Epigenetic control of training adaptation in skeletal muscle
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ABSTRACT:
PROVIDER: PRJNA916268 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22902310.fastq.gz | Fastqsanger.gz | |||
| SRR22902311.fastq.gz | Fastqsanger.gz | |||
| SRR22902312.fastq.gz | Fastqsanger.gz | |||
| SRR22902313.fastq.gz | Fastqsanger.gz | |||
| SRR22902314.fastq.gz | Fastqsanger.gz |
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Project description:Skeletal muscle has an enormous plastic potential and adapts to various stimuli such as mechanical stress, nutrients and hormones. While morphological changes observed in endurance trained muscles are well described, the molecular underpinnings of training adaptation is poorly understood. Therefore, the aim of our study was to define the molecular signature of a trained muscle and unravel the transcriptional responses of untrained and trained muscles to an acute bout of endurance exercise. Our results reveal that even though at baseline, the transcriptome of trained and untrained muscles is very similar, training status substantially affects the transcriptional response to an acute challenge, both quantitatively and qualitatively. Therefore, we provide novel insights into the complex molecular processes that are induced in response to exercise in a temporal- and training status-dependent manner. In addition, our study reveals that the epigenetic landscape contributes to the transcriptional memory of a trained muscle.
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Project description:Skeletal muscle has an enormous plastic potential to adapt to various external and internal
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defining the molecular signature of a trained muscle and unraveling the training status-
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Project description:Skeletal muscle has an enormous plastic potential to adapt to various external and internal perturbations. While morphological changes in endurance trained muscles are well described, the molecular underpinnings of training adaptation are poorly understood. We aimed at defining the molecular signature of a trained muscle and unraveling the training status-dependent responses to an acute bout of exercise. Our results reveal that even though at baseline, the transcriptomes of trained and untrained muscles are very similar, training status substantially affects the transcriptional response to an acute challenge, both quantitatively and qualitatively, in part mediated by epigenetic modifications. Second, proteomic changes were elicited by different transcriptional modalities. Finally, an unexpected resilience to enhance endurance performance even in the absence of key regulatory factors was observed, suggesting a strong evolutionary pressure on enabling muscle plasticity even in unfavorable contexts. Together, these results provide a molecular framework that defines muscle plasticity in training.
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Project description:Transcriptional control of training adaptation in skeletal muscle
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Project description:Skeletal muscle has an enormous plastic potential and adapts to various stimuli such as mechanical stress, nutrients and hormones. While morphological changes observed in endurance trained muscles are well described, the molecular underpinnings of training adaptation is poorly understood. Therefore, the aim of our study was to define the molecular signature of a trained muscle and unravel the transcriptional responses of untrained and trained muscles to an acute bout of endurance exercise. Our results reveal that even though at baseline, the transcriptome of trained and untrained muscles is very similar, training status substantially affects the transcriptional response to an acute challenge, both quantitatively and qualitatively. Therefore, we provide novel insights into the complex molecular processes that are induced in response to exercise in a temporal- and training status-dependent manner. In addition, our study reveals that the epigenetic landscape contributes to the transcriptional memory of a trained muscle.
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Project description:The molecular pathways which are activated and contribute to physiological remodeling of skeletal muscle in response to endurance exercise have not been fully characterized. We previously reported that ~800 gene transcripts are regulated following 6 weeks of supervised endurance training in young sedentary males, referred to as the training responsive transcriptome (TRT). Here we utilized this database together with data on biological variation in muscle adaptation to aerobic endurance training in both humans and a novel out-bred rodent model to study the potential regulatory molecules that coordinate this complex network of genes. We identified three DNA sequences representing RUNX1, SOX9, and PAX3 transcription factor binding sites as over-represented in the TRT. In turn, miRNA profiling indicated that several miRNAs targeting RUNX1, SOX9 and PAX3 were down-regulated by endurance training. The TRT was then examined by contrasting subjects who demonstrated the least vs. the greatest improvement in aerobic capacity (low vs. high responders), and at least 100 of the 800 TRT genes were differentially regulated, thus suggesting regulation of these genes may be important for improving aerobic capacity. In high responders, pro-angiogenic and tissue developmental networks emerged as key candidates for coordinating tissue aerobic adaptation. Beyond RNA level validation there were several DNA variants that associated with VO(2)max trainability in the HERITAGE Family Study but these did not pass conservative Bonferroni adjustment. In addition, in a rat model selected across 10 generations for high aerobic training responsiveness, we found that both the TRT and a homologous subset of the human high responder genes were regulated to a greater degree in high responder rodent skeletal muscle. This analysis provides a comprehensive map of the transcriptomic features important for aerobic exercise-induced improvements in maximal oxygen consumption. This data is from skeletal muscle post 6 weeks of endurance exercise training.
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Project description:Context: Exercise training is a plausible model for identification of molecular mechanisms that cause metabolic-related changes in human skeletal muscle. Objective: The goal was to explore the molecular basis of the adaptation of skeletal muscle to exercise training. Design and Intervention: Obese male subjects were subjected to an individualized supervised training program targeted in order to optimize lipid oxidation during 8 weeks. Main Outcome Measures: Primary outcome measures were gene expression profiling of skeletal muscle. Body composition, oral glucose tolerance test, Resting metabolic rate, respiratory quotient, maximal oxygen uptake and metabolic biochemistry were also assessed. Overall Design The obese (BMI 30-36) male volunteers (age 32-42) were asked to refrain from vigorous physical activity 48h before presenting to the clinical investigation centre, and ate a weight-maintaining diet consisting of 35% fat, 16% protein, and 49% carbohydrates two days before the experiment. Muscle biopsies of Vastus Lateralis weighing 60–100 mg were obtained using the Bergstrom technique, cleaned and snap-frozen in liquid nitrogen. Resting metabolic rate, respiratory quotient and maximal oxygen uptake were assessed. The subjects were investigated at baseline and after 8 weeks of supervised aerobic exercise training program consisting of daily sessions of 45-60 min of endurance exercise, 5 days a week, at least 48-72h after the last acute exercise bout. Skeletal muscle biopsies were obtained at the beginning and at the end of the protocol. Transcriptome analysis compared 8 subjects before vs. after training using arrays using a common reference design (Cy5 dye was incorporated into all muscle RNA samples, while a reference RNA pool made of the mix of commercial human liver, adipose tissue and skeletal muscle RNA was labelled with Cy3 dye (Applied Biosystems/Ambion, Foster City, USA)( and whole genome 4x44k oligonucleotide arrays (Agilent Technologies).
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