Research Progress on the Adaptation Law and Core Mechanism of Animal Models for Exercise Intervention in Inflammatory Bowel Disease: A Systematic Review

Xiwen Yang,1 Sibin Yi2 1School of Physical Education, Pingxiang University, Pingxiang, 337055, People’s Republic of China; 2Department of Surgery, Pingxiang Hospital of Traditional Chinese Medicine, Pingxiang, 337099, People’s Republic of ChinaCorrespondence: Sibin Yi, Email [email protected]: Inflammatory Bowel Disease (IBD), including Crohn’s Disease (CD) and Ulcerative Colitis (UC), is a chronic recurrent intestinal inflammatory disorder with a rising global incidence and younger age trend. Current immunosuppressant-based treatments have limited efficacy due to individual differences, making exercise—a low-cost, safe auxiliary intervention—attractive for improving intestinal inflammation and patient quality of life. However, exercise effects are dually regulated by IBD animal model pathological characteristics and exercise program parameters, with unclear adaptation laws and mechanisms. This PRISMA-compliant systematic review synthesizes evidence from 59 studies (2016– 2025, 9 databases) to clarify the “model-exercise-effect” correlation. We classified IBD animal models into chemical-induced (DSS/TNBS/OXZ, acute inflammation, suitable for short-term low-intensity active exercise), gene-edited (IL-10 KO/IL-2 KO, chronic genetic susceptibility, requiring long-term moderate-intensity exercise), naturally occurring/microbiota-induced (SAMP1/YitFc/microbiota-transplanted, natural disease course, suitable for microbiota-exercise combined intervention), and emerging models (gnotobiotic/humanized microbiota/organoid, high translational value). Exercise type (active > passive), intensity (50– 70% VO2max optimal), cycle (≥ 12 weeks for stable microbiota regulation), and timing (preventive > therapeutic in acute phase) significantly affect outcomes. Core mechanisms include intestinal microbiota modulation (increased Lactobacillus/Bifidobacterium, upregulated SCFAs synthesis), inflammatory factor balance (myokines/SCFAs synergistically inhibiting NF-κB), intestinal barrier enhancement (upregulated tight junction proteins), and immune homeostasis remodeling (Treg differentiation/M2 macrophage polarization). Key challenges include model-human pathological differences and exercise protocol standardization. Future research should focus on precise model matching, multi-omics mechanism analysis, and clinical translation to promote exercise as a non-pharmacological intervention for IBD.Keywords: inflammatory bowel disease, animal model, exercise intervention, intestinal microbiota