 (interleukin 6) [NCBI Gene 3569], SIRT1 (sirtuin 1) [NCBI Gene 23411], PPARGC1A (PPARG coactivator 1 alpha) [NCBI Gene 10891], PPARA (peroxisome proliferator activated receptor alpha) [NCBI Gene 5465], NOS3 (nitric oxide synthase 3) [NCBI Gene 4846], NOS2 (nitric oxide synthase 2) [NCBI Gene 4843], IL10 (interleukin 10) [NCBI Gene 3586], IL1B (interleukin 1 beta) [NCBI Gene 3553], CRP (C-reactive protein) [NCBI Gene 1401]
- **Diseases:** cardiovascular disease (MONDO:0004995), diabetes (MONDO:0005015), obesity (MONDO:0011122)

## Full-text entities

- **Genes:** CREB1 (cAMP responsive element binding protein 1) [NCBI Gene 1385] {aka CREB, CREB-1}, PPARA (peroxisome proliferator activated receptor alpha) [NCBI Gene 5465] {aka NR1C1, PPAR, PPAR-alpha, PPARalpha, hPPAR}, PPARGC1A (PPARG coactivator 1 alpha) [NCBI Gene 10891] {aka LEM6, PGC-1(alpha), PGC-1alpha, PGC-1v, PGC1, PGC1A}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, SIRT1 (sirtuin 1) [NCBI Gene 23411] {aka SIR2, SIR2L1, SIR2alpha}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, NOS3 (nitric oxide synthase 3) [NCBI Gene 4846] {aka EC-NOS, ECNOS, MYMY8, NOSIII, cNOS, eNOS}, BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, ISYNA1 (inositol-3-phosphate synthase 1) [NCBI Gene 51477] {aka INO1, INOS, IPS, IPS 1, IPS-1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}
- **Diseases:** Metabolic Disorders (MESH:D008659), diabetes (MESH:D003920), Inflammatory (MESH:D007249), Neurodegenerative (MESH:D019636), obesity (MESH:D009765), neuroinflammation (MESH:D000090862), Pain (MESH:D010146), fibrosis (MESH:D005355), cardiovascular disease (MESH:D002318)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12564535/full.md

## References

118 references — full list in the complete paper: https://tomesphere.com/paper/PMC12564535/full.md

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Source: https://tomesphere.com/paper/PMC12564535