Abstract
Background: Monitoring cardiac, metabolic, neurological, and aging responses to stressors is critical. This study aimed to investigate the effect of swimming training on HIF-1α and vascular endothelial growth factor (VEGF) levels in heart tissue of rats exposed to chronic stress. Methods: To this end, 30 male Wistar rats (age: 10 - 12 weeks, weight: 220 ± 20 g) were randomly divided into five equal groups of six rats as follows: (1) Con (no treatment for 10 weeks); (2) CS + ST (4 weeks of stress, 4 weeks of swimming); (3) ST (4 weeks of swimming); (4) CS (4 weeks of stress); (5) CS-time (4 weeks of stress, 6 weeks of no treatment). Anxiety-like behaviors were measured by an open field test. Heart tissue was immunohistochemically assessed for HIF-1α expression using a polyclonal antibody. Vascular endothelial growth factor protein levels were also determined using western blot analysis. To analyze the data, Kolmogorov-Smirnov, One-way ANOVA, and Tukey’s post hoc tests were used, and P ≤ 0.05 was considered statistically significant. Results: The results showed that chronic mild stress (CMS) significantly decreased the HIF-1α expression in heart tissue in CS and CS-time groups (P < 0.05). Furthermore, the result revealed that swimming training significantly increased the level of HIF-1α expression in heart tissue in ST and CS + ST groups (P < 0.05). Although swimming training increased HIF-1α levels in the CS + ST group after a period of four weeks of CMS, these increases were smaller than those observed in ST and control groups (P < 0.05). The results from the One-way ANOVA test also demonstrated that the CMS significantly downregulated the VEGF expression in heart tissue in CS and CS-time groups, whereas swimming training significantly increased its level in ST and CS + ST groups (P < 0.05). Although swimming training increased VEGF levels in the CS + ST group after a period of four weeks of CMS, these increases were smaller than those detected in ST and control groups. Conclusions: Although chronic mild stress had the potential to reduce hypoxia-induced factors in heart tissue, swimming training modified these factors.