OBJECTIVETo see the change of capillary of heart in Athlete's Heart, so that to discover the mechanism of pathologic change.

METHOD18 male SD rats were separated randomly into control group (without any exercise), aerobic exercise group (swimming for 75 min every day), and overload group (swimming for 180 min with 5% weight of its body every day). After 5 days per week, 12 weeks, exercise training stopped and heart of rats were observed under Transmission Electron Microscope.

RESULTSIn aerobic exercise group, the capillary cavities in heart expand, the walls of capillary become thick; the number of mitochondrion increases; endothelium cells become active in growth. However, after overload exercise, the walls of capillary cockle and protuberances appear. The mitochondrion swell and the cristae become disorder. Most of endosomes expand and their number increases. The karyons become abnormity in shape and uniformity in electronic density, besides the nuclear envelope cockle. The basilar membranes become thick and unclear.

CONCLUSIONAfter exercise training, both physical and pathologic changes in heart capillary are found. In suitable exercises group, the capillaries change physically; the pathologic changes are becoming visible after overload exercise however.

Animals ; Capillaries ; ultrastructure ; Cardiomegaly ; etiology ; pathology ; Male ; Physical Conditioning, Animal ; adverse effects ; Physical Endurance ; Rats ; Rats, Sprague-Dawley ; Sports

Animals ; Diet ; adverse effects ; Hyperlipidemias ; blood ; etiology ; Lipids ; blood ; Male ; Mice ; Mice, Inbred C57BL ; Physical Conditioning, Animal

OBJECTIVEBased on high fat diet induced the model of atherosclerosis (AS) in C57BL/6J mice, authors studied the effect of endurance exercise on the atherosclerostic formation.

METHODSForty eight 8-week-old C57BL/6J mice were divided into four groups randomly (n=12): control (group N), 12-week atherosclerosis model group(group H), 12-week atherosclerosis model plus 11-week treadmill training group (group H + E) and 22-week atherosclerosis model group (group HS). Then, we observed the effects of endurance exercise on the ultra structure of aorta by electron microscope.

RESULTSTwenty weeks of high fat diet could result in serious AS in mice while endurance exercise could significantly antagonize or restrain the occur of AS. In addition, 10 weeks of endurance exercise could alleviate the symptom of pathological changes which already happened on aorta wall.

CONCLUSIONIt indicated that endurance exercise could effectively prevent and cure AS that induced by high fat diet.

Animals ; Aorta ; ultrastructure ; Atherosclerosis ; etiology ; prevention & control ; Diet, High-Fat ; adverse effects ; Dietary Fats ; administration & dosage ; Male ; Mice ; Mice, Inbred C57BL ; Physical Conditioning, Animal ; physiology ; Physical Endurance ; physiology

Animals ; Beer ; adverse effects ; Blood Glucose ; metabolism ; Diabetes Mellitus, Experimental ; metabolism ; Lipid Metabolism ; Male ; Physical Conditioning, Animal ; physiology ; Rats ; Rats, Wistar

Objective: To investigate the role of clock gene BMAL1 in exercise-induced skeletal muscle injury recovery. Methods: Two hundred and eight 8-week-old SD rats were randomly divided into the control group (Group C, n=104) and the exercise group (Group E, n=104). Group E performed a 90-minute downhill run on the treadmill. After exercise, the gastrocnemius muscle of 8 rats in Group C and Group E were collected at 0 h, 6 h, 12 h, 18 h, 24 h, 30 h, 36 h, 42 h, 48 h, 54 h, 60 h, 66 h and 72 h. The expression of skeletal muscle core clock gene, BMAL1 was measured by real-time fluorescence quantitative PCR. The parameters of fitting cosine curve were obtained by cosine analysis software circacompare (R package), and the change trend of rhythmic oscillation was analyzed. The ultrastructure of skeletal muscle fibers was observed by transmission electron microscope. The expressions of skeletal muscle BMAL1 and DESMIN were detected by Western blot; Immunofluorescence was used to observe the localization and contents of BMAL1 and DESMIN. Results: In Group C, three complete circadian rhythm cycles of mRNA BMAL1 were observed within 72 hours; in Group E, the circadian rhythm of BMAL1 mRNA disappeared at 0 h～24 h. Compared with Group C, the expression level of BMAL1 mRNA was significantly increased at 0 h, 6 h, 12 h, and 18 h after exercise in Group E (P＜0.05), and the expression of BMAL1 protein was significantly increased at 0 h and 12 h after exercise(P＜0.05), and recovered to the level of that in Group C from 24 h to 72 h(P＞0.05). The expression of DESMIN protein was decreased at 0 h and 12 h after exercise(P＜0.05), gradually increased at 24 h, increased significantly at 48 h(P＜0.01), and recovered to the control level at 72 h (P＞0.05). In Group E, BMAL1 and DESMIN were co-localized at 0 h, 12 h, and 24 h after exercise; the colocalization at 0 h～24 h showed a trend of first decreasing and then increasing, and the fluorescence intensity at 24 h reached the highest value. Conclusion: The post-exercise clock gene BMAL1 may be involved in the enhanced synergy of regulating the cytoskeletal protein DESMIN, it is thus related to the promotion of muscle fiber structure recovery.
ARNTL Transcription Factors/metabolism* ; Animals ; Desmin/metabolism* ; Muscle, Skeletal/physiology* ; Physical Conditioning, Animal/adverse effects* ; RNA, Messenger/metabolism* ; Rats ; Rats, Sprague-Dawley

In the present study, we were to screen the specific microRNA (miRNA) of exercise-induced muscle damage (EIMD) and assess the EIMD-specific miRNAs-regulated target of sarcolemmal damage in rats. Twenty-four male Sprague-Dawley (SD) rats were randomly divided into 3 groups, which included sedentary (C), 24 h post-exercise (E24) and 48 h post-exercise (E48) groups. Rat EIMD model was established by an acute eccentric exercise, i.e., a downhill running treatment at -16º gradient. EIMD characteristics were verified by Evans blue dye staining, differentially expressed miRNAs were detected by microarray assay, EIMD-specific miRNAs expressions were further validated by real-time quantitative RT-PCR (RT-qPCR), and targets of the miRNAs were predicted based on mRNA expressions of associated proteins and related pathway core molecules of sarcolemmal damage. Two EIMD-specific expressed miRNAs, including miR-206-3p and miR-139-3p, were found in the study. There was a significantly negative correlation (P < 0.05) between miR-206-3p expression and dystrophin (r = -0.68), utrophin (r = -0.64), JNK (r = -0.62) or ERK1 (r = -0.68) respectively, but no correlation was found between miR-139-3p and these biomolecules. The results suggest that: i) the expression profile of miRNAs in rat is significantly affected by EIMD, ii) miR-206-3p and miR-139-3p are the EIMD-specific miRNAs, and iii) miR-206-3p may control sarcolemmal damage by regulating dystrophin, utrophin, JNK and ERK1.
Animals ; Dystrophin ; genetics ; MAP Kinase Kinase 4 ; genetics ; MAP Kinase Signaling System ; Male ; MicroRNAs ; genetics ; Physical Conditioning, Animal ; adverse effects ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Running ; Sarcolemma ; pathology ; Utrophin ; genetics

OBJECTIVETo evaluate the role of serum tumor necrosis factor-alpha (TNF-alpha) and adiponectin on insulin resistance in different fat diet rats.

METHODSThirty weanling female rats were randomly divided into 3 group (n = 10): a low-fat soybean oil (LFS; 22% of total energy fed as fat), high-fat soybean oil (HFS; 40% of total energy fed as fat), or high-fat soybean oil and swimming training at the same time (HFS + T). After fed for 10 weeks, the level of TNF-alpha, adiponectin in serum of rats were observed.

RESULTS(1) The body weight, percentage of body fat of HFS group increased compared with that of LFS group (P < 0.05), however those of HFS + T group were decreased (P < 0.05). (2) The level of serum insulin and ISI in HFS group were increased by LFS group (P < 0.05), in HFS+ T group the levels decreased. (3) And the serum level of TNF-alpha and IL-6 in HFS group were higher than those in LFS group (P < 0.05), the serum levels of adiponectin in HFS group were lower than those in LFS rats, and in HFS+ T group the levels of TNF-alpha and IL-6 were lower than those in HFS group (P < 0.05), the adiponectin level was higher than that in HFS group, and there were no significant difference between LFS group and HFS + T group.

CONCLUSIONExercises training could improve sugar and fat metabolism disorders, which also contributes to improving insulin resistance caused by high-fat diet.

Adiponectin ; blood ; Animals ; Diet, High-Fat ; adverse effects ; Dietary Fats ; administration & dosage ; Female ; Insulin ; blood ; Interleukin-6 ; blood ; Physical Conditioning, Animal ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVE: To study the effect of 6-week intensive training on renal function in rats and the mechanism of exercise-induced proteinuria. METHODS: Thirty-six male SD rats, aged 6 weeks, were divided into two groups, including a control group(C,=12)and an overtraining group(M,=24). After the rats adapted to feeding for 4 d, group C did not carry out any exercise, and the M group did 6-week of increasing load swimming, 6 days a week, once a day. Started with the load of 1%weight at the beginning of the 4 week,and gradually increased (to 6% weight). Took a single urine from both groups 30 min after the end of the training. Blood was taken from the main ventral vein, and the bilateral kidneys were to be tested. The levels of tested urine protein, microalbumin and neutrophil gelatinase associated lipocalin(NGAL) was determined by using enzyme linked immunosorbent assaytest. The content of urine creatinine was tested with alkaline picric acid method,. The serum levels of colorimetric method to determine serum creatinine and urea nitrogen were determined by colorimetric method. The expression of Nephrin in renal tissue was detected by Western blot and the radioimmunoassay was used to test serum testosterone, corticosterone and renin-angiotensin system related index. RESULTS: Compared with group C, the serum testosterone/cortisone(T/C) of group M was decreased significantly (<0.01). The urine total protein(TP), microalbumin (mAlb), microalbumin/creatinine (mAlb/CRE), NGAL, blood urea nitrogen (BUN) and serum creatinine(SCr) were increased significantly (<0.01). The abnormality of glomerular structure was obvious, and the paller scores were higher. The protein expression of Nephrin was obviously down decreased (<0.01). The renin activity (Ra) and angiotension Ⅱ (Ang Ⅱ) in renal and circulating blood were decreased significantly (<0.01). CONCLUSIONS The effects of 6-week intensive training on renal function in rats and the mechanism of exercise-induced proteinuria may be that overtraining can induce the continuous excitation of Reninrenin activity in renal and circulating blood, down-regulated the expression of Nephrin, lead to abnormality of renal structure and function, and proteinuria.
Animals ; Blood Urea Nitrogen ; Corticosterone ; blood ; Creatinine ; blood ; Kidney ; physiopathology ; Male ; Membrane Proteins ; metabolism ; Physical Conditioning, Animal ; adverse effects ; Proteinuria ; Rats ; Rats, Sprague-Dawley ; Renin-Angiotensin System ; Testosterone ; blood

Animals ; Cardiovascular Diseases ; drug therapy ; etiology ; Creatine Kinase, MB Form ; blood ; Heart ; drug effects ; Interleukin-1 ; blood ; Interleukin-6 ; blood ; Lycium ; chemistry ; Male ; Nitrates ; blood ; Oxidative Stress ; drug effects ; Physical Conditioning, Animal ; adverse effects ; Plant Extracts ; therapeutic use ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; blood

AIMTo investigate the possible role of rate-limiting enzyme of heme metabolism and globin in the development of the low hemoglobin (Hb), red blood (cell) count (RBC) and hematocrit (Hct) after long-term exercise, and effect of nutrition supplement on sports anemia.

METHODSMale Wistar rats were randomly assigned to three groups (n = 10): control (C), exercise (P) and exercise + nutrition (G). Animals in the P and G groups started treadmill running at 30 m/min, 0% grade, 1 min/time. Running time was gradually increased with 2 min/time during initial 5 weeks and final 4 weeks. In addition, running frequency was 2 times/day except initial 2 weeks. At the end of eleventh week, gene expression of 5-aminolevulinate synthase (ALAS), ferrochelatase, alpha-globin and beta-globin in bone marrow were measured with RT-PCR. Mean-while heme oxygenase 1 (HO-1) activity in liver was measured with immunohistochemical method.

RESULTSEleven weeks of exercise induced a significant increase in HO-1 and a significant increase in gene expression of beta-globin (P < 0.01, P < 0.05, respectively). Treatment with anti-sports anemia compound dosage led to no significant differences in rate-limiting enzyme of heme metabolism and globin in the exercised rats. The G group had a significantly higher HO-1 level in liver than the C group (P < 0.01). These finds showed that exercise was associated with no significant difference in heme synthetase and alpha-globin gene expression, and significant difference in heme catabolic enzyme and beta-globin gene expression.

CONCLUSIONThe increase of HO-1 activity in liver might be one of the causes of the lower Hb, RBC and Hct status in exercised rats.

5-Aminolevulinate Synthetase ; genetics ; metabolism ; Anemia ; etiology ; metabolism ; physiopathology ; Animals ; Dietary Supplements ; Ferrochelatase ; genetics ; metabolism ; Gene Expression Regulation, Enzymologic ; physiology ; Globins ; metabolism ; Heme Oxygenase (Decyclizing) ; genetics ; metabolism ; Hydroxymethylbilane Synthase ; genetics ; metabolism ; Male ; Motor Activity ; Physical Conditioning, Animal ; adverse effects ; Random Allocation ; Rats ; Rats, Wistar