Introduction: Badminton is characterized by a high amount of exercise and high intensity of work. Muscle pain and discomfort often occur throughout the game, so some relaxation training is necessary. Objective: Study the effect of relaxation training on recovery from sports fatigue and fitness recovery during badminton. Methods: Badminton training was conducted three times a week. The duration of the exercises of the experimental and control group students was the same. The experimental group adopted the relaxation training form, including stretching, aerobic, and other relaxation actions. The duration of relaxation training was 15 minutes, while the control group continued to use the traditional relaxation method. Results: Lactate in the experimental group showed a continuous downward trend, from 2.09 to 1.93 and then to 1.62; heart rate increased from 84.73 to 85.48, then decreased to 81.57, and finally increased to 85.62. The optimization effect was greater than in the control group. In the experimental group, the speed and strength of the athletes improved considerably. Conclusion: Relaxation training can improve athletes’ fatigue, promoting body development and improving strength and speed in physical fitness. Level of evidence II; Therapeutic studies - investigation of treatment outcomes.

Osteosarcoma (OS) is the most common primary malignant bone tumor and is mainly diagnosed in children. Toll-like receptor 9 (TLR9) is expressed in various tumor cells and was correlated with cancer progression. However, the underlying mechanism of TLR9 on the OS progression remains unclear. Our previous study demonstrated that the expression of TLR9 was positively correlated with the development stage of OS. Herein, we further evaluated the actual roles and the molecular mechanism of TLR9 on regulating OS cell proliferation and metastasis. Our data showed that TLR9 was upregulated in OS cells compared to normal osteoblastic cells, and knockdown of TLR9 inhibited OS cell proliferation and induced cell cycle arrest by the decreased expression of cyclin D1, CDK2, and p-Rb, while TLR9 overexpression exerted the inverse effects. Furthermore, TLR9 overexpression could enhance the migration and invasion activities of the OS cells by the upregulation of matrix metalloproteinases 2 (MMP2) and MMP9, and the opposite result was observed in TLR9-silenced cells. Moreover, the nuclear factor kappa B (NF-κB) signaling pathway was activated by TLR9, and TLR9-induced malignant phenotype of OS cells was abrogated by the NF-κB antagonist BAY11-7082. Our study indicated that TLR9 might play a critical role in facilitating OS progression by activating the NF-κB signaling pathway, which may provide a valuable therapeutic target for OS.