Comparative analysis of skeletal muscle transcriptional signatures associated with aerobic exercise capacity or response to training in humans and rats
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ABSTRACT:
PROVIDER: PRJNA648996 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12333763.fastq.gz | Fastqsanger.gz | |||
| SRR12333764.fastq.gz | Fastqsanger.gz | |||
| SRR12333765.fastq.gz | Fastqsanger.gz | |||
| SRR12333766.fastq.gz | Fastqsanger.gz | |||
| SRR12333767.fastq.gz | Fastqsanger.gz |
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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: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:Maximal aerobic exercise capacity (V̇O2max) is one of the strongest predictors of morbidity and mortality. Aerobic exercise training can increase V̇O2max, but inter-individual variability is marked and unexplained physiologically. The mechanisms underlying this variability have major clinical implications for extending human healthspan. Here, we report the first comprehensive, RNA-seq study of circulating transcriptome signatures related to ΔV̇O2max. We used RNA-seq to characterize transcriptomic predictors of ΔV̇O2max in healthy women who completed a 16-week, randomized controlled trial comparing higher vs. lower aerobic exercise training volume and intensity (four training groups, fully crossed). We found striking baseline gene expression differences in subjects who responded to aerobic exercise training with robust (R) vs. little/no (NR) ΔV̇O2max.
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Project description:Microarray analysis was performed with RNA isolated from vastus lateralis muscle biopsies of lean/overweight subjects following 18 days of aerobic exercise training. Samples from lean active individuals were also included. Exercise training led to robust changes in trained muscle. The lean active group profile was distinct from the pre-exercise samples. These results help define the molecular changes associated with aerobic training and contrast with an active phenotype.
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Project description:Skeletal muscle has a unique ability to remodel in response to stimuli such as contraction and aerobic exercise training. Phenotypic changes in muscle that occur with training such as a switch to a more oxidative fiber type, and increased capillary density contribute to the well-known health benefits of aerobic exercise. The muscle matrisome likely plays an important role in muscle remodeling with exercise. However, due to technical limitations in studying muscle ECM proteins, which are highly insoluble, little is known about the muscle matrisome and how it contributes to muscle remodeling. Here, we utilized two-fraction methodology to extract muscle proteins, combined with multiplexed tandem mass tag proteomic technology to identify 161 unique ECM proteins in mouse skeletal muscle. In addition, we demonstrate that aerobic exercise training induces remodeling of a significant proportion of the muscle matrisome. We performed follow-up experiments to validate exercise-regulated ECM targets in a separate cohort of mice using Western blotting and immunofluorescence imaging. Our data demonstrate that changes in several key ECM targets are strongly associated with muscle remodeling processes such as increased capillary density in mice. We also identify LOXL1 as a novel muscle ECM target associated with aerobic capacity in humans. In addition, publically available data and databases were used for in silico modeling to determine the likely cellular sources of exercise-induced ECM remodeling targets and identify ECM interaction networks. This work greatly enhances our understanding of ECM content and function in skeletal muscle and demonstrates an important role for ECM remodeling in the adaptive response to exercise.
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Project description:In this study, we set out to dissect the intrinsic and response components of aerobic exercise at the transcriptional level in the skeletal muscle.
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Project description:The processes of adaptation to environmental heat and aerobic exercise training improve efficiency in various body systems and bring about acclimatory homeostasis. In order to examine the global genomic responses of the soleus and heart following exposure of rats to these stressors, nylon cDNA Atlas Array was used. Male rats were exposed to one of the following stressors: heat acclimation, aerobic training (treadmill), and combined heat acclimation and aerobic training for short (2, 3 days) and long (1 mo) time period. The study comprised seven experimental groups: Controls-untreated. Heat acclimated groups (2dac, Acc)â exposure to environmental heat at 34C for 2 or 30 days. Exercise groups (3dex, Ex)â graduated training protocol under normothermic conditions for 3 and 30 days at 24C. Exercise training and heat acclimation â (3dexac, ExAc)- exposed to both environmental heat and aerobic exercise as above. The Series data tables appended below: 1) Heart - normalized log2 ratio of geomeans defined as treatment/control 2) Soleus - normalized log2 ratio of geomeans defined as treatment/control 21 samples, 3 pool each, of: 1)Â Control untreated rats 2)Â Long-term heat acclimated rats 3)Â Long-term aerobic-exercised trained rats. 4)Â Rats exposed to long-term heat acclimation and exercise training. 5)Â Short term heat acclimated rats. 6)Â Short term aerobic exercised trained rats 7)Â Rats exposed to short-term heat acclimation and exercise training.
2010-05-27 | E-GEOD-7799 | biostudies-arrayexpress
Project description:The processes of adaptation to environmental heat and aerobic exercise training improve efficiency in various body systems and bring about acclimatory homeostasis. In order to examine the global genomic responses of the soleus and heart following exposure of rats to these stressors, nylon cDNA Atlas Array was used. Male rats were exposed to one of the following stressors: heat acclimation, aerobic training (treadmill), and combined heat acclimation and aerobic training for short (2, 3 days) and long (1 mo) time period. The study comprised seven experimental groups: Controls-untreated. Heat acclimated groups (2dac, Acc)– exposure to environmental heat at 34C for 2 or 30 days. Exercise groups (3dex, Ex)– graduated training protocol under normothermic conditions for 3 and 30 days at 24C. Exercise training and heat acclimation – (3dexac, ExAc)- exposed to both environmental heat and aerobic exercise as above. The Series data tables appended below: 1) Heart - normalized log2 ratio of geomeans defined as treatment/control 2) Soleus - normalized log2 ratio of geomeans defined as treatment/control Keywords: stress response
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