| 1.IntroductionIt is well documented that strenuous and repeated eccentric contractions are associated with EIMD( exercise-induced muscle damage) and DOMD( delayed onset muscle soreness). This occurs in both recreational and elite athletes. With elite athletes, these responses are often related to relatively sudden increases in the volume or intensity of training, or following prolonged rest or injury. For sedentary individuals, a single episode of exercise involving eccentric muscular contractions may produce significant muscle soreness and damage. This is a well researched, but poorly understood area, including the actual mechanisms involved in the muscle damage and repair cycle.Cells have endogenous mechanisms to protect against damage, facilitate recovery from re- versible damage and adapt to prevent subsequent damage. One of the most extensively described of these is the stress response. All nucleated cells respond to a short period of stress by increased synthesis of a family of proteins known as stress or heat shock proteins. HSP are named according to their molecular mass and include the small HSPs such as HSP25, HSP60, HSP70, HSP90, HSP110. HSPs are constitutively expressed in the unstressed cell where they act as molecular chaperones, associating with newly synthesized proteins, facilitating folding and aiding translocation of newly synthesized proteins to intracellular sites such as the mitochondria. When cellular stress leads to the production of unfolded or misfolded proteins, the celluar content of HSPs is increased. Thus, the HSPs content of cells is increased following heat, infection, incorporation of amino acid analogues and various forms of oxidative stress including exercise.A increased cellular content of HSPs can provide cytoprotection against subsequent stress. For example, in the heart, a period of hyperthermia provided substantial protection against damage induced by subsequent ischaemia and reperfusion, the calcium paradox or the oxygen paradox . This protection was associated with a sixfold increase in the HSP70 content of the heart . Definit- ive evidence for the crucial role of HSP70 in this protection was presented by transgenic mice. These studies independently demonstrated significant reductions in damage induced by ischaem- ia-reperfusion in hearts from transgenic mice overexpressing HSP70 in cardiac tissue.A similar protective mechanism has also been reported in studies of skeletal muscle. Hyperthermia or exercise results in an increased content of HSPs in skeletal muscle. In addition, a prior period of hyperthermia or a non-damaging period of ischaemia-reperfusion provides protection against subsequent ischaemia and reperfusion-induced skeletal muscle damage. The induction of HSPs is well established in many organisms and some tissues, but the importance of such proteins in the protection against exercise stress in skeletal muscle, especially exercise-induced damage, is a topic that needs further study.2.Experimental Methods and PurposeTo investigate the mechanisms and protection of the endogenous HSPs against skeletal muscle damage induced by eccentric exercise, in this sudy, experiments were conducted for prior heat stress and 6 weeks eccentric training respectly to induce endogenous HSPs expression. The expression of Hsp70 andαB-crystallin in gastrocnemius muscle and the function of muscle was measured by means of biomechanics, immhistochemistry and molecular biology after eccentric exercise-induce damage. Our objective was to investigate the mechanisms of HSPs promote resto- ration of damaged skeletal muscle and the protection of HSPs, which would provide reference for prevention of skeletal muscle damage induced by eccentric exercise and the study of basis theory.3.Conclusions(1) Heat stress can induce Hsp70 andαB-crystallin expression significantly in rat skeletal muscle, and such expression have protective effect on skeletal muscle against eccentric exercise-induce injury. After eccentric exercise, heat stress group showed apparent recovery of maximum tetanic force of gastrocnemius, serum CK, LDH descreased, and SOD increased, MDA decreased significantly.(2) The mechanisms of HSPs protective effect in prior heat stress adaptation include:①Heat stress can induceαB-crystallin mRNA increased significantly, which provides evidence forαB-crystallin involve in prior heat stress against eccentric exercise injury in rat muscle.②In normal rats, HSP70 is only expression in type I and IIa cytoplasm. Heat stress induce translocation of HSP70 to all muscle cell membrane, includingⅡb type muscle cell membrane, which made specific expression of HSP70 in type I and IIa cytoplasm lose.③Heat stress induce translocation ofαB-crystallin and Hsp70 to Z-disk and cell membrane. Because HSPs have been shown to stabilize cytoskeletal elements, Hsp70 andαB-crystallin may protect the Z-disk and membrane against further injury or aid in their repair in rat skeletal muscle.④Heat stress induce muscle HSPs and SOD levels increased significantly at the same time, which made serum MDA levels decreased significantly.(3) 6 weeks intermittent eccentric training induce gastrocnemiusαB-crystallin expression significantly. Both untrained and trained rats were submitted to the same bout of high intensity eccentric exercise. Trained rats clearly demonstrated higher resistance to exercise , such as desmin disruption is less and CK is decrease significant, which suggestαB-crystallin protect cytoskeletal from exercise stress. In high intensity eccentric exercise, untrained rats experienced a significant stress response, a significant increase inαB-crystallin levels parallel to a decrease in the desmin content, which suggestαB-crystallin acts as complementary protective mechanism in eccentric exercise-induce cytoskeletal injury.
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