Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

The Heritage (HEalth, RIsk factors, exercise Training And GEnetics) family study

ABSTRACT: The overall objective of the heritage project is to study the role of the genotype in cardiovascular,metabolic and hormonal responses to aerobic exercise training and the contribution of regular exercise to changes in several cardiovascular disease and diabetes risk factors. The study cohort in this analysis consists of 473 Caucasian subjects (230 male and 243 female) from 99 nuclear families who completed M-bM-^IM-%58 of the prescribed 60 exercise-training sessions.The phenotypic expression of each individualM-bM-^@M-^Ys genotype is assessed under two well-defined environmental conditions, the pre- and post-training conditions. Here we have made the pre-training data available as used in the article Phillips BE, Williams JP, Gustafsson T, Bouchard C, Rankinen T, et al. (2013) Molecular Networks of Human Muscle Adaptation to Exercise and Age. PLoS Genet 9(3): e1003389. doi:10.1371/journal.pgen.1003389 52 U133+2 profiles (17M-bM-^@M-^S63 yr) generated from pre-exercise muscle biopsy samples from the HERITAGE Family Study. Heritage_pre dataset.

ORGANISM(S): Homo sapiens

SUBMITTER: Jamie Timmons

PROVIDER: E-GEOD-47874 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Molecular networks of human muscle adaptation to exercise and age.

Phillips Bethan E BE Williams John P JP Gustafsson Thomas T Bouchard Claude C Rankinen Tuomo T Knudsen Steen S Smith Kenneth K Timmons James A JA Atherton Philip J PJ

PLoS genetics 20130321 3

Physical activity and molecular ageing presumably interact to precipitate musculoskeletal decline in humans with age. Herein, we have delineated molecular networks for these two major components of sarcopenic risk using multiple independent clinical cohorts. We generated genome-wide transcript profiles from individuals (n = 44) who then undertook 20 weeks of supervised resistance-exercise training (RET). Expectedly, our subjects exhibited a marked range of hypertrophic responses (3% to +28%), an ...[more]

PMID: 23555298

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Project description:While the salutary effects of exercise training on conduit artery endothelial cells have been reported in animals and humans with cardiovascular risk factors or disease, whether a healthy endothelium is alterable with exercise training is less certain. The purpose of this study was to evaluate the impact of exercise training on transcriptional profiles in normal endothelial cells using a genome-wide microarray analysis. Brachial and internal mammary endothelial gene expression was compared between a group of healthy pigs that exercise-trained for 16-20 weeks (n=8) and a group that remained sedentary (n=8). We found that a total of 130 genes were up regulated and 84 genes down regulated in brachial artery endothelial cells with exercise training. In contrast, a total of 113 genes were up regulated and 31 genes down regulated in internal mammary artery endothelial cells (>1.5-fold and false discovery rate<15%). Although there was an overlap of 66 genes (59 up regulated and 7 down regulated with exercise training) between the brachial and internal mammary arteries, the identified endothelial gene networks and biological processes influenced by exercise training were distinctly different between the brachial and internal mammary arteries. These data indicate that a healthy endothelium is indeed responsive to exercise training and support the concept that the influence of physical activity on endothelial gene expression is not homogenously distributed throughout the vasculature. Brachial and internal mammary endothelial gene expression was compared between a group of healthy pigs that exercise-trained for 16-20 weeks (n=8) and a group that remained sedentary (n=8). The arteries were taken from the same animals, and after quality assessment, so there were 29 total arrays (15 unique pigs), 14 with an array for both the brachial artery and the internal mammary artery (IMA), and the remaining 1 having only brachial. One pig had bad RNA quality and is missing from both IMA and brachical. Therefore, there were 15 IMA (7 SED, 8 EX) and 14 brachial arrays (7 SED, 7 EX) that were used in this study.

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.

Dataset Information

The Heritage (HEalth, RIsk factors, exercise Training And GEnetics) family study

Publications

Molecular networks of human muscle adaptation to exercise and age.

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