Effects of mixed exercise training on gene expression in human skeletal muscle
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Milene Catoire
PROVIDER: E-GEOD-53598 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE18583: Baseline skeletal muscle gene expression GSE35659: A transcriptional map of the impact of endurance exercise training on skeletal muscle phenotype (resting muscle after endurance training) Refer to individual Series
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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.
2012-02-10 | E-GEOD-35659 | biostudies-arrayexpress
Project description:The aim of this work was to produce a reproducible molecular signature of human muscle responses to resistance training and examine how such a profile relates to new and established exercise adaptation gene networks. Subjects were recruited from an age range of 18 to 75 y. Before beginning the study all subjects were screened using a medical questionnaire, physical examination and resting ECG with exclusions for overt muscle wasting (>2 SD below age norms)[85], metabolic, respiratory/cardiovascular disorders or other major contraindications to a healthy status. All subjects had normal blood chemistry and were normotensive (BP <140/90). All subjects performed routine activities of daily living and recreation but did not participate in moderate to high intensity aerobic exercise and none had participated in RET in the last 24 months. Body composition was measured at screening and following RET by dual energy X-ray absorptiometry (DEXA) (Lunar Prodigy II, GE Medical Systems). Subject positioning on the DEXA bed was optimized to allow the region of interest (ROI) body compartments to be analyzed separately. The upper leg ROI was selected as the area inferior to the lowest visible point of the coccyx to the mid-point of the patella. The dataset comprises 44 pre-exercise and 44 post-exercise samples. In addition there is a baseline sample NB021_pre-training (D13_NB021F). Therefore there are 89 samples in total. (Note: Singleton baseline sample NB021_pre-training was normalized only using all baseline samples.) Derby dataset.
2013-06-12 | E-GEOD-47881 | biostudies-arrayexpress
Project description:Background: Exercising is know to have an effect on exercising skeletal muscle, but unkown is the effect on non-exercising skeletal muscle. Gene expression changes in the non-exercising skeletal muscle would point to a signalling role of skeletal muscle 9 healthy middle-aged men performed 1 hour of one-legged exercise, before and afterwards muscle biopsies were taken from both legs. Skeletal muscle biopsies were analyzed by microarray.
2012-10-23 | E-GEOD-41769 | biostudies-arrayexpress
Project description:The rates of obesity and sedentary lifestyle are on a dramatic incline, with associated detrimental health effects among women in particular. Although exercise prescriptions are useful for overcoming these problems, success can be hampered by differential responsiveness among individuals in cardiovascular fitness indices (i.e., improvements in strength, lipids, VO2max). Genetic factors appear to play an important role in determining this inter-individual variation in responsiveness. We performed microarray analyses on mRNA in whole blood from 60 sedentary women from a multi-ethnic cohort who underwent 12 weeks of exercise, to identify gene subsets that were differentially expressed between individuals who experienced the greatest and least improvements in fitness based upon a composite fitness score index. We identified 43 transcripts in 39 unique genes (FDR<10%; FC>1.5) whose expression increased the most in “high” versus “low” premenopausal female responders. Several (TIGD7, UQCRH, PSMA6, WDR12, TFB2M, USP15) have reported associations with fitness-related phenotypes. Bioinformatic analysis of the 39 genes identified 4 miRNAs whose expression has been linked to cardiovascular diseases (ANKRD22: miR-637, LRRFIP1: miR-132, PRKAR2B: miR-92a, RSAD2:miR-192). These 39 genes were enriched in 6 biological pathways, including the oxidative phosphorylation pathway (p=8.08 x 10-3). Two genes, LRRFIP1 and SNORD30, were also identified with lower expression in high responding postmenopausal women. In summary, we identified gene signatures based on mRNA analysis that define responsiveness to exercise in a largely minority-based female cohort. Importantly, this study validates several genes/pathways previously associated with exercise responsiveness and extends these findings with additional novel genes. We performed microarray analyses on mRNA in whole blood from 60 sedentary women from a multi-ethnic cohort who underwent 12 weeks of exercise, to identify gene subsets that were differentially expressed between individuals who experienced the greatest and least improvements in fitness based upon a composite fitness score index.
2012-05-31 | E-GEOD-34788 | biostudies-arrayexpress
Project description:There is an association between transcriptome and the exercise-related phenotype. Peripheral blood cells suffer alterations in the gene expression pattern in response to perturbations caused by exercise. The acute response to endurance activates stress and inflammation, as well as growth and tissue repair responses. Peripheral blood mononuclear cell (PBMC) samples were obtained at baseline and after an endurance training protocol from healthy male untrained police recruits. Samples were used to identify differentially expressed transcripts in response to training and further infer about activated metabolic and signalling pathways. Additionally, baseline expression was associated with the oxygen uptake change and stratified individuals according to their percent change in oxygen uptake. Fasting blood samples were withdrawn at baseline and after the exercise training protocol, 48 hours after the last exercise session. RNA was extracted from peripheral blood mononuclear cells, and hybridized into Affymetrix microarrays.
2014-05-30 | E-GEOD-57999 | biostudies-arrayexpress
Project description:Regular endurance exercise training induces beneficial functional and health effects in human skeletal muscle. The putative contribution to the training response of the epigenome as a mediator between genes and environment has not been clarified. Here we investigated the contribution of DNA methylation and associated transcriptomic changes in a well-controlled human intervention study. Training effects were mirrored by significant alterations in DNA methylation and gene expression in regions with a homogeneous muscle energetics and remodeling ontology. Differential DNA methylation predominantly occurred in regulatory enhancer regions, where known binding motifs of MRF, MEF2 and ETS proteins were identified. A transcriptional network analysis revealed modules harboring distinct ontologies, and interestingly the overall direction of the changes of methylation within each module was inversely correlated to expression changes. In conclusion, we show that highly consistent and associated modifications in methylation and expression, concordant with observed health-enhancing phenotypic adaptations, are induced by a physiological stimulus. DNA samples from vastus lateralis muscle bisopsies were included in the study. Specifically, 23 subjects performed three months of supervised endurance training. Biospies were taken at rest, before and after training. DNA methylation levels were profiled using Illumina 450K arrays.
2014-11-04 | E-GEOD-60655 | biostudies-arrayexpress
Project description:Although skeletal muscle metabolism is a well-studied physiological process, little is known about how it is regulated at the transcriptional level. The myogenic transcription factor myogenin is required for skeletal muscle development during embryonic and fetal life, but myogeninâs role in adult skeletal muscle is unclear. We sought to determine myogeninâs function in adult muscle metabolism. A Myog conditional allele and Cre-ER transgene were used to delete Myog in adult mice. Mice were analyzed for exercise capacity by involuntary treadmill running. To assess oxidative and glycolytic metabolism, we monitored blood glucose and lactate levels and performed histochemical analysis on muscle fibers. Surprisingly, we found that Myog-deleted mice performed significantly better than controls in high- and low-intensity treadmill running. This enhanced exercise capacity was due to more efficient oxidative metabolism during low-intensity exercise and more efficient glycolytic metabolism during high-intensity exercise. Furthermore, Myog-deleted mice had an enhanced response to long-term voluntary exercise training on running wheels. We identified several candidate genes whose expression was altered in exercise-stressed muscle of mice lacking myogenin. The results suggest that myogenin plays a critical role as a high-level transcriptional regulator to control the energy balance between aerobic and anaerobic metabolism in adult skeletal muscle. We used microarrays to detail the global program of gene expression underlying enhanced exercise endurance associated with myog-deletion and long-term exercise training. Mouse gastrocnemius muscles were selected after 6 months of myog-deletion and exercise training for RNA extraction and hybridization on Affymetrix microarrays. We chose 3 wild type and 3 myog-deleted mice that best represented the average of each larger group that was tested during our mouse exercise studies.
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