## 1 Introduction  
The metabolic processes during judo training or tournaments predominantly depend on anaerobic mechanisms. These processes can lead to substantial muscle cell damage due to mechanical and metabolic stress, especially in high-temperature environments [1; 2]. Such stress triggers an inflammatory state, marked by cytokine-induced structural and metabolic alterations in the affected areas [3; 4]. At the site of injury, neutrophils and their associated pro-inflammatory cytokines, as well as reactive oxygen and nitrogen species, become evident [5]. Additionally, muscle proteins, such as myoglobin (Mb), are released into the bloodstream [5]. Together with neuroendocrine factors, muscle damage significantly influences the immune response to exercise [3; 6]. Judo athletes in competitions face multiple rounds, each roughly spanning 5 min [7]. The structure of these competitions includes intermittent sequences of combat and rest periods, amounting to approximately 460 s (7 min 40 s) in total [7]. Competing in higher ambient temperatures strains the body's systems more than performing at room temperature, potentially because of shifts in plasma volume indicating dehydration [8]. Muscle damage from exercise prompts a rise in pro-inflammatory interleukin production, especially interleukin-6 (IL-6) and interleukin-1\(\upbeta\) (IL-1\(\upbeta\)), in conjunction with cytokine-driven neutrophil and macrophage reactions [3; 9]. These cytokines also stimulate the production of heat shock proteins (HSPs) that possess anti-inflammatory capabilities [10; 11]. The expression of IL-6 correlates with the \"energy deficit\" encountered during physical exertion, prompting the release of energy compounds [12]. Moreover, skeletal muscle injuries enhance the secretion of pro-inflammatory cytokines such as IL-1\(\upbeta\)[13; 14; 15]. Cytokines also promote the synthesis of acute-phase proteins in the liver. IL-6 activates T lymphocytes, modulates B lymphocyte differentiation, and amplifies HSP production [16]. A rise in internal body temperature by 1 \({}^{\circ}\)C due to physical exercise insigates catecholamine and cytokine release, which in turn affects leukocyte circulation [17]. The liver's increased amino acid uptake for HSP synthesis might lower blood glutamine levels, subsequently affecting immune functionality [18]. There is a paucity of comprehensive data about the inflammation triggered by high-intensity, acyclic workouts, particularly in hot environments [19]. Heat shock proteins (HSPs) serve as chaperones, shielding proteins from atypical alterations under stressful conditions [19]. The synthesis of HSPs can occur both under stress and in standard physiological states [20]. HSP70 also influences immune responses by affecting the major histocompatibility complex (MHC), with its expression induced by multiple factors [21]. Elevated ambient temperatures notably boost HSP70 levels [20; 22]. Physical activity-related cell injuries insigates an inflammatory response, marked by an uptick in acute-phase proteins, predominantly propelled by IL-6 [20]. Exercise intensity, duration, engaged muscle groups, and activated fiber types all affect HSP70 and HSP72 concentrations [19]. HSP70 helps mitigate micro-damage resulting from anaerobic exercises, and individual variability can influence its expression [23]. Acclimating to heat can modify the immune system, leading to increased concentrations of anti-inflammatory interleukin (IL-10) and HSP72 [24]. HSP levels might serve as indicators for heat stress vulnerability [19]. This research addresses an existing knowledge gap regarding high-intensity, acyclic exercises in hotter climates, focusing on their impact on physiological and biochemical markers [19]. The insights gathered could inform optimized training regimens for athletes [25]. The study's primary objective is to ascertain if interval anaerobic workouts targeting both upper and lower limbs, executed in varied ambient temperatures, have a consistent effect on muscle damage indicators and blood-borne biochemical markers.