Training-induced adaptation of oxidative phosphorylation in skeletal muscles.
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ABSTRACT:
SUBMITTER: Korzeniewski B
PROVIDER: S-EPMC1223571 | biostudies-other | 2003 Aug
REPOSITORIES: biostudies-other
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Project description:Exercise training promotes muscle adaptation and remodelling by balancing the processes of anabolism and catabolism; however, the mechanisms by which exercise delays accelerated muscle wasting are not fully understood. Intramuscular extracellular matrix (ECM) proteins are essential to tissue structure and function, as they create a responsive environment for the survival and repair of the muscle fibres. However, their role in muscle adaptation is underappreciated and underinvestigated. The PubMed, COCHRANE, Scopus and CIHNAL databases were systematically searched from inception until February 2021. The inclusion criteria were on ECM adaptation after exercise training in healthy adult population. Evidence from 21 studies on 402 participants demonstrates that exercise training induces muscle remodelling, and this is accompanied by ECM adaptation. All types of exercise interventions promoted a widespread increase in collagens, glycoproteins and proteoglycans ECM transcriptomes in younger and older participants. The ECM controlling mechanisms highlighted here were concerned with myogenic and angiogenic processes during muscle adaptation and remodelling. Further research identifying the mechanisms underlying the link between ECMs and muscle adaptation will support the discovery of novel therapeutic targets and the development of personalised exercise training medicine.
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Project description:BackgroundTo investigate how anatomical cross-sectional area and volume of quadriceps and triceps surae muscles were affected by ageing, and by resistance training in older and younger men, in vivo.MethodsThe old participants were randomly assigned to moderate (O55, n = 13) or high-load (O80, n = 14) resistance training intervention (12 weeks; 3 times/week) corresponding to 55% or 80% of one repetition maximum, respectively. Young men (Y55, n = 11) were assigned to the moderate-intensity strengthening exercise program. Each group received the exact same training volume on triceps surae and quadriceps group (Reps x Sets x Intensity). The fitting polynomial regression equations for each of anatomical cross-sectional area-muscle length curves were used to calculate muscle volume (contractile content) before and after 12 weeks using magnetic resonance imaging scans.ResultsOnly Rectus femoris and medial gastrocnemius muscle showed a higher relative anatomical cross-sectional area in the young than the elderly on the proximal end. The old group displayed a higher absolute volume of non-contractile material than young men in triceps surae (+ 96%). After training, Y55, O55 and O80 showed an increase in total quadriceps (+ 4.3%; + 6.7%; 4.2% respectively) and triceps surae (+ 2.8%; + 7.5%; 4.3% respectively) volume. O55 demonstrated a greater increase on average gains compared to Y55, while no difference between O55 and O80 was observed.ConclusionsMuscle loss with aging is region-specific for some muscles and uniform for others. Equivalent strength training volume at moderate or high intensities increased muscle volume with no differences in muscle volume gains for old men. These data suggest that physical exercise at moderate intensity (55 to 60% of one repetition maximum) can reverse the aging related loss of muscle mass.Trial registrationNCT03079180 in ClinicalTrials.gov . Registration date: March 14, 2017.
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Project description:Skeletal muscle has an enormous plastic potential and adapts to various stimuli such as mechanical stress, nutrients and hormones. While morphological changes observed in endurance trained muscles are well described, the molecular underpinnings of training adaptation is poorly understood. Therefore, the aim of our study was to define the molecular signature of a trained muscle and unravel the transcriptional responses of untrained and trained muscles to an acute bout of endurance exercise. Our results reveal that even though at baseline, the transcriptome of trained and untrained muscles is very similar, training status substantially affects the transcriptional response to an acute challenge, both quantitatively and qualitatively. Therefore, we provide novel insights into the complex molecular processes that are induced in response to exercise in a temporal- and training status-dependent manner. In addition, our study reveals that the epigenetic landscape contributes to the transcriptional memory of a trained muscle.
2023-08-04 | GSE221831 | GEO
Project description:Skeletal muscle has an enormous plastic potential and adapts to various stimuli such as mechanical stress, nutrients and hormones. While morphological changes observed in endurance trained muscles are well described, the molecular underpinnings of training adaptation is poorly understood. Therefore, the aim of our study was to define the molecular signature of a trained muscle and unravel the transcriptional responses of untrained and trained muscles to an acute bout of endurance exercise. Our results reveal that even though at baseline, the transcriptome of trained and untrained muscles is very similar, training status substantially affects the transcriptional response to an acute challenge, both quantitatively and qualitatively. Therefore, we provide novel insights into the complex molecular processes that are induced in response to exercise in a temporal- and training status-dependent manner. In addition, our study reveals that the epigenetic landscape contributes to the transcriptional memory of a trained muscle.
2023-08-04 | GSE221210 | GEO
Project description:Pathological and physiological stimuli, including acute exercise, activate autophagy; however, it is unknown whether exercise training alters basal levels of autophagy and whether autophagy is required for skeletal muscle adaptation to training. We observed greater autophagy flux (i.e., a combination of increased LC3-II/LC3-I ratio and LC3-II levels and reduced p62 protein content indicating a higher rate of initiation and resolution of autophagic events), autophagy protein expression (i.e., Atg6/Beclin1, Atg7, and Atg8/LC3) and mitophagy protein Bnip3 expression in tonic, oxidative muscle compared to muscles of either mixed fiber types or of predominant glycolytic fibers in mice. Long-term voluntary running (4 wk) resulted in increased basal autophagy flux and expression of autophagy proteins and Bnip3 in parallel to mitochondrial biogenesis in plantaris muscle with mixed fiber types. Conversely, exercise training promoted autophagy protein expression with no significant increases of autophagy flux and mitochondrial biogenesis in the oxidative soleus muscle. We also observed increased basal autophagy flux and Bnip3 content without increases in autophagy protein expression in the plantaris muscle of sedentary muscle-specific Pgc-1? transgenic mice, a genetic model of augmented mitochondrial biogenesis. These findings reveal that endurance exercise training-induced increases in basal autophagy, including mitophagy, only take place if an enhanced oxidative phenotype is achieved. However, autophagy protein expression is mainly dictated by contractile activity independently of enhancements in oxidative phenotype. Exercise-trained mice heterozygous for the critical autophagy protein Atg6 showed attenuated increases of basal autophagy flux, mitochondrial content, and angiogenesis in skeletal muscle, along with impaired improvement of endurance capacity. These results demonstrate that increased basal autophagy is required for endurance exercise training-induced skeletal muscle adaptation and improvement of physical performance.
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Project description:BackgroundMicroRNAs (miRNAs) are a type of non-coding small RNA ~22 nucleotides in length that regulate the expression of protein coding genes at the post-transcriptional level. Glycolytic and oxidative myofibers, the two main types of skeletal muscles, play important roles in metabolic health as well as in meat quality and production in the pig industry. Previous expression profile studies of different skeletal muscle types have focused on these aspects of mRNA and proteins; nonetheless, an explanation of the miRNA transcriptome differences between these two distinct muscles types is long overdue.ResultsHerein, we present a comprehensive analysis of miRNA expression profiling between the porcine longissimus doris muscle (LDM) and psoas major muscle (PMM) using a deep sequencing approach. We generated a total of 16.62 M (LDM) and 18.46 M (PMM) counts, which produced 15.22 M and 17.52 M mappable sequences, respectively, and identified 114 conserved miRNAs and 89 novel miRNA*s. Of 668 unique miRNAs, 349 (52.25%) were co-expressed, of which 173 showed significant differences (P?<?0.01) between the two muscle types. Muscle-specific miR-1-3p showed high expression levels in both libraries (LDM, 32.01%; PMM, 20.15%), and miRNAs that potentially affect metabolic pathways (such as the miR-133 and -23) showed significant differences between the two libraries, indicating that the two skeletal muscle types shared mainly muscle-specific miRNAs but expressed at distinct levels according to their metabolic needs. In addition, an analysis of the Gene Ontology (GO) terms and KEGG pathway associated with the predicted target genes of the differentially expressed miRNAs revealed that the target protein coding genes of highly expressed miRNAs are mainly involved in skeletal muscle structural development, regeneration, cell cycle progression, and the regulation of cell motility.ConclusionOur study indicates that miRNAs play essential roles in the phenotypic variations observed in different muscle fiber types.
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Project description:The homeodomain transcription factor Prep1 was previously shown to regulate insulin sensitivity. Our aim was to study the specific role of Prep1 for the regulation of energy metabolism in skeletal muscle. Muscle-specific ablation of Prep1 resulted in increased expression of respiratory chain subunits. This finding was consistent with an increase in mitochondrial enzyme activity without affecting mitochondrial volume fraction as assessed by electron microscopy. Metabolic phenotyping revealed no differences in daily energy expenditure or body composition. However, during treadmill exercise challenge, Prep1 ablation resulted in a higher maximal oxidative capacity and better endurance. Elevated PGC-1? expression was identified as a cause for increased mitochondrial capacity in Prep1 ablated mice. Prep1 stabilizes p160 Mybbp1a, a known inhibitor of PGC-1? activity. Thereby, p160 protein levels were significantly lower in the muscle of Prep1 ablated mice. By a chromatin immunoprecipitation-sequencing (ChIP-seq) approach, PREP1 binding sites in genes encoding mitochondrial components (e.g., Ndufs2) were identified that might be responsible for elevated proteins involved in oxidative phosphorylation (OXPHOS) in the muscle of Prep1 null mutants. These results suggest that Prep1 exhibits additional direct effects on regulation of mitochondrial proteins. We therefore conclude that Prep1 is a regulator of oxidative phosphorylation components via direct and indirect mechanisms.
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Project description:It has been shown previously that direct stimulation of oxidative-phosphorylation complexes in parallel with the stimulation of ATP usage is able to explain the stability of intermediate metabolite (ATP/ADP, phosphocreatine/creatine, NADH/NAD+, protonmotive force) concentrations accompanied by a large increase in oxygen consumption and ATP turnover during transition from rest to intensive exercise in skeletal muscle. It has been also postulated that intensification of parallel activation in the ATP supply-demand system is one of the mechanisms of training-induced adaptation of oxidative phosphorylation in skeletal muscle. In the present paper, it is demonstrated, using the computer model of oxidative phosphorylation in intact skeletal muscle developed previously, that the direct activation of oxidative phosphorylation during muscle contraction can account for the following kinetic properties of oxidative phosphorylation in skeletal muscle encountered in different experimental studies: (i) increase in the respiration rate per mg of mitochondrial protein at a given ADP concentration as a result of muscle training and decrease in this parameter in hypothyroidism; (ii) asymmetry (different half-transition time, t(1/2)) in phosphocreatine concentration time course between on-transient (rest-->work transition) and off-transient (recovery after exercise); (iii) overshoot in phosphocreatine concentration during recovery after exercise; (iv) variability in the kinetic properties of oxidative phosphorylation in different kinds of muscle under different experimental conditions. No other postulated mechanism is able to explain all these phenomena at the same time and therefore the present paper strongly supports the idea of the parallel activation of ATP usage and different oxidative-phosphorylation complexes during muscle contraction.
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