Transcription profiling of rat heart left ventricle after exercise to investigate the role of exercise as a known protective factor against cardiovascular morbidity and mortality
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
SUBMITTER: Betti Giusti
PROVIDER: E-GEOD-7640 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Array analysis of a set of 96 stress and toxicity genes was carried out in left ventricular cardiomyocytes from 8 control and 7 trained rats. The training protocol was very gradual and mild. Animals were sacrificed 48 hrs after the last training session in order to evaluate gene expression during the "second window of cardioprotection". Array results were validated by Real Time PCR of selected genes and Western Blot analysis of selected proteins. Plasma MDA and resistance to ischemia/reperfusion were evaluated as well. A total of 11 genes were found to be upregulated by moderate exercise, 3 to be downregulated. MDA was found to be increased in plasma of trained rats. Myocardial resistance to ischemia-reperfusion was found to be improved in trained rats with respect to controls. Results suggest that such a pattern of mild training does at the same time elicit stress responses, but also the upregulation of a number of defensive genes, that are likely to constitute the core of the adaptive mechanisms. Keywords: exercise training-related stress response and cardioprotection
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Project description:The goal of the endurance exercise training study in young adult rats was to perform exercise training studies in young adult (6-month-old) F344 rats, and from these rats collect multiple tissues in order to provide high quality samples for detailed analysis by chemical analysis sites. Tissues were collected from 10-12 rats sedentary control rats concurrent with the collection of the 8-week training groups. The 8-week training group and controls were from the same cohort and same age at euthanasia. For the older age group, an additional set of controls (n=5-6) were collected with the 1-2 week training group. Rats were either sedentary or underwent an exercise training program. Rats were exercised on the rodent treadmill 5 days per week using a progressive training protocol designed to exercise the rats at approximately 70% of VO2max and training was performed no earlier than 10:00 am and no later than 5:00 pm over 5 consecutive days per week. Training was initiated with the treadmill set at 70% of VO2 max and 5 degrees grade for 20 minutes. The duration of exercise was increased by one minute each day until day 31 of training (start of week 7), when a duration of 50 min was reached. Speed and grade of each training session increased in larger increments due to treadmill parameters. The highest intensity and duration of training began on day 31. This intensity was maintained for the final 10 days of the protocol to ensure steady state had been achieved. If any rats were unable to perform at least 4 days of training per week they were removed from the study and euthanized. It is important to note that the starting treadmill speed varied depending on the sex and age of the rat. The initial and maximum speeds were based on VO2max measurements obtained during the pre-training testing of the compliant rats. Rats assigned to the control group followed a schedule similar to the training group. They were placed in one lane on the treadmill for 15 minutes/day, 5 days per week. The treadmill was set at 0 m/min at an incline that corresponded to the incline being used by the training group.
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Project description:Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise resistant phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFM-NM-2 signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease. Cardiac and skeletal muscle from 3 high and 3 low responder rats were examined for differential miRNA expression using Exiqon microarrays
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