Decreased mitochondrial-related gene expression in adipose tissue after acute sprint exercise in humans
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PROVIDER: PRJNA1113706 | ENA |
REPOSITORIES: ENA
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Project description:The aim was to examine the acute effects of sprint exercise (SIT) on global gene expression in subcutaneous adipose tissue (AT) in healthy subjects to improve the understanding of how SIT may contribute to the maintenance of a healthy body weight. An SIT-induced upregulation of genes related to mitochondrial and fat metabolism was hypothesized. A total of 15 subjects performed three 30-s all-out sprints (SIT). Samples from AT, skeletal muscle (SM) and blood (brachial artery and a superficial subcutaneous abdominal vein) were obtained, up to 15 min after the last sprint. Purines such as hypoxanthine, xanthine or uric acid, sources of oxidative stress, increased markedly by SIT in both the artery and the abdominal vein. Purines also increased in AT and SM tissue. In response to SIT, a decreased signaling was predicted from the differential gene expression (z-score < -2 and -log(p-value) > 4) for mitochondrial related pathways such as oxidative phosphorylation, electron transport, ATP synthesis and heat production by uncoupling, mitochondrial fatty acid beta oxidation. Contrary to the hypothesis, a downregulation of various gene sets related to oxidative metabolism was shown after SIT. This could counteract possible negative effects of SIT-induced oxidative stress by an early stage “shutdown” of the mitochondria.
2024-10-30 | GSE267959 | GEO
Project description:The molecular mechanisms by which different exercise prescriptions dictate mitochondrial remodelling are poorly understood in humans. Here, we show that, compared to moderate-intensity continuous exercise (MICE), sprint-interval exercise (SIE) – a known time-efficient high-intensity exercise – leads to mitochondrial stress and transcriptionally activates the mitochondrial unfolded protein response (UPRmt).
2025-11-06 | GSE302582 | GEO
Project description:Aim: To examine the global gene expression response to the profound metabolic and hormonal stress induced by acute sprint exercise. Methods: Healthy women and men (n=14) performed 3 all-out cycle sprints interspersed by 20 min recovery. Muscle biopsies were obtained before the first and 2h and 20 min after the last sprint. Microarray analysis was performed to analyse the acute gene expression response. Repeated blood sample were also obtained. Results: In skeletal muscle, a set of immediate early genes, FOS, NR4A3, MAFF, EGR1, JUNB were markedly upregulated after sprint exercise. These genes were also upregulated, but to a lesser extent, after other exercise modes and after insulin exposure. Gene ontology analysis from 879 differentially expressed genes revealed predicted activation of extracellular remodelling and fat metabolism, which was in common with the gene expression response to endurance and resistance exercise. Moreover, the gene expression pattern indicated an increased turnover of skeletal muscle mass after sprint exercise, which was in common with data on resistance exercise and GH exposure. Insulin and GH may be involved in sprint-induced changes in the transcriptome, based on the overlap noted between sprint- and hormone exposure-related signatures. Furthermore, there were correlations between sprint-induced changes in hormonal levels and changes in gene expression. Conclusion: This is the first study reporting on global gene expression in skeletal muscle in response to acute sprint exercise. Several novel findings are presented related to novel sprint exercise - regulated genes as well as to shared gene signatures between sprint exercise, other exercise modes and exogenous hormone exposure.
2019-02-09 | GSE126296 | GEO
Project description:Exercise is recognized as a first-line lifestyle therapy for many cardiometabolic diseases, including obesity, type 2 diabetes, and hypertension. Despite the abundant health-promoting effects of exercise, in-depth characterization of circulatory factors mediating these benefits remain understudied in humans. Moreover, how different modes of exercise uniquely regulate these processes is unclear. Here, we address these questions by conducting a multi-cohort human exercise intervention, incorporating sprint-interval exercise (SIE), moderate-intensity exercise (MIE), and treadmill exercise to exhaustion to analyze intensity-dependent regulation of adipocytes and bulk adipose tissue. We find that exercise intensity uniquely influences the plasma proteome and plasma metabolome, and culturing primary human adipocytes with these plasma samples results in robust intensity-dependent transcriptome changes. We confirm many of these genes are similarly regulated by intense exercise in vivo, via RNA-sequencing of bulk adipose tissue following treadmill exercise to exhaustion. These findings underscore intensity-dependent regulation of adipose tissue following exercise.
2026-06-23 | GSE308252 | GEO
Project description:Mitochondria play a central role in cellular metabolism and are crucial for maintaining cellular health. Exercise is a proven intervention to enhance mitochondrial function and prevent non-communicable diseases, yet the molecular mechanisms driving exercise-induced mitochondrial remodelling remain unclear. This study compares the effects of moderate-intensity continuous exercise (MICE) and sprint-interval exercise (SIE) on mitochondrial adaptations. We demonstrate that SIE induces mitochondrial stress and activates the mitochondrial unfolded protein response (UPRmt), alongside disturbances in mitochondrial structure while MICE promotes mitochondrial adaptations characterized by increased mitochondrial content. Over an 8-week training period, moderate-intensity continuous training (MICT) and sprint-interval training (SIT) show divergent mitochondrial remodelling. Findings provide novel insights into the mechanisms by which different exercise prescriptions modulate mitochondrial signalling and remodelling in human skeletal muscle, offering a basis for personalized exercise strategies to optimize mitochondrial health.
2026-01-12 | PXD059070 | Pride
Project description:Sprint interval exercise (SIE) induces mitochondrial adaptations in skeletal muscle, comparable to or greater than moderate-intensity continuous exercise (MICE), despite lower training volume. These effects are partly due to enhanced mitochondrial bioenergetics, including increased Ca²⁺ uptake and pyruvate dehydrogenase (PDH) activation. Oleuropein (OLE), a compound from olive leaf extract, also promotes mitochondrial Ca²⁺ uptake and PDH activation in mice. The current study tested whether OLE could enhance these adaptations in humans during MICE or SIE. In a double-blind crossover design, healthy males performed either MICE or SIE with OLE supplementation. To elucidate the acute molecular response of skeletal muscle following exercise, we performed mass spectrometry-based proteomic analysis.
2026-05-13 | PXD072766 | Pride
Project description: Not available
| S-EPMC11492148 | biostudies-literature
Project description:Adipose Energy Homeostasis is the important guarantee to maintain the body's energy balance. Recently, it is reported that, in the adipose cell, Kisspeptins play important role in cell proliferation, differentiation, lipid metabolism and some adipocytokine secretion, so Kisspeptins maybe the novel targets of adipose energy homeostasis regulation. Adipose tissue is the core organs that regulates adipose energy homeostasis. Our early studies observed that there is organizational difference that exercise regulated adipose energy homeostasis, and the response of the Kisspeptins to exercise is closely related to the energy state of the body, so we speculated that Kisspeptins play some important role in the exercise regulated adipose energy homeostasis. Based on the cell experiments to clarify the role of Kisspeptins in regulating adipose energy homeostasis, the role of Kisspeptins in the regulation of adipose energy homeostasis were determined in the adipose tissue of conditioned Kiss1 gene knockout mice of CRISPR/Cas9, then we use the single cell transcriptome sequencing, untargeted proteome and targeted metabolome techniques to further explore and elucidate the possible pathways and mechanisms of Kisspeptins mediated adipose energy homeostasis regulated by exercise.
| PXD051630 |
Project description:Extracellular vesicles (EVs) have emerged as important mediators of inter-tissue signaling and exercise adaptations. In this human study (n=32), muscle-specific microRNA-1 (miR-1) was delivered to adipose tissue via EVs following an acute bout of resistance exercise. Using a multi-model machine learning automation tool, we discovered muscle primary miR-1 transcript and CD63+ EV count in circulation as top explanatory features for changes in adipose miR-1 levels in response to resistance exercise. RNA-sequencing (RNA-seq) and in-silico prediction of miR-1 target genes identified CAV2 and TRIM6 as miR-1 target genes upregulated in adipose tissue of participants with high increases in miR-1 levels following resistance exercise. Overexpression of miR-1 in differentiated human adipocyte-derived stem cells downregulated these miR-1 targets and enhanced catecholamine-induced lipolysis. These data identify a novel mechanism by which skeletal muscle communicates to adipose tissue and modulates lipolysis via delivery of miR-1-containing EVs.
2024-10-15 | GSE262576 | GEO
Project description:Exercise improves health and well-being across diverse organ systems, and elucidating mechanisms underlying the beneficial effects of exercise on health can lead to new therapies for disease. We find that exercise training in humans causes profound changes in subcutaneous adipose tissue (scWAT) gene expression, including genes encoding secreted proteins. In addition, we used our previously published microarray dataset derived from scWAT from mice housed in static cages (sedentary controls) or mice housed in cages with running wheels for 11 days. Genes that were significantly changed by exercise training in humans and mice were further selected by annotation for Extracellular Space in Gene Ontology. Of these genes, the most significantly correlated with the total wheel running distance in the trained mice was Tgfb2. We validated that exercise training increased TGFB2 mRNA in scWAT of human subjects using RT-qPCR. This led us to hypothesize that TGF-β2 is an exercise-induced adipokine. To determine the therapeutic potential and mechanism for increased TGF-β2, we investigated mouse models of exercise training and obesity. Our findings indicate that exercise training improves metabolism through inter-organ communication with fat via a TGF-β2 signaling, providing a novel mechanism for counteracting metabolic disease.
2018-11-21 | GSE116801 | GEO