Ontology highlight
ABSTRACT:
PROVIDER: PRJNA430461 | ENA |
REPOSITORIES: ENA
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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 TGFβ 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.
2014-05-23 | GSE57880 | GEO
Project description:Skeletal muscle adapts to exercise training of various modes, intensities and durations with a programmed gene expression response. This study dissects the independent and combined effects of exercise mode, intensity and duration to identify which exercise has the most positive effects on skeletal muscle health. Full details on exercise groups can be found in: Kraus et al Med Sci Sports Exerc. 2001 Oct;33(10):1774-84 and Bateman et al Am J Cardiol. 2011 Sep 15;108(6):838-44. This study uses a middle aged group of subjects that have 3+ markers of metabolic syndrome. One group remains an inactive control, while 5 groups undergo 9 mo supervised exercise training. Exercise groups are as follows: Inactive control (group B); Mild aerobic exercise - low amount/mod intensity (group A); Moderate aerobic exercise - low amt/vig intensity (group D); High aerobic exercise - high amt/vig intensity (group C); resistance training only (group F); and mod aerobic + resistance training (group E). Each group has 10 subjects (5 men and 5 women), however 3 subjects failed array QC, leaving 8 subjects in group E and 9 subjects in group F. Data were all analyzed pre to post training in a RM ANCOVA, covaried for age and sex or regression to determine genotype/phenotype interactions.
2015-05-14 | E-GEOD-48278 | biostudies-arrayexpress
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
2014-05-23 | E-GEOD-57880 | biostudies-arrayexpress
Project description:Low aerobic exercise capacity increases susceptibility to smoking-induced inflammation and tissue damage
2016-02-15 | GSE22456 | GEO
Project description:This 12-week, exercise study will assess the feasibility of a home-based high-intensity interval training (HIIT) program among colorectal cancer survivors and explore the impact of home-based HIIT compared to a standard home-based moderate-intensity continuous aerobic exercise program on physical outcomes linked with survival from colorectal cancer and surrogate blood markers of colorectal cancer recurrence.
HIIT is a type of aerobic exercise that includes short bursts (i.e. 1-4 minutes) of vigorous exercise followed by longer periods of moderate to lower intensity exercise (i.e. 1-10 minutes). Participants in this study will be randomly assigned into a personalized home based exercise program - either high-intensity interval training (HIIT) or moderate-intensity continuous aerobic exercise (MICE).
This pilot study will provide us with preliminary evidence for a larger trial aimed to compare the effectiveness of these two different types of home-based exercise programs on physical outcomes linked with survival, quality of life, and surrogate blood markers of colorectal cancer recurrence.
| 2315575 | ecrin-mdr-crc
Project description:Low aerobic exercise capacity increases susceptibility to smoking-induced inflammation and tissue damage 38 animals total: 12 HCR Smoke, 12 LCR Smoke, 7 HCR sham, 7 LCR sham
2016-02-15 | E-GEOD-22456 | biostudies-arrayexpress
Project description:Epidemiological studies reveal a strong link between low aerobic capacity and metabolic and cardiovascular diseases. Two-way artificial selection of rats based on low and high intrinsic exercise capacity has produced two strains that also differ in risk for metabolic syndrome (Koch LG, Britton SL. Artificial selection for intrinsic aerobic endurance running capacity in rats. Physiol Genomics 5:45-52, 2001). Here we investigated skeletal muscle characteristics and genotype-phenotype relationships behind high and low inherited aerobic exercise capacity and the link between oxygen metabolism and metabolic disease risk factors in rats derived from generation 18. This population (n=24) of high capacity runners (HCR) and low capacity runners (LCR) differed by 615% in maximal treadmill running capacity. LCR were significantly significantly heavier and had increased blood glucose, serum insulin and triglyceride concentration. HCR had higher resting metabolic rate than LCR. Capillaries/mm2 and capillary-to-fiber ratio were significantly greater in HCR rats in soleus and gastrocnemius and capillary-to-fiber ratio in extensor digitorum longus (EDL) muscle. Subsarcolemmal mitochondrial area was 96% (p<0.01) and intermyofibrillar area was 32% (p<0.05) larger in HCR soleus. Microarray results showed that 126 genes were significantly up-regulated and 113 genes were down-regulated in HCR (p<0.05). Functional clustering and unbiased correlation analysis of muscle microarray data revealed that genes up-regulated in HCR were related to mitochondria, carboxylic acid and lipid metabolism, and oxidoreductase activity. In conclusion, our data show that aerobic capacity is strongly linked to the architecture of energy transfer and corroborate the importance of oxygen metabolism as the determinant of metabolic health and complex metabolic diseases such as metabolic syndrome and type 2 diabetes. Total RNA obtained from gastrocnemius muscle was compared between rat strains of low and high inherited aerobic exercise capacity.
2010-04-13 | E-GEOD-17190 | biostudies-arrayexpress
Project description:To investigate the effect of aerobic exercise on liver injury in nonalcoholic steatohepatitis (NASH), we established a NASH model induced by atherosclerotic (Ath) diet and intervened with aerobic exercise training.
2023-01-11 | GSE217155 | GEO
Project description:High intensity aerobic exercise (90% of the maximum heart rate) can effectively suppress cancer proliferation in vivo. However, the molecular effect of aerobic exercise and its relevance to cancer prevention remains uninvestigated. The mRNA-sequencing technique (mRNA-seq) can provide a genome-wide depiction of gene expression changes by aerobic exercise. Mice with colorectal cancer were subjected to high intensity aerobic exercise, and mRNA-seq analysis was performed on heart, lung, and skeletal muscle tissues to analyze the molecular effects of the exercise in a genome-wide manner. The skeletal muscle-derived genes with exercise-dependent differential expressions were further evaluated for their effects on colorectal cancer cell viability. Regular and high intensity aerobic physical activity in the mice produced positive results in comprehensive parameters (i.e., food intake, weight, and survival rate) compared to those in the control groups (healthy and cancer with no exercise). A heatmap of differentially expressed genes revealed markedly different expression patterns between these groups. RNA-seq analysis of 23,282 skeletal muscle-derived genes identified a number of anticancer effector genes. Knockdown and overexpression of selected anticancer genes significantly repressed CT26 proliferation by 20% (p<0.05). Our finding based on the aerobic exercise cancer mouses model suggest that the high intensity exercise resulted in a global change in gene expression patterns, particularly those that affect cancer cell viability.
2022-07-13 | GSE191284 | GEO
Project description:High intensity aerobic exercise (90% of the maximum heart rate) can effectively suppress cancer proliferation in vivo. However, the molecular effect of aerobic exercise and its relevance to cancer prevention remains uninvestigated. The mRNA-sequencing technique (mRNA-seq) can provide a genome-wide depiction of gene expression changes by aerobic exercise. Mice with colorectal cancer were subjected to high intensity aerobic exercise, and mRNA-seq analysis was performed on heart, lung, and skeletal muscle tissues to analyze the molecular effects of the exercise in a genome-wide manner. The skeletal muscle-derived genes with exercise-dependent differential expressions were further evaluated for their effects on colorectal cancer cell viability. Regular and high intensity aerobic physical activity in the mice produced positive results in comprehensive parameters (i.e., food intake, weight, and survival rate) compared to those in the control groups (healthy and cancer with no exercise). A heatmap of differentially expressed genes revealed markedly different expression patterns between these groups. RNA-seq analysis of 23,282 skeletal muscle-derived genes identified a number of anticancer effector genes. Knockdown and overexpression of selected anticancer genes significantly repressed CT26 proliferation by 20% (p<0.05). Our finding based on the aerobic exercise cancer mouses model suggest that the high intensity exercise resulted in a global change in gene expression patterns, particularly those that affect cancer cell viability.
2022-07-13 | GSE191283 | GEO