Korkmaz, K.Duzova, H.Taslidere, A. CetinKoc, A.Karaca, Z. M.Durmus, K.2024-08-042024-08-0420230765-1597https://doi.org/10.1016/j.scispo.2022.04.009https://hdl.handle.net/11616/101190Objectives. - 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. Equipment and methods. - 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. Results. - 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). Conclusions. - 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. (c) 2023 Elsevier Masson SAS. All rights reserved.eninfo:eu-repo/semantics/closedAccessWeight-loading swimming exerciseER stressGRP78ATF4IL-17IL-23BDNFNGFNT-3caspase-3Article38410.1016/j.scispo.2022.04.0092-s2.0-85148755649Q3WOS:001016413300001Q4