## 4 Discussion
Changes in Mb correlated with IL-6 levels [50]. Lactate dehydrogenase (LDH) activity increased by 28.2% at 21 \({}^{\circ}\)C and 31.66% at 31 \({}^{\circ}\)C post-exercise [50]. Monitoring muscle damage markers helps athletes and coaches tailor training loads, safeguarding against unfavorable muscle changes [52]. When exercise is performed in higher temperatures, the inflammatory process might be connected to blood redistribution [57]. Cytokines like IL-6 and IL-1B are released by immune cells, affecting thermoregulatory centers and potentially leading to hyperthermia [58; 59]. Scientific findings [60] reveal that cytokine release, including IL-6 and IL-1B, is influenced by exercise type (duration, intensity, muscle engagement). For exercise exceeding 2 h, IL-6 increased 120-fold and IL-1B by 3-fold. Shorter exercises saw a 6-fold IL-6 increase,while IL-1\(\upbeta\) remained relatively stable. Eccentric and concentric exercises induced IL-6 mRNA production, suggesting its production is not solely due to muscle damage, possibly linking it to muscle glycogen levels or glucose production. Some theories connect IL-6 to muscle pain post-exercise [61]. IL-6 plays a central role in the body's response to exercise, affecting fatigue perception and concentration. It is released during exercise and can rise significantly during infections [62]. The IL-6 increase might be linked to muscle cell damage, but it is not closely correlated with effector structure damage biomarkers (LDH, CK, Mb). IL-6 also influences muscle mass growth through satellite cell division [63]. IL-6 concentrations change based on exercise type, duration, muscle volume, and thermal stimuli [62]. Exercise-induced temperature elevation can influence IL-6 changes [62]. Antioxidants like vitamins C and E might limit the action of RFT in reducing muscle damage [64]. Training specialization can lead to decreased IL-6 levels due to receptor expression and heightened cell sensitivity [65]. Lower physical activity increases IL-6, while training reduces resting IL-6 levels [62]. In the study, IL-6 concentration increased after exercise in both ambient temperatures. At 21 \({}^{\circ}\)C, it increased by 113.5% in the first hour and 61.22% after 24 h, while at 31 \({}^{\circ}\)C, it rose by 97.9% and 5.36%, respectively [53]. IL-1\(\upbeta\), produced by macrophages and monocytes, triggers an inflammatory response and affects muscle damage. Early studies mistakenly identified IL-1\(\upbeta\) as the main inflammatory factor; however, it is IL-6 that holds that role [62]. IL-1\(\upbeta\)'s concentration can remain elevated for days post-exercise. It plays a role in skeletal muscle reconstruction and oxidative stress response [66]. This study did not find significant changes in IL-1\(\upbeta\) concentration due to anaerobic pulsatile exercises [53]. Heat shock proteins (HSPs) have anti-inflammatory effects and protect muscles from damage. They are affected by exercise, thermal stimuli, and stressors [20]. HSP70 concentration decreased by 40% an hour after exercise at 21 \({}^{\circ}\)C, and increased by 53.3% after 24 h. At 31 \({}^{\circ}\)C, it increased by 7.29% in the first hour and 51.04% in 24 h after exercise [53]. HSPs are influenced by training and temperature variations [25]. Athletes have higher HSP70 levels [25]. Differences in anaerobic power between upper and lower limbs can influence judo training. Higher ambient temperatures affect physiological and biochemical responses, impacting performance [53]. Evaluating muscle damage markers in judokas helps assess damage levels, regeneration effectiveness, and training adjustments. It also aids in understanding muscle damage and recovery processes [53]. Comparing results between novice and experienced judokas could provide insights into the impact of effort intensity on muscle damage [53].