Abstract
Aims: The efficacy of swimming in managing knee osteoarthritis (KOA) is well documented. However, the potential of swimming to regulate the Hif-1α/VEGFa pathway and thereby hindering the formation of subchondral bone H-type vessels, remains to be fully elucidated. Methods: A mouse model of KOA was established by intra-articular injection of papain solution, followed by a swimming intervention. Symptomatic changes were observed by measuring body weight and knee joint diameter. Behavioural tests were used to assess exercise-related functions. HE staining was used to observe bone tissue morphology, while immunofluorescence staining was used to observe variations in H-type vessels of the subchondral bone. Quantitative PCR and western blotting were used to determine the expression levels of the pathway mRNA and protein. Results: The results obtained from this study revealed that KOA mice exhibited activation of the Hif-1α/VEGFa pathway in the tibial plateau bone, increased H-type vessels in the subchondral bone, and significant cartilage degeneration. In contrast, mice in the swimming exercise group demonstrated faster recovery from body weight and knee swelling, and exhibited superior performance in the balance beam test, rotarod test, and open field test. The swimming exercise group exhibited reduced articular cartilage destruction, diminished formation of H-type vessels in the subchondral bone, and decreased mRNA and protein expression of the Hif-1α/VEGFa pathway. Conclusion: Articular cartilage in KOA mice exhibited signs of degradation and joint function was impaired. The findings of this study demonstrate that swimming exercise led to a down-regulation of the Hif-1α/VEGFa pathway in the tibial plateau bone of KOA mice, an inhibition of H-type vessels in the subchondral bone, and an improvement in cartilage morphology. Supplementary Information: The online version contains supplementary material available at 10.1186/s12891-025-08903-6.