Precision High Intensity Training through Epigenetics (PHITE)
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PROVIDER: PRJNA1202221 | ENA |
REPOSITORIES: ENA
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Project description:Precision High Intensity Training through Epigenetics (PHITE)
| PRJNA1202222 | ENA
Project description:Twenty healthy subjects (25±5yrs) completed two high-intensity interval training interventions (training and retraining) lasting 8 weeks separated by 12 weeks of detraining. Measurements at baseline and after training, detraining and retraining included maximal oxygen consumption (V̇O2max), along with vastus lateralis biopsy for genome wide DNA methylation using Illumina Epic arrays in 5 of the participants for all conditions (baseline, training, detraining and retraining).
2024-05-30 | GSE268211 | GEO
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:High-intensity intermittent exercise training (HIIT) has been proposed as an effective approach for improving both anaerobic and aerobic capacities. However, the molecular response of muscles to HIIT remains unknown. We used microarray to examine the effects of HIIT on global gene expression in human skeletal muscle.
2018-11-30 | GSE109657 | GEO
Project description:Human skeletal muscle transcriptome in response to high-intensity interval training
| PRJNA685799 | ENA
Project description:High intensity exercise (HIE) has become a prominent training modality used to ameliorate cardiac disease conditions. The effects of HIE training on Hypertrophic Cardiomyopathy (HCM) have not been previously studied in animal models or in patients, largely due to concerns about triggering sudden arrhythmic events. Employing a transgenic cardiac troponin (cTnT-160E or TG) preclinical murine model that closely recapitulates human HCM, we evaluated the effects of a High Intensity Interval Training (HIIT) protocol on cardiorespiratory capacity (i.e., peak oxygen consumption or pVO2), which is a significant prognostic indicator of disease trajectory. 14 month old TG male mice had lower peak VO2 than non-transgenic (NTG) male mice of the same age at baseline, but there was no difference in pVO2 in female TG compared to nTG mice. HIIT significantly improved pVO2 in both nTG female (18%) , nTG male (18%), TG female (16%) and TG male (12%) mice compared to sedentary controls. There were no changes in structure, function or LV mass as measured by echocardiography or post mortem analyses in any of the groups, and no effect of HIIT on cardiac fibrosis. HIIT led to significant increases in lean muscle mass in both nTG and TG male mice, and nTG female mice but not TG female mice. The results of our study provide foundational evidence that HIE can improve pVO2 in HCM without adverse effects on disease phenotype.
2025-05-20 | GSE297707 | GEO
Project description:Skeletal muscle response to high-intensity intermittent exercise training in young men
| PRJNA431609 | ENA
Project description:Human skeletal muscle possesses an epigenetic memory of high intensity interval training
| PRJNA1115137 | ENA
Project description:Methods for studying mitochondrial adaptations in skeletal muscle have mostly used whole-muscle samples, where results may be confounded by the presence of a mixture of type I and II skeletal muscle fibres. In this project, we utilised the latest Mass spectrometry (MS) techniques to provide new insights into mitochondrial adaptations in type I and II fibres in response to two different types of training – moderate-intensity-continuous training (MICT) and sprint-interval training (SIT). An 8-week training intervention was undertaken by 23 men who performed either MICT or SIT. Single muscle fibres from skeletal muscle biopsies were collected at rest, before and after the 8 weeks of training, and pooled for subsequent MS analysis. A proteomic workflow was applied that permitted a three-tiered comparison and quantification of mitochondrial proteins in different fibre types. Our protocol includes tandem mass tag labelling for increased identification of low-abundant proteins. We quantified more than 45% of known mitochondrial proteins in skeletal muscle. When comparing type I to type II fibres,24 mitochondrial proteins were differentially expressed following MICT and 10 following SIT. These altered proteins were associated with known cellular pathways within the mitochondria, including oxidative phosphorylation, the TCA cycle and fatty acid oxidation. There were distinct trends for fibre-type-specific protein responses to different types of exercise training. Following MICT proteins mostly increased in abundance in type I fibres, without analogous changes observed following SIT. This greater upregulation of mitochondrial proteins observed following MICT, suggests exercise volume is a powerful stimulus for mitochondrial adaptations. This upregulation mostly seen in type I fibres is consistent with the predominate recruitment of this fibre type with MICT. When normalised to mitochondrial content further evidence to fibre-specific non-stoichiometrically induced increases in the expression of fatty acid mitochondrial proteins is presented, highlighting mitochondria as a pivotal subcellular site in facilitating substrate utilisation to increase ATP production in type I fibres. Conversely, the research suggests very high-intensity exercise training altered the systematic biogenesis of oxidative phosphorylation (OXPHOS) components, in particular complex IV subunits of the OXPHOS pathway. These results question the existing knowledge of fibre-type-specific changes to mitochondrial proteins in response to exercise training and provide a valuable contribution to understanding the mechanisms by which exercise helps to improve health and prevent disease.
2024-10-17 | PXD036010 | Pride
Project description:Exercise is an effective strategy in the prevention and treatment of metabolic diseases. Alterations in the skeletal muscle proteome, including post-translational modifications, regulate its metabolic adaptations to exercise. Here, we examined the effect of high-intensity interval training (HIIT) on the proteome and acetylome of human skeletal muscle, revealing the response of 3168 proteins and 1263 lysine acetyl-sites on 464 acetylated proteins. We identified novel protein adaptations to exercise training involved in metabolism and excitation-contraction coupling. Furthermore, HIIT increased the acetylation of mitochondrial proteins, particularly those of complex V, likely via non-enzymatic mechanisms. We also highlight the regulation of novel exercise-responsive histone acetyl-sites. These data demonstrate the plasticity of the skeletal muscle proteome and acetylome, providing insight into the regulation of contractile, metabolic and transcriptional processes within skeletal muscle. Herein, we provide a substantial hypothesis-generating resource to stimulate further mechanistic research investigating how exercise improves metabolic health.
2022-06-09 | PXD023084 | Pride