High-intensity interval training upregulates adiponectin receptor 1 expression and modulates serum antioxidant enzymes in a Murine model of breast cancer

چکیده

Aim: This study aimed to investigate the effects of high-intensity interval training (HIIT) on Adiponectin receptor 1 (AdipR1) gene expression in breast tumor tissue and serum levels of glutathione peroxidase (GPX) and glutathione reductase (GR) in a murine model of breast cancer.

Methods: Sixteen male BALB/c mice were inoculated subcutaneously with 4T1 murine mammary carcinoma cells (5 × 10⁵ cells/mouse). One week post-inoculation, mice were randomly assigned to either a tumor-bearing control group (Tumor, n=8) or a tumor-bearing group subjected to HIIT (Tumor+HIIT, n=8). The HIIT protocol was performed on a motor-driven treadmill five days/week for four weeks, consisting of six 2-minute high-intensity intervals (18–25 m/min, 80–90% VO₂max) interspersed with 3-minute active recovery periods (5–9 m/min). Twenty-four hours after the final session, tumor tissues were excised for AdipR1 gene expression analysis via quantitative real-time PCR (2^-ΔΔCT method), and serum samples were collected for assessment of GPX and GR levels using ELISA. Statistical comparisons were performed using independent samples t-tests (p<0.05).

Results: HIIT significantly upregulated AdipR1 gene expression in breast tumor tissue compared to the control group (p<0.0001). Serum GPX levels were significantly decreased in the Tumor+HIIT group compared to the Tumor control group (p<0.0001). However, no significant difference was observed in serum GR levels between the two groups (p=0.7499).

Conclusion: Four weeks of HIIT effectively enhanced AdipR1 expression in tumor tissue and modulated the antioxidant profile by reducing serum GPX in tumor-bearing mice. These findings suggest that HIIT may influence breast cancer progression through adiponectin-mediated pathways and oxidative stress regulation, providing a potential non-pharmacological adjunctive strategy for breast cancer management. Further studies are warranted to elucidate the underlying molecular mechanisms and clinical implications.