The Heritage (HEalth, RIsk factors, exercise Training And GEnetics) family study
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE47874 | GEO | 2013/06/12
SECONDARY ACCESSION(S): PRJNA208217
REPOSITORIES: GEO
Similar Datasets
Project description: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.
2013-06-12 | E-GEOD-47874 | biostudies-arrayexpress
Project description:Experiment designed to identify differences in gene expression patterns in previously sedentary individuals before an endurance exercise training program. This series compares 2 groups of individuals that display high and low insulin sensitivity (SI) response (HSIR and LSIR) after 20 weeks of exercise (a 4-fold difference in SI response). There were no differences before training for SI, sex, age, BMI or body fat in the individuals integrating the LSIR and HSIR groups. Keywords = skeletal muscle Keywords = exercise-training Keywords = insulin sensitivity Keywords: repeat sample
2005-02-14 | GSE1718 | GEO
Project description:Gene expression profiles generated from skeletal muscle biopsies taken from participants of the HERITAGE family study. Participants completed an endurance training regime in which a skeletal muscle biopsy was taken prior to the start and after the final session of the program. Biopsies were used to generate Affymetrix gene expression microarrays.
2018-07-14 | GSE117070 | GEO
Project description:The overall objective of the Heritage Family Study 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 used in this analysis was derived from the pool of 473 Caucasian subjects (230 male and 243 female) from 99 nuclear families who completed ≥58 of the prescribed 60 exercise-training sessions. Utilizing a subsample of this Caucasian cohort, we selected family members from the Quebec center (N=125) to assess the metabolome and lipidome of circulating plasma under two well-defined environmental conditions, the pre- and post-training conditions.
2016-04-26 | ST000387 | MetabolomicsWorkbench
Project description:We reported that skeletal muscle insulin sensitivity was restored to a lean phenotype with exercise training in patients undergoing RYGB surgery. For that, the goals of this study is to identify changes in the skeletal muscle transcriptome profiling (RNA-seq) that could explain the insulin sensitivity improvement of RYGB + exercise training group.
2020-05-19 | GSE137631 | GEO
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:Skeletal muscle tissue is a highly adaptable tissue, responding to the specific demands it is subjected to. High-intensity interval training (HIIT) has been shown to generate similar, or even greater, molecular changes in skeletal muscle as that of constant load longer-lasting endurance-type training at moderate intensities. Despite shorter exposure times, the higher intensity provided by HIIT training leads to greater metabolic perturbations and thereby larger improvements in mitochondrial content and maximal oxygen uptake. During a period of regular exercise training, the performance improvements follow a non-linear pattern with a relatively faster pace initially and a gradual ‘plateauing-off’ after weeks and months. It is believed that this ‘plateau effect’ is due to a blunting of the molecular responses to acute exercise with exercise training. In the present study we utilised an explorative global transcriptomic approach to investigate the phenomenon of transcriptional-level blunting of the acute exercise response in human skeletal muscle over the course of a three-week HIIT intervention. We hypothesize that the blunting of transcription at this time-point is specific to certain pathways, including metabolic regulation and that these genes have communal transcriptional regulation.
2021-09-01 | GSE163356 | GEO
Project description:Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise resistant phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFβ signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease.
2014-05-23 | GSE57880 | GEO
Project description:A single bout of exercise induces changes in gene expression in skeletal muscle. Regular exercise results in an adaptive response involving changes in muscle architecture and biochemistry, and is an effective way to manage and prevent common human diseases such as obesity, cardiovascular disorders and type II diabetes. Our study is a transcriptome-wide analysis of skeletal muscle tissue in a large cohort of untrained Thoroughbred horses before and after a bout of high-intensity exercise and again after an extended period of training. We hypothesized that regular high-intensity exercise training primes the transcriptome for the demands of high-intensity exercise.
2018-08-07 | E-MTAB-5447 | biostudies-arrayexpress
Project description:Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise resistant phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFM-NM-2 signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease. Cardiac and skeletal muscle from 3 high and 3 low responder rats were examined for differential miRNA expression using Exiqon microarrays
2014-05-23 | E-GEOD-57880 | biostudies-arrayexpress