Dataset Information

Adaptation-dependent alterations in the human skeletal muscle proteome and phosphoproteome of human skeletal muscle in response to damaging resistance exercise

ABSTRACT: Resistance exercise (RE) enhances strength, muscle mass, and overall health. Intense RE also triggers rapid muscle damage that is efficiently restored through proteostatic mechanisms in healthy individuals. However, the specific factors and signalling processes active at sites of damage remain poorly understood. In this study, human subjects underwent acute, recurring, and interrupted high-intensity RE to induce, adapt, and deadapt skeletal muscle. Muscle biopsies were taken at thee time points to analyse the skeletal muscle proteome's localization and phosphorylation under these conditions. RE-induced lesions were reduced through continued training but quickly reestablished upon detraining.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Skeletal Muscle

SUBMITTER: Pitter Huesgen

LAB HEAD: Pitter Huesgen

PROVIDER: PXD044976 | Pride | 2026-04-28

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	210920_A_MA_DIA_sportschool_human_M5_05_RH3_1_2778.d.zip	Other
	210920_A_MA_DIA_sportschool_human_M5_06_RH4_1_2779.d.zip	Other
	210920_A_MA_DIA_sportschool_human_M5_13_RG9_1_2766.d.zip	Other
	210920_A_MA_DIA_sportschool_human_M5_14_RG10_1_2767.d.zip	Other
	210920_A_MA_DIA_sportschool_human_M5_21_RG11_1_2771.d.zip	Other

Items per page:

1 - 5 of 173

Similar Datasets

Project description:The rates of obesity and sedentary lifestyle are on a dramatic incline, with associated detrimental health effects among women in particular. Although exercise prescriptions are useful for overcoming these problems, success can be hampered by differential responsiveness among individuals in cardiovascular fitness indices (i.e., improvements in strength, lipids, VO2max). Genetic factors appear to play an important role in determining this inter-individual variation in responsiveness. We performed microarray analyses on mRNA in whole blood from 60 sedentary women from a multi-ethnic cohort who underwent 12 weeks of exercise, to identify gene subsets that were differentially expressed between individuals who experienced the greatest and least improvements in fitness based upon a composite fitness score index. We identified 43 transcripts in 39 unique genes (FDR<10%; FC>1.5) whose expression increased the most in “high” versus “low” premenopausal female responders. Several (TIGD7, UQCRH, PSMA6, WDR12, TFB2M, USP15) have reported associations with fitness-related phenotypes. Bioinformatic analysis of the 39 genes identified 4 miRNAs whose expression has been linked to cardiovascular diseases (ANKRD22: miR-637, LRRFIP1: miR-132, PRKAR2B: miR-92a, RSAD2:miR-192). These 39 genes were enriched in 6 biological pathways, including the oxidative phosphorylation pathway (p=8.08 x 10-3). Two genes, LRRFIP1 and SNORD30, were also identified with lower expression in high responding postmenopausal women. In summary, we identified gene signatures based on mRNA analysis that define responsiveness to exercise in a largely minority-based female cohort. Importantly, this study validates several genes/pathways previously associated with exercise responsiveness and extends these findings with additional novel genes. We performed microarray analyses on mRNA in whole blood from 60 sedentary women from a multi-ethnic cohort who underwent 12 weeks of exercise, to identify gene subsets that were differentially expressed between individuals who experienced the greatest and least improvements in fitness based upon a composite fitness score index.

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.

Dataset Information

Adaptation-dependent alterations in the human skeletal muscle proteome and phosphoproteome of human skeletal muscle in response to damaging resistance exercise

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets