Acute Aerobic Exercise Alters PBMC microRNA Expression: Insights into Sport- and Sex-Specific Variations
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PROVIDER: PRJNA1219210 | ENA |
REPOSITORIES: ENA
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Project description:Studying microRNAs in the immune cells of athletes offers a novel perspective on the molecular regulation of immune function and recovery, potentially uncovering strategies to enhance performance and resilience to physical stress. However, PBMC microRNA expression in endurance athletes, such as runners and cyclists, remains underexplored, especially with regard to sex differences. This study aimed to (i) assess sport- and sex-specific differences in PBMC microRNA expression induced by acute aerobic exercise in runners and cyclists, (ii) evaluate the impact of maximal (trial A) and sub-maximal (trial B) exercises, and (iii) examine correlations between PBMC microRNAs and exercise performance. Methods: A total of 58 participants were included: 22 runners (9 females), 18 cyclists (9 females), and 18 active controls (9 females). Participants underwent VO2max and time-to-exhaustion tests, with blood samples collected pre- and post-exercise to analyze PBMC microRNA levels. Results: Runners exhibited a stronger microRNA response than cyclists or controls, with significant sex-based differences. After maximal intensity exercise, 279 microRNAs (255 upregulated) were altered in runners, compared to only 7 microRNAs (none upregulated) in cyclists. Exercise intensity and duration had sport-specific effects on microRNA expression. Time-to-exhaustion in runners and weekly training volume in both groups were significantly associated with changes in PBMC microRNA profiles. Conclusion: This study reveals that PBMC microRNA expression in response to acute aerobic exercise is sport- and sex-specific, providing new insights into the molecular adaptations of endurance athletes and their relationship to athletic performance.
2025-07-02 | GSE288760 | GEO
Project description:To investigate the effect of aerobic exercise on liver injury in nonalcoholic steatohepatitis (NASH), we established a NASH model induced by atherosclerotic (Ath) diet and intervened with aerobic exercise training.
2023-01-11 | GSE217155 | 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: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
Project description:Microarray analysis was performed with RNA isolated from vastus lateralis muscle biopsies of lean/overweight subjects following 18 days of aerobic exercise training. Samples from lean active individuals were also included. Exercise training led to robust changes in trained muscle. The lean active group profile was distinct from the pre-exercise samples. These results help define the molecular changes associated with aerobic training and contrast with an active phenotype.
2020-05-01 | GSE139258 | GEO
Project description:10 male subjects performed ~45 min one-legged cycling and 4 x 7 maximal concentric-eccentric knee extensions for each leg 15 min later. Thus, one limb performed aerobic and resistance exercise (AE+RE), while the opposing leg did resistance exercise only (RE). Biopsies were obtained from m. vastus lateralis of each leg 3 h after the resistance exercise bout. Gene expression analysis was carried out on the Affymetrix HuGene-2.1-st platform.
2016-05-24 | GSE74194 | GEO
Project description:High intensity aerobic exercise (90% of the maximum heart rate) can effectively suppress cancer proliferation in vivo. However, the molecular effect of aerobic exercise and its relevance to cancer prevention remains uninvestigated. The mRNA-sequencing technique (mRNA-seq) can provide a genome-wide depiction of gene expression changes by aerobic exercise. Mice with colorectal cancer were subjected to high intensity aerobic exercise, and mRNA-seq analysis was performed on heart, lung, and skeletal muscle tissues to analyze the molecular effects of the exercise in a genome-wide manner. The skeletal muscle-derived genes with exercise-dependent differential expressions were further evaluated for their effects on colorectal cancer cell viability. Regular and high intensity aerobic physical activity in the mice produced positive results in comprehensive parameters (i.e., food intake, weight, and survival rate) compared to those in the control groups (healthy and cancer with no exercise). A heatmap of differentially expressed genes revealed markedly different expression patterns between these groups. RNA-seq analysis of 23,282 skeletal muscle-derived genes identified a number of anticancer effector genes. Knockdown and overexpression of selected anticancer genes significantly repressed CT26 proliferation by 20% (p<0.05). Our finding based on the aerobic exercise cancer mouses model suggest that the high intensity exercise resulted in a global change in gene expression patterns, particularly those that affect cancer cell viability.
2022-07-13 | GSE191284 | GEO
Project description:High intensity aerobic exercise (90% of the maximum heart rate) can effectively suppress cancer proliferation in vivo. However, the molecular effect of aerobic exercise and its relevance to cancer prevention remains uninvestigated. The mRNA-sequencing technique (mRNA-seq) can provide a genome-wide depiction of gene expression changes by aerobic exercise. Mice with colorectal cancer were subjected to high intensity aerobic exercise, and mRNA-seq analysis was performed on heart, lung, and skeletal muscle tissues to analyze the molecular effects of the exercise in a genome-wide manner. The skeletal muscle-derived genes with exercise-dependent differential expressions were further evaluated for their effects on colorectal cancer cell viability. Regular and high intensity aerobic physical activity in the mice produced positive results in comprehensive parameters (i.e., food intake, weight, and survival rate) compared to those in the control groups (healthy and cancer with no exercise). A heatmap of differentially expressed genes revealed markedly different expression patterns between these groups. RNA-seq analysis of 23,282 skeletal muscle-derived genes identified a number of anticancer effector genes. Knockdown and overexpression of selected anticancer genes significantly repressed CT26 proliferation by 20% (p<0.05). Our finding based on the aerobic exercise cancer mouses model suggest that the high intensity exercise resulted in a global change in gene expression patterns, particularly those that affect cancer cell viability.
2022-07-13 | GSE191283 | GEO
Project description:High intensity aerobic exercise (90% of the maximum heart rate) can effectively suppress cancer proliferation in vivo. However, the molecular effect of aerobic exercise and its relevance to cancer prevention remains uninvestigated. The mRNA-sequencing technique (mRNA-seq) can provide a genome-wide depiction of gene expression changes by aerobic exercise. Mice with colorectal cancer were subjected to high intensity aerobic exercise, and mRNA-seq analysis was performed on heart, lung, and skeletal muscle tissues to analyze the molecular effects of the exercise in a genome-wide manner. The skeletal muscle-derived genes with exercise-dependent differential expressions were further evaluated for their effects on colorectal cancer cell viability. Regular and high intensity aerobic physical activity in the mice produced positive results in comprehensive parameters (i.e., food intake, weight, and survival rate) compared to those in the control groups (healthy and cancer with no exercise). A heatmap of differentially expressed genes revealed markedly different expression patterns between these groups. RNA-seq analysis of 23,282 skeletal muscle-derived genes identified a number of anticancer effector genes. Knockdown and overexpression of selected anticancer genes significantly repressed CT26 proliferation by 20% (p<0.05). Our finding based on the aerobic exercise cancer mouses model suggest that the high intensity exercise resulted in a global change in gene expression patterns, particularly those that affect cancer cell viability.
2022-07-13 | GSE191281 | GEO
Project description:Regulated in DNA Damage and Development 1 (REDD1) is a stress induced protein whose expression is highly induced in skeletal muscle following a single bout of aerobic exercise. However, the role of this induction is unknown We used microarrays to detail the change in gene signature within skeletal muscle following a single bout of aerobic exercise in wild type and REDD1 null mice
2017-10-05 | GSE97415 | GEO