Epigenetic control of training adaptation in skeletal muscle
Ontology highlight
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
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-
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baseline, the transcriptomes of trained and untrained muscles are very similar, training status
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2023-06-19 | MSV000092203 | MassIVE
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: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.
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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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