Skeletal Muscle Adaptations to Exercise Training in Young and Aged Horses
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ABSTRACT:
SUBMITTER: Latham C
PROVIDER: S-EPMC9261331 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundWe have recently shown that 12 weeks of progressive aerobic exercise training improves whole-muscle size and function in older women. The purpose of this investigation was to evaluate molecular markers that may be associated with muscle hypertrophy after aerobic training in aging skeletal muscle.MethodsMuscle biopsies were obtained before and after 12 weeks of aerobic exercise training on a cycle ergometer in nine older women (70 ± 2 years) to determine basal levels of messenger RNA and protein content of select myogenic, proteolytic, and mitochondrial factors.ResultsThe training program increased (p < .05) aerobic capacity 30 ± 9%, whole-muscle cross-sectional area 11 ± 2%, and whole-muscle force production 29 ± 8%. Basal messenger RNA levels of FOXO3A, myostatin, HSP70, and MRF4 were lower (p < .05) after aerobic training. FOXO3A, FOXO3A phosphorylation, and HSP70 protein content were unaltered after training. Mitochondrial protein COX IV was elevated (p < .05) 33 ± 7% after aerobic training, whereas PGC-1α protein content was 20 ± 5% lower (p < .05).ConclusionsThese data suggest that reductions in FOXO3A and myostatin messenger RNA are potentially associated with exercise-induced muscle hypertrophy. Additionally, it appears that mitochondrial biogenesis can occur with aerobic training in older women independent of increased PGC-1α protein. Aerobic exercise training alters molecular factors related to the regulation of skeletal muscle, which supports the beneficial role of aerobic training for improving muscle health in older women.
| S-EPMC2954235 | biostudies-literature
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:BackgroundA single bout of exercise induces changes in gene expression in skeletal muscle. Regular exercise results in an adaptive response involving changes in muscle architecture and biochemistry, and is an effective way to manage and prevent common human diseases such as obesity, cardiovascular disorders and type II diabetes. However, the biomolecular mechanisms underlying such responses still need to be fully elucidated. Here we performed a transcriptome-wide analysis of skeletal muscle tissue in a large cohort of untrained Thoroughbred horses (n = 51) before and after a bout of high-intensity exercise and again after an extended period of training. We hypothesized that regular high-intensity exercise training primes the transcriptome for the demands of high-intensity exercise.ResultsAn extensive set of genes was observed to be significantly differentially regulated in response to a single bout of high-intensity exercise in the untrained cohort (3241 genes) and following multiple bouts of high-intensity exercise training over a six-month period (3405 genes). Approximately one-third of these genes (1025) and several biological processes related to energy metabolism were common to both the exercise and training responses. We then developed a novel network-based computational analysis pipeline to test the hypothesis that these transcriptional changes also influence the contextual molecular interactome and its dynamics in response to exercise and training. The contextual network analysis identified several important hub genes, including the autophagosomal-related gene GABARAPL1, and dynamic functional modules, including those enriched for mitochondrial respiratory chain complexes I and V, that were differentially regulated and had their putative interactions 're-wired' in the exercise and/or training responses.ConclusionHere we have generated for the first time, a comprehensive set of genes that are differentially expressed in Thoroughbred skeletal muscle in response to both exercise and training. These data indicate that consecutive bouts of high-intensity exercise result in a priming of the skeletal muscle transcriptome for the demands of the next exercise bout. Furthermore, this may also lead to an extensive 're-wiring' of the molecular interactome in both exercise and training and include key genes and functional modules related to autophagy and the mitochondrion.
| S-EPMC5551008 | biostudies-literature
Project description:The molecular mechanisms underlying the response to exercise and inactivity are not fully understood. We propose an innovative approach to profile the skeletal muscle transcriptome to exercise and inactivity using 66 published datasets. Data collected from human studies of aerobic and resistance exercise, including acute and chronic exercise training, were integrated using meta-analysis methods (www.metamex.eu). Here we use gene ontology and pathway analyses to reveal selective pathways activated by inactivity, aerobic versus resistance and acute versus chronic exercise training. We identify NR4A3 as one of the most exercise- and inactivity-responsive genes, and establish a role for this nuclear receptor in mediating the metabolic responses to exercise-like stimuli in vitro. The meta-analysis (MetaMEx) also highlights the differential response to exercise in individuals with metabolic impairments. MetaMEx provides the most extensive dataset of skeletal muscle transcriptional responses to different modes of exercise and an online interface to readily interrogate the database.
| S-EPMC6981202 | biostudies-literature
Project description:ObjectiveMitochondria are organelles primarily responsible for energy production, and recent evidence indicates that alterations in size, shape, location, and quantity occur in response to fluctuations in energy supply and demand. We tested the impact of acute and chronic exercise on mitochondrial dynamics signaling and determined the impact of the mitochondrial fission regulator Dynamin related protein (Drp)1 on exercise performance and muscle adaptations to training.MethodsWildtype and muscle-specific Drp1 heterozygote (mDrp1+/-) mice, as well as dysglycemic (DG) and healthy normoglycemic men (control) performed acute and chronic exercise. The Hybrid Mouse Diversity Panel, including 100 murine strains of recombinant inbred mice, was used to identify muscle Dnm1L (encodes Drp1)-gene relationships.ResultsEndurance exercise impacted all aspects of the mitochondrial life cycle, i.e. fission-fusion, biogenesis, and mitophagy. Dnm1L gene expression and Drp1Ser616 phosphorylation were markedly increased by acute exercise and declined to baseline during post-exercise recovery. Dnm1L expression was strongly associated with transcripts known to regulate mitochondrial metabolism and adaptations to exercise. Exercise increased the expression of DNM1L in skeletal muscle of healthy control and DG subjects, despite a 15% ↓(P = 0.01) in muscle DNM1L expression in DG at baseline. To interrogate the role of Dnm1L further, we exercise trained male mDrp1+/- mice and found that Drp1 deficiency reduced muscle endurance and running performance, and altered muscle adaptations in response to exercise training.ConclusionOur findings highlight the importance of mitochondrial dynamics, specifically Drp1 signaling, in the regulation of exercise performance and adaptations to endurance exercise training.
| S-EPMC6407367 | biostudies-literature
Project description:Investigate the effects loss of skeletal muscle Bmal1 has on exercise training via transcriptional analysis (RNA-sequencing).
2024-07-02 | GSE240653 | GEO
Project description:Purpose: RNA-seq method was used to select genes expressed in muscle tissue and are potentially associated with exercise adaptation in Arabian horses. Methods: Whole transcriptomes between three time points of muscle tissue collection were compared: T0 (untrained horses), T1 (horses after intense gallop phase) and T2 (at the end of the racing season), in total 23 samples. The biopsy of gluteus medius muscle was performed by using minimally invasive ProMag™ Ultra Automatic Biopsy Instrument with a 2 mm diameter biopsy needle. The total RNA was isolated using by TriReagent and 300ng was used to cDNA libraries preparation. The NGS sequencing was performed on HiScan SQ (Illumina). The quantifying transcript abundances was made using the RSEM supported by STAR aligner. The raw reads were aligned to the Equus caballus reference genome. Differentially expressed genes were detected by DESeq2. The RNA-seq results were validated using by qPCR. Results: To detected differentially expressed genes during training preparing to the flat racing, whole transcriptomes between three time points of muscle tissue collection were compared: T0 (untrained horses), T1 (horses after intense gallop phase) and T2 (at the end of the racing season). We identified 1168 DEGs between T0 vs T1; 1593 between T1 vs T2 and 763 between T2 vs T0. The analysis for all DEGs allow to detect 11 pathways which ale significant over represented between at last two training periods. The numerous group of exercise-regulated DEGs was related with muscle cell structure and signaling (‘focal adhesion’, ‘adherens juntion’ and ‘PI3-ATK signaling’) and included insulin-like growth factor 1 receptor (IGF1R); insulin receptor (INSR); transforming growth factor beta receptors 1 and 2 (TGFBR1; TGFBR2); vascular endothelial growth factor B (VEGFB); epidermal growth factor (EGF); hepatocyte growth factor (HGF) and vascular endothelial growth factor D (FIGF). Our results showed that in Arabian horses exercise modified the expression of genes belonging to the ‘PPAR signaling pathway’ (e.g. PPARA; PPARD; PLIN2); ‘calcium signaling pathway’ (e.g. PLN; PLCD1; TNNC1; TNNC2) as well as pathways associated with metabolism processes - ‘oxidative phosphorylation’; ‘fatty acid metabolism’; ‘glycolysis/gluconeogenesis’ and ‘citrate cycle’. Conclusions: Our research allowed to identify the group of exercise-regulated genes which was related with muscle cell structure as well as signaling and pinpointed the significant metabolic processes critical for adaptive response during training. We confirmed that in Arabians, the exercise switch energy generation towards fatty acid utilization, enhance glycogen transport and calcium signaling. The sequencing of skeletal muscle transcriptome allowed to propose the panel of new candidate genes (such as SLC16A1; ME3; ACTN3; PPARα; SH3RF2; TPM3; TNNC1; TNNI3; TGFBR1; TGFBR2; FABP3) potentially related with body homeostasis maintenance and race performance in Arabian horse.
2016-10-21 | GSE88951 | GEO
Project description:Maximal strength training (MST) results in robust improvements in skeletal muscle force production, efficiency, and mass. However, the effects of MST on muscle mitochondria are still unknown. Accordingly, the purpose of this study was to examine, from the molecular level to whole-muscle, mitochondrial adaptations induced by 8 weeks of knee-extension MST in the quadriceps of 10 older adults using immunoblotting, spectrophotometry, high-resolution respirometry in permeabilized muscle fibers, in vivo 31P magnetic resonance spectroscopy (31P-MRS), and gas exchange. As anticipated, MST resulted in an increased isometric knee-extensor force from 133 ± 36 to 147 ± 49 Nm (p < .05) and quadriceps muscle volume from 1,410 ± 103 to 1,555 ± 455 cm3 (p < .05). Mitochondrial complex (I-V) protein abundance and citrate synthase activity were not significantly altered by MST. Assessed ex vivo, maximal ADP-stimulated respiration (state 3CI+CII, PRE: 23 ± 6 and POST: 14 ± 5 ρM·mg-1·s-1, p < .05), was decreased by MST, predominantly, as a result of a decline in complex I-linked respiration (p < .05). Additionally, state 3 free-fatty acid linked respiration was decreased following MST (PRE: 19 ± 5 and POST: 14 ± 3 ρM·mg-1·s-1, p < .05). Assessed in vivo, MST slowed the PCr recovery time constant (PRE: 49 ± 13 and POST: 57 ± 16 seconds, p < .05) and lowered, by ~20% (p = .055), the quadriceps peak rate of oxidative ATP synthesis, but did not significantly alter the oxidation of lipid. Although these, likely qualitative, mitochondrial adaptations are potentially negative in terms of skeletal muscle energetic capacity, they need to be considered in light of the many improvements in muscle function that MST affords older adults.
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Project description:Skeletal muscle is highly plastic and dynamically regulated by the body's physical demands. This study aimed to determine the plasticity of skeletal muscle DNA methylation in response to 8 weeks of supervised exercise training in volunteers with a range of insulin sensitivities. We studied 13 sedentary participants and performed euglycemic hyperinsulinemic clamps with basal vastus lateralis muscle biopsies and peak aerobic activity (VO2 peak) tests before and after training. We extracted DNA from the muscle biopsies and performed global methylation using Illumina's Methylation EPIC 850K BeadChip. Training significantly increased peak aerobic capacity and insulin-stimulated glucose disposal. Fasting serum insulin and insulin levels during the steady state of the clamp were significantly lower post-training. Insulin clearance rates during the clamp increased following the training. We identified 13 increased and 90 decreased differentially methylated cytosines (DMCs) in response to 8 weeks of training. Of the 13 increased DMCs, 2 were within the following genes, FSTL3, and RP11-624M8.1. Of the 90 decreased DMCs, 9 were within the genes CNGA1, FCGR2A, KIF21A, MEIS1, NT5DC1, OR4D1, PRPF4B, SLC26A7, and ZNF280C. Moreover, pathway analysis showed an enrichment in metabolic and actin-cytoskeleton pathways for the decreased DMCs, and for the increased DMCs, an enrichment in signal-dependent regulation of myogenesis, NOTCH2 activation and transmission, and SMAD2/3: SMAD4 transcriptional activity pathways. Our findings showed that 8 weeks of exercise training alters skeletal muscle DNA methylation of specific genes and pathways in people with varying degrees of insulin sensitivity.
| S-EPMC8953782 | biostudies-literature
Project description:Exercise decreases adiposity and improves metabolic health; however, the physiological and molecular underpinnings of these phenomena remain unknown. Here, we investigate the effect of endurance training on adipose progenitor lineage commitment. Using mice with genetically labeled adipose progenitors, we show that these cells react to exercise by decreasing their proliferation and differentiation potential. Analyses of mouse models that mimic the skeletal muscle adaptation to exercise indicate that muscle, in a non-autonomous manner, regulates adipose progenitor homeostasis, highlighting a role for muscle-derived secreted factors. These findings support a humoral link between skeletal muscle and adipose progenitors and indicate that manipulation of adipose stem cell function may help address obesity and diabetes.
| S-EPMC4807773 | biostudies-literature