OBJECTIVE: To analyze the possible mechanism of Fas mediated apoptosis, investigate the correlation of exercise with apoptosis of cardiomyocytes,skeletal muscle and lymphocytes, and explain the changes of histocyte injury under exercise training from a new level of recognition, so as to provide scientific theoretical evidences for the prevention and treatment of overtraining.DATA SOURCES: A computer-based online search of Springlinker and Pubmed databases was undertaken to identify articles related to Fas mediated apoptosis of cardiomyocytes, skeletal muscle and lymphocytes published in English from January 1994 to December 2004 by using the keywords of "Fas, apoptosis, exercise, skeletal muscle, cardiomyocyte, lymphocyte". Meanwhile, Chinese relevant articles published from January 1994 to December 2004 were searched in the Chinese journal full-text database with the keywords of "apoptosis, exercise, skeletal muscle, cardiomyocyte, lymphocyte" in Chinese.STUDY SELECTION: The data were checked firstly. Inclusive criteria:studies related to Fas mediated apoptosis of cardiomyocytes, skeletal muscle and lymphocytes. The repetitive ones were excluded.DATA EXTRACTION: Totally 58 literatures were collected, 29 repetitive studies were excluded, and the other 29 were accorded with the inclusive criteria.DATA SYNTHESIS: Apoptosis is a gene-controlled process of spontaneous death for cells, and it is the physiological cell death. As a death factor inducing apoptosis, Fas is of important biological significance in regulating apoptosis. The study on exercise and the mechanism of apoptosis signal conduction will explain the changes of histocyte injury under exercise training from a new level of recognition, and provide scientific theoretical evidences for the prevention and treatment of overtraining, Besides,Fas plays an important role in various tumors, diseases of immune system and spinal cord injury.CONCLUSION: The deeper investigation on exercise and Fas mediated apoptosis may disclose the mechanism for the treatment of disease, and introduce new methods of exercise treatment, which undoubtably has important practical significance in accelerating healthy of human being.

BACKGROUND: To explore the effect of negative feedback mechanism of adipose tissue in the pathogenesis of obesity and type 2 diabetes through analyzing the function of the adipocytokines in regulating energy metabolism and fat accumulation.DATA SOURCES: We searched in the PubMed database of National Library of Medicine in USA for the articles on negative feedback action of adipocytokine, obesity and type 2 diabetes published from Jan 1962 to Nov 2005, using the key words of "adipocytokines, obesity, tumor necrosis factor-α, interleukin-6, leptin, adiponectin, resistin and PGAR" and limited the language to English.STUDY SELECTION: The articles of original researches and associated with energy metabolism and fat accumulation were included. The articles of repetitive researches, reviews and little associated with energy metabolism and fat accumulation were excluded.DATA EXTRACTION: A total of 158 articles were collected, of which 35 were closely correlated with this paper, and the 123 excluded articles were all repetitive studies, reviews and little correlated with this paper.DATA SYNTHESIS: Researches show that the fat tissue is able to secrete adipocytokines to regulate the fat mass, While the mass of body fat increases, the adipocytokines will inhibit lipogenesis and promote lipolysis.Adipocytokines can either resist the action of insulin or suppress the secretion of insulin. Thus lead to lipogenesis inhibition, lipolysis increasing and suppressing the utilization of blood glucose.CONCLUSION: When man develops obesity going up to certain degree,the negative feedback action of adipocytokines may lead to insulin resistance and type 2 diabetes.

BACKGROUND: The regeneration and repair of skeletal muscle after injury relies on the new nucleus formed through muscle satellite cell proliferation. However, there are few reports on the relationship between the skeletal muscle cell proliferation and the vimentin expression.OBJECTIVE: To explore the relationship between the skeletal muscle cell proliferation and the vimentin expression, as well as the mechanism underlying the repair of exercise-induced skeletal muscle micro-injury. DESIGN, TIME AND SETTING: A randomized controlled animal experiment was done at the Sports Human Science Experimental Center in Hunan Normal University between December 2007 and September 2008. MATERIALS: A total of 50 male SD rats, aged 8 weeks, were randomly divided into a control group and a training group which were subdivided in to four groups at the time points of immediate post-exercise, hour 3, hour 24 and hour 48 post-exercise, with 10 ones in each of the five groups.METHODS: Rats in the training group underwent 3 days of repetitive exhausting eccentric exercise on a treadmill of-16° slope at the speed of 16 m/min. Rats in the control group underwent no running. MAIN OUTCOME MEASURES: Rats in the training group was taken for measurement immediate, 3 hours, 24 hours and 48 hours post-exercise respectively. Immunohistochemistry was adopted to determine the proliferating coil nuclear antigen (PCNA) A expression and the vimentin expression in medial head of triceps brachii muscle cells in each group at different phases of repair.RESULTS: The skeletal muscle cell showed sequentially-changed proliferation. The proliferation index of the training group was significantly higher than that of the control group immediately post-exercise. At hour 24 post-exercise, it reached the peak. Hour 48 post-exercise saw the decreased proliferation. The expression of vimentin also exhibits a sequential change after exercise. Moreover, its immunoreaction score changed with time in the same direction with the proliferation index, but there is no correlation between the two.CONCLUSION: Three days of repeated exhausting eccentric exercise can induce the sequential changes of skeletal muscle cell proliferation and vimentin expressions. Vimentin expression has some kinds of correlations with skeletal muscle cell proliferation, but it is not the only factor that matters.

BACKGROUND: Many experiments have proved that heavy-load movement training causes the acute increase of free radicals. The increase of endogenous free radicals and caused cellular and subcellular lipid peroxidation strengthening injure the structure and function of tissue cells, thereby, decrease motor ability. Sleep deprivation also causes the increase of oxygen free radicals.OBJECTIVE: To observe the changes in malondialdehyde (MDA) and glutathione (GSH) levels as well as superoxide dismutase (SOD) activity in serum of acute exhaustive exercise rats following different time periods of sleep deprivation.DESIGN: A randomized controlled animal experiment.SETTING: Laboratory of Exercise Sciences & Sports Medicine, Physical College, Hunan Normal University.MATERIALS: Thirty healthy male SD rats of clean grade, weighing about (220±13)g, provided by Experimental Animal Center of Hunan Agricultural University, were involved in this study.METHODS: This experiment was carried out in the Laboratory of Exercise Sciences & Sports Medicine, Physical College,Hunan Normal University from April 2006 to May 2006. Thirty rats were randomized into 5 groups: blank control group,simple exercise group, sleep deprivation 24 hours group, sleep deprivation 48 hours group and sleep deprivation 72 hours group, with 6 rats in each group; Rats in the blank control group were allowed to sleep normally, but not do exercise; Rats in the simple exercise group were allowed to sleep normally and executed after acute exhaustive exercise; Rats in the sleep deprivation 24, 48 and 72 hours groups were deprived their sleep for 24, 48 and 72 hours,respectively, then they were executed after acute exhaustive exercise. Method of gentle handling was used in creating rat models of sleep deprivation; Rats in the simple exercise group and sleep deprivation groups were forced to do exercise according to the rat exercise model project established by Bedford: treadmill gradient 10°, speed 19.3 m/min, all the exercise rats were exhaustive (Exhaustion criteria: At the end of exercise, rats reached 1/3 of runway over 3 times;Various stimulations for expelling were invalid. After running, rats presented with breathlessness, expression lassitude,ventral decubitus, slow stimulus response, weaker escape response in being captured). After experiment, rats in each group were executed under the anesthetic state, and their blood was taken out, and centrifuged after natural clotting.Supernatant fluid was taken for detecting MDA and GSH levels as well as SOD activity.MAIN OUTCOME MEASURES: Changes in MDA and GSH levels, and SOD activity in rat serum.RESULTS: Thirty rats were involved in the final analysis. ① MDA level in the simple exercise group was higher than that in the blank control group (P＜ 0.01). MDA level in the sleep deprivation 24 hours, 48 hours and 72 hours was higher than that in the simple exercise group, respectively (P ＜ 0.01). MDA level in the sleep deprivation 72 hours was statistically higher than that in the other sleep deprivation groups, respectively (P ＜ 0.01). ②GSH level in the simple exercise group was lower than that in the blank control group (P ＜ 0.01). GSH level in the sleep deprivation 24 hours group was higher than that in the simple exercise group [(P ＜ 0.01). GSH level in the sleep deprivation 24 hours and 48 hours groups was lower than that in the simple exercise group, respectively (P ＜ 0.05, 0.01). There were statistical differences in GSH level among sleep deprivation groups (all P＜ 0.01). ③ SOD activity in the simple exercise group was lower than that in the blank control group (P ＜ 0.01); SOD activity in the sleep deprivation 24, 48 and 72 hours groups was lower than that in the simple exercise group, respectively (P ＜ 0.01); SOD activity in the sleep deprivation 48 and 72 hours groups was significantly lower than that in the blank control group, respectively (P ＜ 0.01); There were statistical differences in SOD activity among sleep deprivation groups (P ＜ 0.01).CONCLUSION: Sleep deprivation can cause serumal oxidative stress injury of rats; With elongation of time of sleep deprivation and exhaustive exercise, oxygen free radical production in serum of rats accumulates more and more, ability to get rid of oxygen free radical becomes weaker and weaker, and injury to body is more and more obvious.Serumal oxidative stress status of acute exhaustive exercise rats following sleep deprivation