ABSTRACT
Mitochondrial dynamics, involving mitochondrial fusion, fission and autophagy, plays an important role in maintaining cellular physiological function and homeostasis. Mitochondria are the "energy plant" of human body, so the changes of mitochondrial fusion, division and autophagy are important for cell respiration and energy production. On the other hand, energy metabolism influences mitochondrial dynamics in turn. This paper reviewed the recent advances in studies on the relationship between energy metabolism and the proteins regulating mitochondrial fusion, fission and autophagy. The association of mitochondrial dynamics with electron chain complex expression, oxidative phosphorylation and ATP synthesis upon exercise intervention will provide theoretical references for the further studies in sports training and disease intervention.
Subject(s)
Humans , Adenosine Triphosphate , Autophagy , Energy Metabolism , Exercise , Mitochondria , Physiology , Mitochondrial Dynamics , Mitochondrial Proteins , MetabolismABSTRACT
OBJECTIVE@#To detect the levels of miR-1, miR-21 and their targeted proteins in hearts of mice after different exercise training, and discuss potential molecular mechanism.@*METHODS@#Male C57BL/6 mice were randomly divided to 3 groups:sedentary (SE), exercise training 1(ET1) and exercise training 2 (ET2). SE did not do any exercise; ET1 undertook swimming training for 8 weeks, once a day, 5 days/week. Swimming 30 min in the 1 week, and the duration was increased 10 min per week to 90 min and maintained in the 7 and 8 week. ET2 performed the same work as ET1 and switched to twice a day by the end of the 5th week. TUNEL assay was applied to test myocardial apoptosis. Western blot and RT-PCR were used to detect proteins and miRs levels respectively.@*RESULTS@#Compared with SE, in ET1, myocardial apoptosis and miR-1 level did not change, but its targeted protein Bcl-2 increased significantly(<0.01). miR-21 and its targeted protein PDCD4 did not change significantly. In ET2, myocardial apoptosis and miR-1 level were decreased significantly(<0.05). Bcl-2 was increased significantly(<0.01). miR-21 also increased significantly (<0.05), but PDCD4 did not decrease significantly.@*CONCLUSIONS@#Exercise training in ET2 other than ET1 could down-regulate myocardial apoptosis. Alterations of miR-1 and Bcl-2 may be responsible for this cardioprotection. PDCD4 is not sensitive to exercise training, it is likely that miR-21 and other targeted proteins participate in exercise-regulative apoptosis.
Subject(s)
Animals , Male , Mice , Apoptosis , Apoptosis Regulatory Proteins , Metabolism , Mice, Inbred C57BL , MicroRNAs , Metabolism , Myocardium , Metabolism , Pathology , Myocytes, Cardiac , Cell Biology , Metabolism , Physical Conditioning, Animal , Proto-Oncogene Proteins c-bcl-2 , Metabolism , RNA-Binding Proteins , Metabolism , Random AllocationABSTRACT
<p><b>OBJECTIVE</b>To detect the levels of miR-499 and relative proteins in hearts of mice after exercise training, and investigate the mechanism of exercise-regulative apoptosis.</p><p><b>METHODS</b>Male C57BL/6 mice were randomly divided into 3 groups( n = 14): sedentary (SE), exercise training 1 (ET1) and exercise training 2 (ET2) group. SE did not do any exercise. ET1 performed swimming training for 8 weeks. ET2 performed the same work as ET1 until the 5th week. Then, mice trained twice a day until the end of training. TUNEL assay was applied to test myocardial apoptosis, RT-PCR and Western blot were used to detect miR-499 and proteins levels respectively.</p><p><b>RESULTS</b>Compared with SE, stress in ET1 failed to affect apoptotic index (AI) and miR-499-CaN-Drp-1 pathway (P > 0.05). In contrast, exercise load in ET2 increased miR-499 level, decreased Drp-1 level and AI with statistical significance respectively (P < 0.05), but neither CaN expression nor CaN activity was changed significantly (P > 0.05).</p><p><b>CONCLUSION</b>Swimming training can inhibit myocardial apoptosis, and the decrease in Drp-l may be responsible for the reduced myocardial apoptosis. CaN, the upstream protein, does not participate in exercise-regulative apoptosis.</p>
Subject(s)
Animals , Male , Mice , Apoptosis , Dynamins , Metabolism , Heart , Mice, Inbred C57BL , MicroRNAs , Metabolism , Mitochondria, Heart , Physiology , Myocardium , Pathology , Physical Conditioning, Animal , SwimmingABSTRACT
<p><b>OBJECTIVE</b>To investigate effects of exercise training on vascular regulators and discuss its antihypertensive mechanism.</p><p><b>METHODS</b>Rats were divided into three groups (n = 7): spontaneous hypertensive rats control group (SHR-C), training group (SHR-T) and normotensive wistar-kyoto control group (WKY-C). Aerobic exercise consisted of 10 weeks of swimming training for 5 days/week. Exercise duration was 40 min in the first week, then 50 min in the second week, from the third week to the end of training, duration was maintained at 60 min. After training, vascular endothelial growth factor (VEGF) and other biomarkers in soleus were measured by RT-PCR and immunoblotting.</p><p><b>RESULTS</b>VEGF and endothelial NO synthase (eNOS) in SHR-C were lower than that in WKY-C (P < 0.05). Blood pressure in SHR-C and SHR-T were higher than that in WKY-C before training; After training, compared with SHR-C, VEGFR2, eNOS, VEGF and VEGF mRNA increased significantly in SHR-T paralleled with marked decreases in blood pressure and heart rate respectively (P < 0.05, P < 0.01).</p><p><b>CONCLUSION</b>Aerobic exercise training lowered the blood pressure in spontaneous hypertensive rats, and promoted VEGF mRNA level and expressions of VEGF, VEGFR2 and eNOS. The up-regulations of these vascular regulators could benefit angiogenesis and contribute to the antihypertensive effects.</p>
Subject(s)
Animals , Male , Rats , Blood Pressure , Hypertension , Metabolism , Therapeutics , Muscle, Skeletal , Metabolism , Nitric Oxide Synthase Type III , Metabolism , Physical Conditioning, Animal , Physiology , Rats, Inbred SHR , Vascular Endothelial Growth Factor A , Metabolism , Vascular Endothelial Growth Factor Receptor-2 , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of living high-training low (HiLo) on innate immunity in blood of elite swimmers.</p><p><b>METHODS</b>Six female swimmers undertook HiLo for two weeks, erythrocyte adhesion function and counts of leukocyte were tested in different time of training period.</p><p><b>RESULTS</b>Red blood cell C3b receptor ring rate (RBC-C3bRR) decreased and red blood cell immune complex matter ring rate (RBC-ICR) increased significantly (P < 0.05), the two markers returned to base line 1 week after training. Counts of leukocyte and granulocyte decreased significantly (P < 0.05), and they recovered 1 week after training; Counts of lymphocyte and monocyte decreased without significance during training and did not recovered after training.</p><p><b>CONCLUSION</b>Immunity of erythrocyte and granulocyte decreased quickly, but lymphocyte and monocyte recovered slowly, swimmers were adaptive to the training.</p>