Expression of serum HSP27 under exercise-induced muscle damage in elite greco-roman wrestlers

P. Żurek, A. Kasperska, Marcin Krzysztoszek, E. Hübner-Woźniak, A. Zembroń-Łacny
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Abstract

The effectiveness of physical training depends on the training load, the individual toleration ability and an imbalance between the two may lead to under or over-training. One of the unique features of an exercise is that it leads to a simultaneous increase of antagonistic mediators. On the one hand, exercise elevates catabolic molecules such as stress hormo nes, pro-inflammatory cytokines etc. On the other hand, exercise stimulates anabolic components such as heat shock proteins (HSPs) which protect against stressors. If the anabolic response is stronger, exercise will probably lead ultimately to an increased muscle mass and exercise adaptation [1,2]. HSPs represent cell-protective system that may be induc ed by reactive oxygen/nitrogen species (RO/NS). Under phy sio logical conditions, constitutively expressed HSPs function as molecular chaperones, whereas under metabolic stress, HSPs protect proteins against misfolding, aggregation and denaturation. In addition, HSPs may directly regulate specific stress-responsive signalling pathways and may antagonize signalling cascades that result in apoptosis [3,2]. Exerciseinduced stress and muscle damage is considered to be one of the stimulus which induce HSPs [4]. HSPs increase the stress tolerance and participate in the cellular repair process during overtraining. Among the subset of stress-responsive proteins, evaluation of HSP27 level is considered to be a new approach to monitoring exercise training and adaptive mechanisms [5]. Currently, reactive oxygen/nitrogen species NO and H2O2 are perceived as important signalling molecules generated during muscle contraction and involved in the regeneration and adaptation of skeletal muscle to physical work [6]. NO
精英古典式摔跤运动员运动损伤后血清HSP27的表达
体能训练的效果取决于训练负荷和个人的承受能力,两者之间的不平衡可能导致训练不足或过度训练。运动的一个独特特征是它会导致拮抗介质的同时增加。一方面,运动可以提高分解代谢分子,如应激激素、促炎细胞因子等。另一方面,运动刺激合成代谢成分,如热休克蛋白(HSPs),防止压力源。如果合成代谢反应更强,运动可能最终导致肌肉量增加和运动适应[1,2]。热休克蛋白是一种可能由活性氧/氮(RO/NS)诱导的细胞保护系统。在生理条件下,组成性表达的热休克蛋白作为分子伴侣,而在代谢应激下,热休克蛋白保护蛋白质不发生错误折叠、聚集和变性。此外,热休克蛋白可能直接调节特定的应激反应信号通路,并可能拮抗导致细胞凋亡的信号级联反应[3,2]。运动引起的应激和肌肉损伤被认为是诱发热休克蛋白的刺激之一[4]。热休克蛋白增加应激耐受性,并参与过度训练期间的细胞修复过程。在应激反应蛋白的子集中,评估HSP27水平被认为是监测运动训练和适应机制的新方法[5]。目前,活性氧/氮类NO和H2O2被认为是肌肉收缩过程中产生的重要信号分子,参与骨骼肌对体力劳动的再生和适应[6]。没有
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