Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1115089 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29141513.fastq.gz | Fastqsanger.gz | |||
| SRR29141513_1.fastq.gz | Fastqsanger.gz | |||
| SRR29141513_2.fastq.gz | Fastqsanger.gz | |||
| SRR29141514.fastq.gz | Fastqsanger.gz | |||
| SRR29141514_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Purpose: Aerobic capacity is a strong predictor of cardiovascular mortality. To determine the relationship between inborn aerobic capacity and soleus gene expression we examined genome-wide gene expression in soleus muscle of rats artificially selected for high and low running capacity (HCR and LCR, respectively) over 16 generations. The artificial selection of LCR caused accumulation of risk factors of cardiovascular disease similar to the metabolic syndrome seen in man, whereas HCR had markedly better cardiac function. We also studied alterations in gene expression in response to exercise training in the two groups, since accumulating evidence indicates that exercise has profound beneficial effects on the metabolic syndrome. Methods:; Soleus gene expression of both sedentary and exercise trained HCR and LCR was characterized by microarray- and gene ontology analysis. Results: Although HCR and LCR had an inborn 347% difference in running capacity, only three genes were found differentially expressed in the soleus muscle between the two groups. Up-regulation of the mitochondrial enzyme leucyl-transferRNA synthetase (LARS2) was found in the sedentary LCR. Increased expression of LARS2 has been associated with a mitochondrial DNA mutation linked to maternally inherited diabetes and mitochondrial dysfunction. In line with our findings, a growing body of evidence suggests that LCR have compromised mitochondrial function. After exercise training, 58 genes were altered in the soleus muscle of HCR, in contrast to only one in the LCR group. This suggests that animals born with different levels of fitness respond different to the same type of exercise training. Adaptations to exercise in HCR seemed to be associated with increased lipid metabolism and fatty acid elongation in the mitochondria. Also, genes associated with the peroxisomes, seemed to be central in the adaptation to exercise. Conclusion: The results indicate that (i) LCR might have mitochondrial dysfunction, which may be a contributing factor of the low inborn aerobic capacity, (ii) animals born with different levels of fitness respond different to the same exercise program. Experiment Overall Design: There are 16 samples in this study.
2008-06-18 | E-GEOD-10527 | biostudies-arrayexpress
Project description:Strenuous physical exercise causes a massive elevation in the concentration of circulating cell-free DNA (cfDNA), which correlates with effort intensity and duration. The cellular sources and physiological drivers of this phenomenon are unknown. Using methylation patterns of cfDNA and associated histones, we show that cfDNA in exercise originates mostly in extramedullary polymorphonuclear neutrophils. Strikingly, the concentration of cardiomyocyte cfDNA increases after a marathon, consistent with elevated troponin levels and indicating low-level, delayed cardiac cell death. Physical impact, low oxygen levels and elevated core body temperature contribute to the release of neutrophil cfDNA, while muscle contraction, increased heart rate, beta-adrenergic signaling or steroid treatment fail to cause elevation of cfDNA. Physical training reduces the release of neutrophil cfDNA after a standard exercise, revealing an inverse relationship between exercise-induced cfDNA release and training level. We speculate that the release of cfDNA from neutrophils in exercise relates to the activation of neutrophils in the context of exercise-induced muscle damage.
| EGAS00001007157 | EGA
Project description:Purpose: Aerobic capacity is a strong predictor of cardiovascular mortality. To determine the relationship between inborn aerobic capacity and soleus gene expression we examined genome-wide gene expression in soleus muscle of rats artificially selected for high and low running capacity (HCR and LCR, respectively) over 16 generations. The artificial selection of LCR caused accumulation of risk factors of cardiovascular disease similar to the metabolic syndrome seen in man, whereas HCR had markedly better cardiac function. We also studied alterations in gene expression in response to exercise training in the two groups, since accumulating evidence indicates that exercise has profound beneficial effects on the metabolic syndrome. Methods: Soleus gene expression of both sedentary and exercise trained HCR and LCR was characterized by microarray- and gene ontology analysis. Results: Although HCR and LCR had an inborn 347% difference in running capacity, only three genes were found differentially expressed in the soleus muscle between the two groups. Up-regulation of the mitochondrial enzyme leucyl-transferRNA synthetase (LARS2) was found in the sedentary LCR. Increased expression of LARS2 has been associated with a mitochondrial DNA mutation linked to maternally inherited diabetes and mitochondrial dysfunction. In line with our findings, a growing body of evidence suggests that LCR have compromised mitochondrial function. After exercise training, 58 genes were altered in the soleus muscle of HCR, in contrast to only one in the LCR group. This suggests that animals born with different levels of fitness respond different to the same type of exercise training. Adaptations to exercise in HCR seemed to be associated with increased lipid metabolism and fatty acid elongation in the mitochondria. Also, genes associated with the peroxisomes, seemed to be central in the adaptation to exercise. Conclusion: The results indicate that (i) LCR might have mitochondrial dysfunction, which may be a contributing factor of the low inborn aerobic capacity, (ii) animals born with different levels of fitness respond different to the same exercise program. Keywords: aerobic capacity, metabolic syndrome, soleus muscle, gene expression, metabolism
2008-06-01 | GSE10527 | GEO
Project description:Physical performance relies on the concerted action of myriad responses, many of which are under circadian clock control. Little is known, however, regarding the time-dependent effect on exercise performance at the molecular level. We found that both mice and humans exhibit day-time variance in exercise capacity between the early and late part of their active phase. The day-time variance in mice was dependent on exercise intensity and relied on the circadian clock proteins PER1/2. High throughput gene expression and metabolic profiling of skeletal muscle revealed metabolic pathways that are differently activated upon exercise in a day-time dependent manner. Remarkably, we discovered that ZMP, an endogenous AMPK activator, is induced by exercise in a time-dependent manner to regulate key steps in glycolytic and fatty acid oxidation pathways and potentially enhance exercise capacity. Overall, we propose that time of the day is a major modifier of exercise capacity and associated metabolic pathways.
2019-04-07 | GSE117161 | GEO
Project description:Physical activity promotes metabolic and cardiovascular health benefits that derive in part from the transcriptional responses to exercise that occur within skeletal muscle and other organs. There is interest in discovering a pharmacologic exercise mimetic that could imbue wellness and alleviate disease burden. However, the molecular physiology by which exercise signals the transcriptional response is highly complex, making it challenging to identify a single target for pharmacological mimicry. The current studies evaluated the transcriptome responses in skeletal muscle, heart, liver, and white and brown adipose to novel small molecule activators of AMPK (pan-activators for all AMPK isoforms) compared to that of exercise. A striking level of congruence between exercise and pharmacological AMPK activation was observed across the induced transcriptome of these five tissues. However, differences in acute metabolic response between exercise and pharmacologic AMPK activation were observed, notably for acute glycogen balances and related to the energy expenditure induced by exercise but not pharmacologic AMPK activation. Nevertheless, intervention with repeated daily administration of short-acting activation of AMPK was found to mitigate hyperglycemia and hyperinsulinemia in four rodent models of metabolic disease and without the cardiac glycogen accretion noted with sustained pharmacologic AMPK activation. These findings affirm that activation of AMPK is a key node governing exercise mediated transcription and is an attractive target as an exercise mimetic.
2019-02-27 | GSE92719 | GEO
Project description:The pathophysiological effects of a number of metabolic and age-related disorders can be prevented to some extent by exercise and increased physical activity. However, the molecular mechanisms that contribute to the beneficial effects of muscle activity remain poorly explored. Availability of a fast, inexpensive, and genetically tractable model for muscle activity and exercise will allow rapid identification and characterization of the molecular mechanisms that mediate the beneficial effects of muscle activity. Here, we report the development and characterization of an optogenetically-inducible muscle contraction (OMC) model in Drosophila larvae that we used to model acute exercise-like physiological responses. To characterize muscle-specific transcriptional responses to acute exercise, we performed bulk mRNA-sequencing, revealing striking similarities between acute exercise-induced genes in flies and those previously identified in humans. Our larval muscle contraction model opens a path for rapid identification and characterization of exercise-induced factors.
2022-09-15 | GSE196850 | GEO
Project description:Objective: Physical exercise and vitamin E are considered effective treatments of nonalcoholic fatty liver and other metabolic diseases. However, vitamin E has also been shown to interfere with the adaptation to exercise training, in particular for the skeletal muscle. Here, we studied the hypothesis that vitamin E also interferes with the metabolic adaptation of the liver to acute exercise. Methods: Male C57BL6/N mice were fed either control or vitamin E (α-tocopherol)- supplemented antioxidant diet during four weeks before being subjected to a non-exhaustive treadmill run. We assessed the acute transcriptional response of the liver as well as plasma corticosterone and free fatty acid (FFA) concentrations and monitored respiration in the exercising mice. Results: Vitamin E counteracted exercise-induced hepatic inflammation and altered the metabolic adaptation of the liver on the level of gene transcription. Vitamin E interfered with the upregulation of key metabolic regulators and caused a paradoxical increase in transcripts involved in lipid and cholesterol synthesis, processes negatively regulated by FFA and usually suspended during physical exercise. Whole-body energy consumption as well as corticosterone levels and signalling were similar, arguing against acute differences in fatty acid oxidation or glucocorticoid action. Conclusions: Our results show that vitamin E supplementation alters the inflammatory and transcriptional response of the liver to physical exercise. These effects of vitamin E could, on the long run, result in an impaired adaptation of the liver to physical exercise. Since exercise is clearly beneficial for general health and in reducing inflammation and dyslipidemia in nonalcoholic fatty liver disease, the interference of vitamin E with these processes may speak for a cautious use as dietary supplement.
2018-04-26 | GSE110747 | GEO
Project description:Physical exercise is a cornerstone for preventing diet-induced obesity, while it is unclear whether physical exercise could offset high-fat, high-calories diet (HFCD)-induced cardiac dysfunction. Here, mice were fed with HFCD and simultaneously subjected to physical exercise. As expected, physical exercise prevented HFCD-induced whole-body fat deposition. However, physical exercise exacerbated HFCD-induced cardiac damage. Further metabolomic analysis results showed that physical exercise induced circulating lipid redistribution, leading to excessive cardiac lipid uptake and lipotoxicity. Our study provides valuable insights into the cardiac effects of exercise in mice fed with HFCD, suggesting that counteracting the negative effect of HFCD by simultaneous physical exercise might be detrimental. Moreover, inappropriate physical exercise may damage certain organs even though it leads to weight loss and overall metabolic benefits. Of note, the current findings are based on animal experiments, the generalizability of these findings beyond this specific diet and mouse strain remains to be further explored.
2024-11-30 | PXD058460 |
Project description:Background: Physical exercise is beneficial to keep physical and mental health. The molecular mechanisms underlying exercise are still worth exploring. Methods: The healthy adult mice after six weeks of moderate-intensity exercise (experimental group) and sedentary mice (control group) were used to perform transcriptomic, proteomic, lactylation modification, and metabolomics analysis. In addition, gene sets related to hypoxia, glycolysis, and fatty acid metabolism were used to aid in the screening of hub genes. The mMCP-counter was employed to evaluate infiltration of immune cells in murine liver tissues. Results: Transcriptomics analysis revealed 82 intersection genes related to hypoxia, glycolysis, and fatty acid metabolism. Proteomics and lactylation modification analysis identified 577 proteins and 141 differentially lactylation modification proteins. By overlapping 82 intersection genes with 577 differentially expressed proteins and 141 differentially lactylation modification proteins, three hub genes (Aldoa, Acsl1, and Hadhb) were obtained. The immune infiltration analysis revealed a decreased score for monocytes/macrophages and an increased score for endothelial cells in the experimental group. Then, 459 metabolites in positive mode and 181 metabolites in negative mode were identified. The “Metabolic pathways” (mmu01100) was a common pathway between intersection genes-enriched pathways and metabolites-enriched pathways. Conclusion: These findings highlight the pivotal roles of hub genes in the glycolysis and fatty acid metabolism under the context of chronic exercise.
2025-02-10 | PXD057080 | Pride
Project description:The high physical activity/high aerobic fitness phenotype predicts low morbidity and mortality more strongly than any other known biological risk factor. Inherited and/or acquired properties of skeletal muscle seem to be linked with aerobic fitness and other cardio-metabolic risk factors. However, physical activity-induced changes in muscle and fat tissue-related complex molecular networks and their links with cardio-metabolic disease risk are not comprehensively understood. In the present study, we show that among the physically active members of twin pairs, as compared to their inactive co-twins, gene expression in musculus vastus lateralis tissue samples is chronically up-regulated for the central pathways or genes related to energy metabolism, including oxidative phosphorylation, lipid metabolism and supportive metabolic pathways. In addition to aerobic fitness, upregulation of these pathways is associated in particular with high HDL cholesterol levels. In fat tissue we found physical activity-induced increases in the expression of polyunsaturated fatty acid metabolism and in branched chain amino acid degradation genes, increases which were associated with decreased ‘high-risk’ ectopic body fat and low glucose levels. Consistent with other findings, plasma lipidomics analyses showed up-regulation of the triacylglycerols containing the polyunsaturated fatty acids. The findings indicate the main pathways in skeletal muscle and fat tissue that mediate the chronic effects of physical activity on reduced cardio-metabolic disease risk, including the increase in aerobic fitness. Up-regulation of oxidative energy metabolism seems to be a common underlying mechanism.
2010-07-31 | GSE20536 | GEO