SCIENCE AND SPORTS, cilt.1, sa.1, ss.1-10, 2023 (SCI-Expanded)
High-intensity exercise impairs ER functions and elevates pro-inflammatory cytokines and neurotrophins levels. We investigated the effects of different intensity swimming exercises on ER stress of muscle damage with the impact of IL-23 and neurotrophic factors.
Rats were divided into three groups control (n = 9), normal swimming exercise (NSE) (n = 8), and weight-loaded swimming exercise (WLSE) (n = 9). Ventricle and skeletal muscle ATF4 and GRP78 levels were measured by Western Blot, and serum IL-17, IL-23, BDNF, NT-3, and NGF levels by ELISA method. Caspase-3 immunohistochemistry evaluation of skeletal muscle tissues was performed.
The GRP78 level in the gastrocnemius muscle in the NSE group decreased, while the ATF4 level increased compared to other groups (P < 0.05). The ATF4 levels in heart muscle in the NSE group increased compared to the WLSE group (P < 0.05). The serum NT-3 level in the WLSE group rats increased compared to the other groups (P < 0.008). Intense Caspase-3 positive staining muscle cells were observed in the WLSE group compared to the control group (P ≤ 0.0001).
In response to high-intensity exercise, while pro-inflammatory cytokines, BDNF, and NGF adaptation in the body take place, also NT-3 secretion causing cell damage by the caspase system to cope with ER stress increasement is seen. In conclusion, this study shows us that high-intensity exercise may cause myopathy in the heart and skeletal muscle.