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However, a growing amount of animal research suggests hyperplasia is a result of ATP-PC training, but only a few studies represent hyperplasia occurring in humans. Myosin heavy chain II: In addition to cross sectional muscle area increases hypertrophy ,.

additional myosin heavy chain II isoforms are present as a result of ATP-PC training. Type I and Type II fiber area: ATP-PC training also has the ability to alter muscle fiber area. Heavily trained subjects depending on training intensity and volume have experienced major alteration in type II muscle fiber diameter in comparison to type I.

Chronic ATP-PC training can have the ability to affect the aerobic metabolism of type I fibers. As type II fibers increase in cross-sectional size, mitochondrial and capillary densities decrease.

The absolute mitochondrial and capillary volumes remain unchanged, however, substrate transport, oxygen utilization and carbon dioxide withdraw may be limited. The end result is a theorized decrease in cardiovascular capacity. ATP-PC training of high intensity and slow-speed utilizing Isokinetic loading may increase several biochemical mechanisms.

Muscle glycogen content, CP, ATP, ADP, creatine, phosphorylase, phosphofructokinase and Krebs cycle enzyme activity are all speculated to experience increased levels under the presence of ATP-PC training. However, ATP-PC training at higher speeds, more related to Power Training, do not replicate the same biochemical results.

Power training will elicit similar results as experienced with ATP-PC training, particularly the neuromuscular effects. However, in addition to the neural adaptations of muscle with ATP-PC training, power training also stresses the elastic components.

Power training, often carried out with the utilization of plyometric loading and emphasizes the stress of the stretch shortening cycle SSC. More specifically, power training generally involves sudden eccentric stress the stretch of the muscle followed by a sudden, rapid fast movement concentric contraction.

The results of power training are not only increases in muscle strength but also shortening muscle contractile time.

Primary neuromuscular adaptations witnessed with power training are shortening the time of motor unit recruitment, particularly of the type IIx and IIa fibers and heightening the tolerance of motor neurons to greater intervention frequencies. Power training also activates greater intramuscular coordination.

Improved linkage between nerve impulses and skeletal muscle, results in greater neuromuscular coordination of the agonist and antagonist muscles. This adaptation is similar to the discussion above regarding co activation.

The magnitude of change and adaptation within skeletal muscle is vast. Largely contingent on the stress placed on upon the body from a training standpoint, muscle will respond and adapt differently, based on the type and modality of exercise.

These adaptations are the major players for improved performance. Specifically, capillary content creates improved interchange of gasses, heat, waste and nutrients between the working skeletal muscle and the blood delivered during exercise.

Increased myoglobin content has the capacity to store oxygen and release it, particularly when oxygen becomes sparse during muscle contraction during prolonged cardiovascular exercise. Given aerobic energy production occurs within the mitochondria, the improvement of its function, particularly in size and number, becomes an obvious player in improved cardiovascular performance.

Lastly, from a cardiovascular standpoint, the efficiency of enzymatic activity is demonstrated to create mitochondrial changes which therefore serves as a vehicle for slower use of muscle glycogen and a reduced production of lactate during exercise at given intensities.

This adaptation likely serves as a major prayer in a heighted lactate threshold. This neutralizing muscle adaption limits effect lactate has on skeletal muscle, therefore delaying performance fatigue. Training within the energy system of the ATP-PC system, results in primarily neuromuscular and contractile component adaptations such as hypertrophy and co-coordination of the muscles.

Finally co-activation agonist and antagonist muscles improvements by reducing the amount of resistive force of antagonist muscle, is supported to contribute to greater force production of agonist muscles.

Similarly, power training results in significant neuromuscular adaptations, however, the elasticity of muscle, specifically the SSC, is more pronounced within power training.

Given that most power training involves sudden eccentric stress the stretch of the muscle followed by a sudden, rapid fast movement concentric contraction, chronic power training may lead to increases in muscle strength but also shortening muscle contractile time. Training for power also shortens the time of motor unit recruitment, particularly of the type IIx and IIa fibers, therefore heightening the tolerance of motor neurons to improve intervention frequencies.

Specifically, a more expedited initiation and excitement of the discharge rate of type IIx and IIa muscle fibers will in turn increase the synchronization of motor units and the rate of firing. The plasticity of muscle is highly contingent on the stress placed upon it and the adaptions are extensively different and described above.

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Home MOJSM Physiological and physical adaptations within the working muscle specific to cardiovascular training lactate training adenosine triphosphate phosphocreatine training and power training.

Research Article Volume 1 Issue 4. ATP-PC: Adensosine Triphosphate-Phosphocreatine; SSC: Stretch Shortening Cycle. Neuromuscular One of the most significant adaptations of ATP-PC training that explains much of the gains that are made by the athletes that are trained are neural.

The first, Transient lasts only a short time immediately after a training bout and is caused by fluid buildup from blood plasma in the interstitial and intercellular spaces within muscle. Author declares there is no conflict of interest in publishing the article.

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Physiological and physical adaptations within the working muscle specific to cardiovascular training, lactate training, adenosine triphosphate-phosphocreatine training and power training.

MOJ Sports Med. DOI: Download PDF. Objectives: The purpose of the present review study is to review the existing literature regarding the physiological and physical adaptations within working skeletal muscle specific to cardiovascular training, lactate training, adenosine triphosphate-phosphocreatine training and power training.

Methods: A search was conducted on the wide-body of research that exists in and around the skeletal muscle and sports performance and aligns the research in a clear manner, specifically describing the physiological response of various training to cellular muscle.

Literature gathered involved trails of comparative analysis with control groups in various exercise settings. Results : In an attempt to clarify the physiological adaptations to working skeletal muscle, the purpose of this review is to determine what affect 4 different types of conditioning reflects in terms of structural, metabolic, enzymatic, neuromuscular and contractile.

The present study identifies each adaptation specific to the training modality to clarify the scientific evidence for the sport practitioner.

Keywords: Muscle adaptations; Adenosine triphosphate; Cardiovascular training; Power training. The capacity for change within skeletal muscle is immense. Represented by gene expression on a molecular level, the alteration of muscle generally results in an increase or decrease in the amount of muscle proteins.

When exercise stress is placed upon the skeletal muscle, the magnitude of adaptation is highly contingent upon plasticity of muscle. Thus, the Principal of Myoplasticityis the specific term that represents the capacity of muscle that is modifiable for adaptation and applies to the ensuing discussion related to muscular training adaptations.

Cardiovascular training on a structural level elicits a significant increase in activation frequency of motor units and a slight increase in oppositional load against motor units. Quintessential cardiovascular training that presents this stimulus to the muscle is represented in weight bearing settings i.

Cardiovascular training results in little to no effect on the cross-sectional area of muscle and muscle fibers. However, specific to type I slow-twitch fibers, these fibers may experience slight increases in cross sectional size due to increases glycogen storage as well as oxidative metabolism.

The adaptations to muscle under the influence of cardiovascular training produce changes in fiber type, capillary supply, myoglobin content, mitochondrial function and oxidative enzymes. Cardiovascular training relies primarily on type I, slow-twitch muscle fibers.

In response to the volume and intensity of training, type I fibers have the capability to become larger in cross-sectional area. Similarly, most literature suggests little change in muscle fiber percentage in slow-twitch and fast-twitch fibers; however, changes have been documented in fast-twitch subtypes.

Type IIx fast-twitch fibers have called upon less during cardiovascular training, consequently, possess a lower aerobic capacity. Recent literature produced by the HERITAGE study suggests that type IIx fast-twitch fibers may transform to type IIa and it is even speculated they may be capable of transitioning to slow-twitch.

However, very minuscule results have been published. A significant adaptation to cardiovascular training is the increase in capillaries surrounding the muscle fibers. Literature has documented that cardiovascular trained individuals have significantly greater amounts of capillary density than compared to sedentary populations.

Upon entering the muscle, oxygen binds with an iron-containing compound that resembles hemoglobin called myoglobin. Myoglobin transports oxygen molecules from the cell membrane to the mitochondria. Of importance to cardiovascular training, myoglobin has the capacity to store oxygen and release it, particularly when oxygen becomes sparse during muscle contraction.

The release of oxygen often occurs during the lag time between the beginning of exercise and the amplified cardiovascular transportation of oxygen. This adaption of muscle significantly impacts the ability for oxidative metabolism.

Aerobic energy production occurs within the mitochondria. Therefore the affect on the mitochondrial function is obvious. The major adaptations with cardiovascular training on the mitochondria are increases in size and number.

As the volume of cardiovascular training rises, so do the number and the size of the mitochondria. Mitochondrial efficiency and the oxidative formation of ATP are increased by oxidative enzymes.

Training induced enzyme activity contributes not only to the number and size of the mitochondria, but also to the metabolic consequence of mitochondrial changes.

It is suggested that increased enzyme activity creating mitochondrial changes creates a slower use of muscle glycogen and a reduced production of lactate during exercise at given intensities.

This adaptation is likely to have great importance to ones lactate threshold. Muscle glycogen is often the primary substrate for cardiovascular exercise. The primary response for depleted glycogen storage is a heighted resynthesis capacity.

With proper recover and dietary intake, cardiovascularly trained muscle stores significantly greater amounts of glycogen. Furthermore, muscular enzymes responsible for lipid breakdown are increased with cardiovascular training. This adaptation allows for trained muscle to oxidize lipids, decreasing the breakdown of glycogen.

In addition to the cardiovascular adaptations and benefits discussed above, lactate training results in a few other key muscle adaptations. Lactate training places high stress on the glycolytic system within the muscle resulting in high amounts of lactate accumulation.

Training under the presence of lactate will lead to increased removal avenues. Increased lactate transporter, monocarboxylate MCT and mitochondrial proteins are expressed in greater capacities in response of higher lactate concentrations and heighten the muscles potential for lactate removal.

Intercellular buffer capacity also contributes to the removal of lactate during lactate training. Physicochemical buffering proteins, dipeptides and phosphates within skeletal muscle increase the efficiency of lactate removal when lactate training is performed.

Similarly, the local formation of lactate within skeletal muscle is theorized as a potential mechanism for adaptation of muscular pH regulation.

PH displacement during lactate training may result in adaptations for improved lactate clearance. The overall adaptation of lactate training is to increase lactate tolerance of skeletal muscle. Buffering and removal capacities of skeletal muscle allow for increased concentration of muscle and blood lactate.

Thus, neutralizing the effect lactate plays on muscle, therefore delaying performance fatigue. One of the most significant adaptations of ATP-PC training that explains much of the gains that are made by the athletes that are trained are neural. Motor unit recruitment and synchronization explain much of the gains that are made during ATP-PC training in the absence of hypertrophy.

Similarly, the more units recruited to perform muscle actions, lead to maximal contraction capabilities. Autogenic inhibitory mechanisms i. Co-activation agonist and antagonist muscles may be another neural factor to ATP-PC training.

Reducing the amount of resistive force of antagonist muscle may contribute to greater force production of agonist muscles. Although speculated to provide minimal contribution, the reduction of co-activation may contribute to neuromuscular adaptations leading to greater force production.

Finally, rate coding may be a contributing neuromuscular factor contributing to greater force production succeeding ATP-PC training. The firing frequency of motor units, known as rate coding, may also lead to force generating improvements.

Although not well documented, evidence does exist to underpin this ATP-PC training mechanism. Hypertrophy: Two types of muscle hypertrophy occur with ATP-PC training. The first,. Transient lasts only a short time immediately after a training bout and is caused by fluid buildup from blood plasma in the interstitial and intercellular spaces within muscle.

Chronic hypertrophy reflects the actual muscle structure size increases that are a result of fiber hypertrophy increase in existing fiber size or fiber hyperplasia increase in actual number of fibers.

Early research established that the number of muscle fibers an individual possess is genetic and the alteration of muscle size rests solely in fiber hypertrophy. However, a growing amount of animal research suggests hyperplasia is a result of ATP-PC training, but only a few studies represent hyperplasia occurring in humans.

Myosin heavy chain II: In addition to cross sectional muscle area increases hypertrophy ,. additional myosin heavy chain II isoforms are present as a result of ATP-PC training.

Type I and Type II fiber area: ATP-PC training also has the ability to alter muscle fiber area. Heavily trained subjects depending on training intensity and volume have experienced major alteration in type II muscle fiber diameter in comparison to type I.

Chronic ATP-PC training can have the ability to affect the aerobic metabolism of type I fibers. As type II fibers increase in cross-sectional size, mitochondrial and capillary densities decrease. The absolute mitochondrial and capillary volumes remain unchanged, however, substrate transport, oxygen utilization and carbon dioxide withdraw may be limited.

The end result is a theorized decrease in cardiovascular capacity. ATP-PC training of high intensity and slow-speed utilizing Isokinetic loading may increase several biochemical mechanisms. Muscle glycogen content, CP, ATP, ADP, creatine, phosphorylase, phosphofructokinase and Krebs cycle enzyme activity are all speculated to experience increased levels under the presence of ATP-PC training.

However, ATP-PC training at higher speeds, more related to Power Training, do not replicate the same biochemical results. Power training will elicit similar results as experienced with ATP-PC training, particularly the neuromuscular effects. Assuming an alpha level of 0. All data are presented as mean ± standard deviation SD.

A group SIT, SSIT, and CON × time pre-training, post-training repeated-measures analysis of variance ANOVA compared the differences between groups. Significant interactions or main effects were subsequently analyzed using a Bonferroni post-hoc test. The statistical analysis was performed utilizing the SPSS statistical software, version No significant pre- to post-training change was observed for SLJ in SIT and SSIT groups Figure 4, B.

The present study aimed to compare the effects of traditional SIT and sport-specific SIT SSIT on physiological and biochemical adaptations and bio-motor abilities in male basketball players.

The most striking finding of the present study was that both traditional SIT and SSIT significantly improved the abovementioned parameters. However, effect size values indicate greater effects of SSIT on aerobic and anaerobic performance than SIT.

Research has shown a positive relationship between aerobic fitness and power recovery between repeated bouts of intensive interval exercise Laursen and Buchheit, This observation implies that aerobic fitness plays a pivotal role in a crucial aspect of basketball performance, i.

The increased running distance completed during the Yo-Yo IR1 test in both SIT and SSIT groups could also verify this improvement. In the present study, both SIT and SSIT imposed an effective stimulus for improving V̇O 2max and significantly enhanced this indicator. Our findings corroborate previous studies reporting enhanced aerobic fitness following game-based Arslan et al.

The enhancement of V̇O 2max can be attributed to increases in two fundamental aspects of aerobic fitness: the central component, involving the improved delivery of oxygen, and the peripheral component, which signifies the enhanced utilization of oxygen by the active muscles Sheykhlouvand et al.

Anaerobic energy metabolism is the primary determinant of high-intensity movement performance, such as jumping, sprinting, and change of direction Arslan et al. Both SIT and SSIT significantly enhanced these sport-specific bio-motor abilities, indicating their positive effects on anaerobic power.

The increase in VJ observed in this study SIT: 7. However, some researchers failed to show the positive effects of SIT on VJ Aschendorf et al. The observed disparities in the outcomes might stem from variations in the duration of the training, gender, fitness levels of the participants, and the specific mode of training employed.

Enhanced explosiveness in VJ could be attributed to parameters such as reactive strength and muscular power Panoutsakopoulos and Bassa, However, neither SIT nor SSIT enhanced 1RM LP , indicating that enhanced neuromuscular adaptations such as increasing rate of force development and firing rate of muscles Buchheit and Laursen, and anaerobic power production of plantar flexors and knee extensors Maffiuletti et al.

We can speculate implementing SSIT, involving sport-specific drills such as dribbling, passing, and shooting exercises, resulted in more significant neuromuscular adaptations than regular SIT, leading to greater training effects with an effect size of 0.

Nonetheless, further investigations are necessary to elucidate the specific adaptations achieved through this approach. Regarding the sprint performance, both SIT and SSIT groups enhanced this locomotor ability after six weeks. An increase in sprint acceleration and velocity due to interval intervention involves fast-twitch muscle fiber and also improvements in stride length resulting in sprint gains Lee et al.

Our finding is in accordance with previous studies reporting a positive transfer of SIT to sprint performance Clemente et al. SSIT indicated greater changes in the m sprint than SIT medium vs. small ES. The possible mechanism explaining such a difference could be the enhanced acceleration component of the maximal sprint test due to sport-specific movements during SSIT Arslan et al.

Both SIT and SSIT significantly diminished TT and IAT time. In addition, the changes in IAT were significantly greater in the SSIT than in the SIT. Likewise, Arslan and colleagues have shown small vs. moderate training effects of HIIT and small-sided games on these parameters.

COD presents a key attribute in basketball. A quick COD requires rapid force development and high power generation by the lower extremities Miller et al. In COD ability tasks, the leg extensor muscles undergo swift transitions between eccentric and concentric muscle actions, accompanied by minimal ground contact time Miller et al.

Effect size results indicate a greater impact of SSIT on COD, which could be attributed to the sport-specific drill during SSIT i. By challenging the neuromuscular system and decision-making ability through basketball-specific drills, such movements may indirectly benefit the ultimate COD better than linear running Arslan et al.

Both SIT interventions were associated with an increase in TEST levels and a decrease in serum CORT concentrations. Our results corroborate previous findings Sheykhlouvand et al. Typically, elevations in resting TEST with reductions in CORT show an anabolic environment and increase performance capacity in athletes.

Enhanced resting TEST levels represent a favorable hormonal environment when attempting to maximize performance adaptations. This study possesses certain limitations that warrant consideration when interpreting its findings.

Firstly, the study exclusively involved male subjects, which restricts the generalizability of our results to the broader population. Gender-based differences in physiology and responses to interventions may exist, and further research with diverse participant groups is necessary to ascertain the applicability of our findings to women.

Secondly, the study acknowledges the potential influence of external factors outside of the intervention, such as dietary habits, sleep patterns, and overall training load. While we tried to control these variables and maintain consistency among participants, we cannot entirely exclude the impact of these factors on the observed outcomes.

Future research could employ more rigorous control measures or investigate these external factors as variables of interest to understand their effects on the studied intervention better.

Specifically, the post-training analysis indicated that both interventions were linked with enhanced aerobic fitness, VJ, COD, linear speed, and anabolic hormonal status. The effect size values indicated more significant effects of SSIT than SIT in most physiological and sport-specific adaptations.

Moreover, sport-specific practices may impose more challenging movements mimicking the game and cause more significant gains than SIT performed on a direct track. This article for the national fitness and sports industry research center project "The basis of sports industry and regional economic development correlation analysis" project number: GT There is no conflict of interest.

The present study complies with the current laws of the country in which it was performed. The datasets generated and analyzed during the current study are not publicly available but are available from the corresponding author, who was an organizer of the study.

Citations in ScholarGoogle. Publish Date Received: Accepted: Published online : Journal of Sports Science and Medicine 22 , - Tao Song, Jilikeha, Yujie Deng. Abstract Introduction Methods Results Discussion Author biography References.

Study design Figure 1 illustrates a summary of the study design. Anthropometric measures Height was assessed employing a stadiometer affixed to the wall Seca , Terre Haute, IN , with measurements recorded to the closest 0. Muscular strength Using a leg press machine Body Solid, Model GLPH , USA , one repetition maximum in leg press 1RM LP was measured to determine lower body maximal strength according to the guidelines of Kraemer and Fry Jumping test Jumping ability was evaluated using the vertical jump VJ and standing long jump SLJ tests.

Change of direction COD tests The T-test TT and Illinois Agility test IAT were applied to measure COD. Blood sampling and analysis After overnight fasting exceeding 8 hours, a mL of blood was collected from the antecubital vein in the pre- and post-training. Training protocols All participants engaged in their formal basketball training twice a week i.

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Download references. We thank D. Wainer, J. Locke and 4omix. com for the shiny app application, M. Rüegg for the critical feedback on the paper and the Genomics Facility Basel, sciCORE, Proteomics Core Facility and the animal facility caretakers of the Biozentrum for their help.

This work was supported by grants from the Swiss National Science Foundation grant no. and S. and the University of Basel to R.

and C. and K. were supported by grants of the German Federal Ministry of Research and Education for de. NBI grant no. Biozentrum, University of Basel, Basel, Switzerland. Regula Furrer, Barbara Heim, Svenia Schmid, Sedat Dilbaz, Volkan Adak, Danilo Ritz, Stefan A.

Laboratory of EpiGenetics, Saarland University, Saarbrücken, Germany. You can also search for this author in PubMed Google Scholar. conceived the project. provided the methodology. conducted the investigations. analysed and interpreted the data.

provided the resources. acquired the funding. supervised the project. wrote the original draft. and J. reviewed and edited the paper. Correspondence to Christoph Handschin. Nature Metabolism thanks the anonymous reviewers for their contribution to the peer review of this work.

Primary Handling Editor: Ashley Castellanos-Jankiewicz, in collaboration with the Nature Metabolism team. b-c , Examples of proteins represented in the annotations clusters of b mitochondrial respiration and lipid metabolic process and c proteasomal catabolic process in a sedentary untrained light gray and training dark gray muscle.

e , Correlation plot of the transcriptome and proteome of trained muscle. Genes representing the different scenarios: same direction in both trained muscle as well as after an acute bout of maximal exercise; only changed in trained muscle; only regulated after an acute maximal exercise bout; or upregulated after an acute challenge and downregulated after training.

Data from 5 biological replicates if not otherwise indicated. Exact p -values of proteomics data and FDR-values of RNA-seq data are displayed in the Source Data file. See also Fig.

c , Examples of gene trajectories in untrained light gray and trained dark gray muscle involved in ECM organization. Exact FDR-values are displayed in Source Data file. d , Schematic representation of genes involved in axon guidance and the possible functional consequences.

The left square below each gene name represents the untrained response and the right square the trained response. Data from 5 biological replicates. Statistics of RNA-seq data were performed with the CLC genomics workbench software.

b , Venn diagram of all the predicted motifs that are changes in untrained light gray and trained dark gray muscle after an acute exercise bout. c-d , Trajectories of motif activity of transcription factors from ISMARA in untrained light gray and trained dark gray muscle post-exercise that are either specific to training status c or show an exacerbation after training d.

e , Example of a possible transcriptional cascade including a top predicted transcription factor by ISMARA and one of the downstream targets gene expression and motif activities.

Exact FDR-values of RNA-seq data and z -scores of ISMARA data are displayed in the Source Data file. b-c , Deconvolution of genes involved in ECM remodeling b and axon guidance c that are upregulated in untrained and downregulated in trained muscle.

a , Representative examples of genes with the same maximal amplitude of gene expression up- or downregulated that show a phase shift towards an earlier time point in trained muscle after acute maximal exercise dark gray compared to untrained muscle light gray.

b , Representation of the time points when peak expression is reached in either the commonly upregulated genes or all upregulated genes in untrained and trained muscle post-exercise. c-e , Examples of differentially methylated genes involved in transcription c , Wnt signaling d and axon guidance e in untrained light gray and trained dark gray muscle post-exercise.

f , Pie chart of the proteome of a trained muscle with the corresponding correlation with the transcriptome of an unperturbed trained muscle or an untrained or trained muscle after an acute bout of maximal exercise.

The gray area depicts the proportion of proteins that are not regulated on a transcriptional level. All exact FDR-values are displayed in Source Data file. b , Volcano plot of the proteome of trained mKO muscle compared to trained WT muscle. Exact p -values are displayed in Supplementary Table 1.

f , Volcano plot of the transcriptome of untrained sedentary mKO muscle compared to that of untrained sedentary WT muscle. g , Venn diagram of all predicted motifs that are changes in unperturbed trained WT gray and mKO blue muscle.

b , Venn diagram of all predicted motifs that are changes after an acute maximal exercise bout in untrained WT gray and mKO blue animals.

All time points are merged. The third column represents genes that are downregulated in both the trained WT and mKO compared to the respective control. e , Venn diagram of all predicted motifs that are changes after an acute exercise bout in trained WT gray and mKO blue animals.

See also Figs. a , Bar Venn diagram of differentially methylated regions DMRs of an unperturbed trained WT dark gray and mKO dark blue muscle. The common DMR are striped gray and blue. b , Venn diagram of DMRs of an unperturbed trained mKO muscle open circle and differentially expressed genes DEG after acute maximal exercise in trained mKO muscle blue circle.

c , Bar Venn diagram of the DMRs that are associated with acute gene expression changes overlap Fig. e , Trajectories of transcription factors in untrained light blue and trained blue mKO mice that are differentially methylated after training.

The common DMRs are striped gray and blue. g-h , Venn diagram of WT g and mKO muscle h depicting all DMRs in untrained muscle after an acute bout of maximal exercise open circles and DEGs upon an acute bout of maximal exercise colored circle.

j , Bar Venn diagram of DMRs of an unperturbed trained WT dark gray and untrained mTG pink muscle. The common DMRs are striped gray and pink. k , Venn diagram of DMRs open circle and DEG blue circle of an untrained sedentary mTG muscle.

l , Venn diagrams of all up- and downregulated genes in untrained sedentary mTG muscle pink and after an acute bout of exercise in untrained light orange or blue and trained darker orange and blue muscle. m , Top 3 functional annotation clusters of the up- orange and downregulated blue proteins in sedentary mTG muscle compared to sedentary WT.

Exact FDR-values of RNA-seq data are displayed in the Source Data file. a, b , Principal component analysis PCA scatter plots of RNA-seq data of untrained a and trained b WT muscle after an acute bout of maximal exercise. c , PCA scatter plot of RNA-seq data of untrained and trained unperturbed WT and mKO muscle.

d, e , PCA scatter plots of RNA-seq data of untrained d and trained e mKO muscle after an acute bout of maximal exercise. Supplementary Table 4 All predicted motifs with significantly changed activities using ISMARA of WT and mKO animals in response to an acute bout of exercise or after training.

Open Access This article is licensed under a Creative Commons Attribution 4. Reprints and permissions. Molecular control of endurance training adaptation in male mouse skeletal muscle. Nat Metab 5 , — Download citation.

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Skip to main content Thank you for visiting nature. nature nature metabolism resources article. Download PDF. Subjects DNA methylation Metabolism Proteomics Transcriptomics. Abstract Skeletal muscle has an enormous plastic potential to adapt to various external and internal perturbations. Main Skeletal muscle exerts pleiotropic functions, from thermoregulation to endocrine signalling by myokines and myometabolites, and detoxification of endogenous compounds, for example, kynurenines or aberrantly high levels of ketone bodies 1 , 2 , 3 , 4 , 5.

Other: Control Trial. Other: Exercise Trial. Full description. Read more. Study type. Funder types. NCT EXERCISE-OBESITY-DUTH.

Take notes. Trial design 20 participants in 2 patient groups. Active Comparator group. Experimental group. Patient eligibility Sex Male. Ages 35 to 50 years old. Volunteers Accepts Healthy Volunteers. Institutional subscriptions. Alp, P. Google Scholar. Andersen, P. Baldwin, K. Bendall, J.

A reinvestigation. Bennett, A. Brace, R. Carey, C. Dissertation, University of Michigan Costill, D. Crabtree, B. Dohm, G. Gleeson, T. Gollnick, P. Fitts, R. Hammond, B. Canada 23 , 65—83 Henriksson, J. Acta Physiol. Hermansen, L. In: Muscle metabolism during exercise. Pernow, B. New York: Plenum Holloszy, J.