Sprint exercise shares gene signatures with other exercise modes and hormone exposure and induces stronger upregulation of immediate early genes
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PROVIDER: PRJNA521490 | ENA |
REPOSITORIES: ENA
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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: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:Decreased mitochondrial-related gene expression in adipose tissue after acute sprint exercise in humans
| PRJNA1113706 | ENA
Project description:The methylome and transcriptome signatures following exercise that are physiologically and metabolically relevant to sporting contexts such as team sports or health prescription scenarios (e.g. high intensity interval training/HIIT) has not been investigated. To explore this, we performed two different sport/exercise relevant high-intensity running protocols in 5 male sport team members using a repeated measures design of: 1) Change of direction (COD) versus; 2) straight line (ST) exercise with a wash-out period of at least 2 weeks between trials. Skeletal muscle biopsies collected from the vastus lateralis 30 minutes and 24 hours post exercise, were assayed using 850K methylation arrays and a comparative analysis with recent (subject-unmatched) sprint and acute aerobic exercise meta-analysis transcriptomes was performed. Despite COD and ST exercise being matched for classically defined intensity measures (speed x distance and number of accelerations/decelerations), COD exercise elicited greater movement (GPS-Playerload), physiological (HR), metabolic (lactate) as well as central and peripheral (differential RPE) measures compared with ST exercise, suggesting COD exercise evoked a higher exercise intensity. The exercise response alone across both conditions evoked extensive alterations in the methylome 30 mins and 24 hrs post exercise, particularly in MAPK, AMPK and axon guidance pathways. COD evoked a considerably greater hypomethylated signature across the genome compared with ST exercise, particularly at 30 minutes post exercise, enriched in: Protein binding, MAPK, AMPK, insulin, and axon guidance pathways. Comparative methylome analysis with sprint running transcriptomes identified considerable overlap, with 49% of genes that were altered at the expression level also differentially methylated after COD exercise. After differential methylated region analysis, we observed that VEGFA and its downstream nuclear transcription factor, NR4A1 had enriched hypomethylation within their promoter regions. VEGFA and NR4A1 were also significantly upregulated in the sprint transcriptome and meta-analysis of exercise transcriptomes. We confirmed increased gene expression of VEGFA, and considerably larger increases in the expression of canonical metabolic genes, PPARGC1A (that encodes PGC1-α) and NR4A3 in COD vs. ST exercise. Overall, we demonstrate that increased physiological/metabolic load via change of direction exercise in human skeletal muscle evokes considerable epigenetic modifications that are associated with changes in expression of genes responsible for adaptation to exercise.
2021-01-21 | GSE162288 | GEO
Project description:To characterize phosphorylation-based signaling events across different exercise modalities we subjected eight healthy young men (age, 26.3±1.3 years; BMI, 23.5±0.7 kg/m2; maximal oxygen uptake (VO2 max), 42.6±1.5 ml/kg/min) that did not perform regular physical activity apart from local bicycling to an acute bout of endurance (90 min ~60% of VO2 max), sprint (3 x 30-s all-out cycling), or resistance exercise (6 sets of 10 RM knee extensions) in the fasting state. All participants completed the three types of exercise in a randomized crossover design with 14 days washout between each exercise bout.
2022-07-18 | PXD031049 | Pride
Project description:Comparative analysis of mouse cardiac left ventricle gene expression: voluntary wheel exercise and pregnancy-induced cardiac hypertrophy We performed microarray analysis on RNA from left ventricles of mice in non-pregnant diestrus cycle, mid-pregnancy (MP), late-pregnancy (LP), and immediate post-partum (0PP). These were compared to 7days (7EX) and 21 days (21EX) of voluntary wheel running exercise.
2012-03-08 | E-GEOD-36330 | biostudies-arrayexpress
Project description:Systolic Blood Pressure Intervention Trial (SPRINT-Imaging)
| PRJNA1079434 | ENA
Project description:Systolic Blood Pressure Intervention Trial (SPRINT-BioLINCC)
| PRJNA1047941 | ENA
Project description:Systolic Blood Pressure Intervention Trial (SPRINT-BioLINCC)
| PRJNA1047942 | ENA
Project description:Objective: Athletes increasingly engage in repeated sprint training that consists of repeated short all-out effort interspersed by short periods of recovery. When performed in hypoxia (RSH), it may lead to greater training effects than in normoxia (RSN), however the underlying molecular mechanisms remain unclear. This study aimed at elucidating the effects of RSH on skeletal muscle oxidative and glycolytic adaptations as compared to RSN. Methods: Healthy young men performed nine repeated sprint training sessions in three weeks. Each training session consisted in six series of six sprints in either normoxia (FiO2 = 20.9%, RSN, n = 7) or normobaric hypoxia (FiO2 = 13.6%, RSH, n = 9). Before and after the training period, exercise performance was assessed by using repeated sprint ability (RSA) and Wingate tests. Vastus lateralis muscle biopsies were performed to investigate muscle metabolic adaptations using proteomic combined to western blotting analyses. Results: We observed similar improvements in RSA and Wingate tests in both RSH and RSN groups. Proteomic analysis revealed a decrease in several proteins involved in oxidative phosphorylation (OXPHOS) in both groups and this was confirmed with western blot showing significant reductions in complexes I and V protein levels. RSN and RSH increased protein levels of the glycolytic enzyme hexokinase II, while only RSH induced a significant increase in the glucose transporter 4 (GLUT4) protein levels, suggesting superior glycolytic adaptations in response to hypoxia. This phenotype is further supported by proteomics data showing significant increase of proteins involved in glycolysis. Our proteomics data showed in the RSH group a specific increase in several S100A family proteins, among which S100A13 was the most modified, a result confirmed by western blot. S100A proteins have recently been shown to accelerate glycolytic phenotype of cancer cells by activating the protein kinase B (Akt) pathway. Our data corroborate these findings by showing in RSH group increased Akt phosphorylation as well as increased levels of proteins related to Akt downstream effects such as enhanced translation. Conclusions: Altogether our data indicate that RSH, as compared to RSN, potentiates the muscle glycolytic phenotype, possibly through the activation of S100A13 and the Akt pathway.
2024-05-05 | PXD040779 | Pride