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Experimental Physiology Dec 2020What is the central question of this study? Does combining endurance and hypertrophic stimuli blunt the adaptations to both modalities and is this effect greater in...
NEW FINDINGS
What is the central question of this study? Does combining endurance and hypertrophic stimuli blunt the adaptations to both modalities and is this effect greater in muscles with larger baseline fibre cross sectional area? What is the main finding and its importance? Endurance exercise and hypertrophic stimuli can be combined to increase fatigue resistance and fibre size without blunting either adaptation regardless of baseline fibre size.
ABSTRACT
Previous studies have demonstrated that fibre cross-sectional area (FCSA) is inversely related to oxidative capacity, which is thought to be determined by diffusion limitations of oxygen, ADP and ATP. Consequently, it is hypothesised that (1) when endurance training is combined with a hypertrophic stimulus the response to each will be blunted, and (2) muscles with a smaller FCSA will show a larger hypertrophic response than those with a large FCSA. To investigate this, we combined overload with endurance exercise in 12-month-old male mice from three different strains with different FCSA: Berlin High (BEH) (large fibres), C57BL/6J (C57) (normal-sized fibres) and Berlin Low (BEL) (small fibres). The right plantaris muscle was subjected to overload through denervation of synergists with the left muscle acting as an internal control. Half the animals trained 30 min per day for 6 weeks. The overload-induced hypertrophy was not blunted by endurance exercise, and the exercise-induced increase in fatigue resistance was not impaired by overload. All strains demonstrated similar absolute increases in FCSA, although the BEH mice with more fibres than the C57 mice demonstrated the largest increase in muscle mass and BEL mice with fewer fibres the smallest increase in muscle mass. This study suggests that endurance exercise and hypertrophic stimuli can be combined without attenuating adaptations to either modality, and that increases in FCSA are independent of baseline fibre size.
Topics: Adaptation, Physiological; Animals; Exercise Therapy; Hypertrophy; Male; Mice; Mice, Inbred C57BL; Muscle Fatigue; Muscle, Skeletal; Muscular Diseases; Physical Conditioning, Animal; Physical Endurance
PubMed: 33140456
DOI: 10.1113/EP089096 -
Physiological Reports Nov 2023Recently, the gut microbiome has emerged as a potent modulator of exercise-induced systemic adaptation and appears to be crucial for mediating some of the benefits of...
Recently, the gut microbiome has emerged as a potent modulator of exercise-induced systemic adaptation and appears to be crucial for mediating some of the benefits of exercise. This study builds upon previous evidence establishing a gut microbiome-skeletal muscle axis, identifying exercise-induced changes in microbiome composition. Metagenomics sequencing of fecal samples from non-exercise-trained controls or exercise-trained mice was conducted. Biodiversity indices indicated exercise training did not change alpha diversity. However, there were notable differences in beta-diversity between trained and untrained microbiomes. Exercise significantly increased the level of the bacterial species Muribaculaceae bacterium DSM 103720. Computation simulation of bacterial growth was used to predict metabolites that accumulate under in silico culture of exercise-responsive bacteria. We identified acetate and succinate as potential gut microbial metabolites that are produced by Muribaculaceae bacterium, which were then administered to mice during a period of mechanical overload-induced muscle hypertrophy. Although no differences were observed for the overall muscle growth response to succinate or acetate administration during the first 5 days of mechanical overload-induced hypertrophy, acetate and succinate increased skeletal muscle mitochondrial respiration. When given as post-biotics, succinate or acetate treatment may improve oxidative metabolism during muscle hypertrophy.
Topics: Mice; Animals; Succinic Acid; Muscle, Skeletal; Microbiota; Bacteria; Bacteroidetes; Acetates; Hypertrophy
PubMed: 37940330
DOI: 10.14814/phy2.15848 -
Trends in Cardiovascular Medicine Nov 2011In response to injury, the myocardium hypertrophies in an attempt to maintain or augment function, which is associated with ventricular remodeling and changes in... (Review)
Review
In response to injury, the myocardium hypertrophies in an attempt to maintain or augment function, which is associated with ventricular remodeling and changes in capillary density. During the compensatory phase of the hypertrophic response, the myocardium maintains output and is characterized by a coordinated neo-angiogenic and fibrotic response that supports cardiomyocyte health and survival. Emerging evidence shows that paracrine-mediated cross talk between cardiac myocytes and nonmyocytes within the heart is critical for cardiac adaptation to stress, including the extent of hypertrophy and angiogenesis. This review discusses recent results indicating that placental growth factor (PGF; also called PlGF), a secreted factor within the vascular endothelial growth factor superfamily, is a pivotal mediator of adaptive cardiac hypertrophy and beneficial angiogenesis through its ability to coordinate the intercellular communication between different cell types in the heart.
Topics: Adaptation, Physiological; Animals; Cardiomegaly; Humans; Myocardium; Neovascularization, Physiologic; Paracrine Communication; Placenta Growth Factor; Pregnancy Proteins; Signal Transduction; Ventricular Remodeling
PubMed: 22902069
DOI: 10.1016/j.tcm.2012.05.014 -
American Journal of Physiology. Cell... Oct 2019It is postulated that testosterone-induced skeletal muscle hypertrophy is driven by myonuclear accretion as the result of satellite cell fusion. To directly test this...
It is postulated that testosterone-induced skeletal muscle hypertrophy is driven by myonuclear accretion as the result of satellite cell fusion. To directly test this hypothesis, we utilized the Pax7-DTA mouse model to deplete satellite cells in skeletal muscle followed by testosterone administration. Pax7-DTA mice (6 mo of age) were treated for 5 days with either vehicle [satellite cell replete (SC+)] or tamoxifen [satellite cell depleted (SC-)]. Following a washout period, a testosterone propionate or sham pellet was implanted for 21 days. Testosterone administration caused a significant increase in muscle fiber cross-sectional area in SC+ and SC- mice in both oxidative (soleus) and glycolytic (plantaris and extensor digitorum longus) muscles. In SC+ mice treated with testosterone, there was a significant increase in both satellite cell abundance and myonuclei that was completely absent in testosterone-treated SC- mice. These findings provide direct evidence that testosterone-induced muscle fiber hypertrophy does not require an increase in satellite cell abundance or myonuclear accretion.Listen to a podcast about this Rapid Report with senior author E. E. Dupont-Versteegden (https://ajpcell.podbean.com/e/podcast-on-paper-that-shows-testosterone-induced-skeletal-muscle-hypertrophy-does-not-need-muscle-stem-cells/).
Topics: Animals; Disease Models, Animal; Hypertrophy; Mice, Transgenic; Muscle Fibers, Skeletal; PAX7 Transcription Factor; Satellite Cells, Skeletal Muscle; Stem Cells; Testosterone
PubMed: 31314585
DOI: 10.1152/ajpcell.00260.2019 -
The Journal of Physiology Jul 2021Ribosome biogenesis and MYC transcription are associated with acute resistance exercise (RE) and are distinct from endurance exercise in human skeletal muscle throughout...
KEY POINTS
Ribosome biogenesis and MYC transcription are associated with acute resistance exercise (RE) and are distinct from endurance exercise in human skeletal muscle throughout a 24 h time course of recovery. A PCR-based method for relative ribosomal DNA (rDNA) copy number estimation was validated by whole genome sequencing and revealed that rDNA dosage is positively correlated with ribosome biogenesis in response to RE. Acute RE modifies rDNA methylation patterns in enhancer, intergenic spacer and non-canonical MYC-associated regions, but not the promoter. Myonuclear-specific rDNA methylation patterns with acute mechanical overload in mice corroborate and expand on rDNA findings with RE in humans. A genetic predisposition for hypertrophic responsiveness may exist based on rDNA gene dosage.
ABSTRACT
Ribosomes are the macromolecular engines of protein synthesis. Skeletal muscle ribosome biogenesis is stimulated by exercise, although the contribution of ribosomal DNA (rDNA) copy number and methylation to exercise-induced rDNA transcription is unclear. To investigate the genetic and epigenetic regulation of ribosome biogenesis with exercise, a time course of skeletal muscle biopsies was obtained from 30 participants (18 men and 12 women; 31 ± 8 years, 25 ± 4 kg m ) at rest and 30 min, 3 h, 8 h and 24 h after acute endurance (n = 10, 45 min cycling, 70% ) or resistance exercise (n = 10, 4 × 7 × 2 exercises); 10 control participants underwent biopsies without exercise. rDNA transcription and dosage were assessed using quantitative PCR and whole genome sequencing. rDNA promoter methylation was investigated using massARRAY EpiTYPER and global rDNA CpG methylation was assessed using reduced-representation bisulphite sequencing. Ribosome biogenesis and MYC transcription were associated primarily with resistance but not endurance exercise, indicating preferential up-regulation during hypertrophic processes. With resistance exercise, ribosome biogenesis was associated with rDNA gene dosage, as well as epigenetic changes in enhancer and non-canonical MYC-associated areas in rDNA, but not the promoter. A mouse model of in vivo metabolic RNA labelling and genetic myonuclear fluorescence labelling validated the effects of an acute hypertrophic stimulus on ribosome biogenesis and Myc transcription, and also corroborated rDNA enhancer and Myc-associated methylation alterations specifically in myonuclei. The present study provides the first information on skeletal muscle genetic and rDNA gene-wide epigenetic regulation of ribosome biogenesis in response to exercise, revealing novel roles for rDNA dosage and CpG methylation.
Topics: Animals; Epigenesis, Genetic; Humans; Hypertrophy; Mice; Muscle, Skeletal; Protein Biosynthesis; Ribosomes
PubMed: 33913170
DOI: 10.1113/JP281244 -
European Journal of Sport Science May 2018Currently, it is unclear whether manipulation of movement velocity during resistance exercise has an effect on hypertrophy of specific muscles. The purpose of this... (Review)
Review
Currently, it is unclear whether manipulation of movement velocity during resistance exercise has an effect on hypertrophy of specific muscles. The purpose of this systematic review of literature was to investigate the effect of movement velocity during resistance training on muscle hypertrophy. Five electronic databases were searched using terms related to movement velocity and resistance training. Inclusion criteria were randomised and non-randomised comparative studies; published in English; included healthy adults; used dynamic resistance exercise interventions directly comparing fast training to slower movement velocity training; matched in prescribed intensity and volume; duration ≥4 weeks; and measured muscle hypertrophy. A total of six studies were included involving 119 untrained participants. Hypertrophy of the quadriceps was examined in five studies and of the biceps brachii in two studies. Three studies found significantly greater increases in hypertrophy of the quadriceps for moderate-slow compared to fast training. For the remaining studies examining the quadriceps, significant within-group increase in hypertrophy was found for only moderate-slow training in one study and for only fast training in the other study. The two studies that examined hypertrophy of the biceps brachii found greater increases for fast compared to moderate-slow training. Caution is required when interpreting the findings from this review due to the low number of studies, hence insufficient data. Future longitudinal randomised controlled studies in cohorts of healthy adults are required to confirm and extend our findings.
Topics: Humans; Hypertrophy; Muscle Strength; Muscle, Skeletal; Randomized Controlled Trials as Topic; Resistance Training
PubMed: 29431597
DOI: 10.1080/17461391.2018.1434563 -
Physiological Reports Apr 2022Mitochondria in the skeletal muscle are essential for maintaining metabolic plasticity and function. Mitochondrial quality control encompasses the dynamics of the...
Mitochondria in the skeletal muscle are essential for maintaining metabolic plasticity and function. Mitochondrial quality control encompasses the dynamics of the biogenesis and remodeling of mitochondria, characterized by the constant fission and fusion of mitochondria in response to metabolic stressors. However, the roles of mitochondrial fission or fusion in muscle hypertrophy and atrophy remain unclear. The aim of this study was to determine whether mitochondrial fusion and fission events are influenced by muscle hypertrophy or atrophy stimulation. Twenty-six male F344 rats were randomly assigned to a control group or were subjected to up to 14 days of either plantaris overload (via tenotomy of the gastrocnemius and soleus muscles; hypertrophy group) or hindlimb cast immobilization (atrophy group). After 14 days of treatment, plantaris muscle samples were collected to determine the expression levels of mitochondrial fusion- and fission-related proteins. Muscle weight and total muscle protein content increased following plantaris overload in the hypertrophy group, but decreased following immobilization for 14 days in the atrophy group. In the hypertrophied muscle, the level of activated dynamin-related protein 1 (Drp1), phosphorylated at Ser616, significantly increased by 25.8% (p = 0.014). Moreover, the protein expression level of mitochondrial fission factor significantly decreased by 36.5% in the hypertrophy group compared with that of the control group (p = 0.017). In contrast, total Drp1 level significantly decreased in the atrophied plantaris muscle (p = 0.011). Our data suggest that mitochondrial fission events may be influenced by both muscle hypertrophy and atrophy stimulation, and that mitochondrial fission- related protein Drp1 plays an important role in the regulation of skeletal muscle in response to mechanical stimulation.
Topics: Animals; Atrophy; Hypertrophy; Male; Mitochondrial Dynamics; Mitochondrial Proteins; Muscle, Skeletal; Rats; Rats, Inbred F344
PubMed: 35439362
DOI: 10.14814/phy2.15281 -
BMJ Case Reports Sep 2011Hypertrophy refers to an enlargement caused by an increase in the size but not in the number of cells. Generalised masticatory muscle hypertrophy may affect the...
Hypertrophy refers to an enlargement caused by an increase in the size but not in the number of cells. Generalised masticatory muscle hypertrophy may affect the temporalis muscle, masseters and medial pterygoids in a variety of combinations. Masseteric hypertrophy may present as either unilateral or bilateral painless swelling of unknown origin in the region of angle of mandible. It is a relatively rare condition and presents a diagnostic dilemma. While the history and clinical examination are important in differentiating this benign condition from parotid or dental pathology, they cannot necessarily exclude rare malignant lesion within the muscle. Advanced imaging modalities like CT and MRI are essential to confirm the diagnosis. Here the authors are reporting a unique case of masseter muscle hypertrophy along with medial pterygoid hypertrophy which was missed clinically but confirmed using CT and MRI.
Topics: Diagnosis, Differential; Facial Asymmetry; Humans; Hypertrophy; Magnetic Resonance Imaging; Male; Masseter Muscle; Pterygoid Muscles; Radiography, Panoramic; Tomography, X-Ray Computed; Young Adult
PubMed: 22679271
DOI: 10.1136/bcr.07.2011.4557 -
FEBS Open Bio Sep 2023Autophagy plays a vital role in cell homeostasis by eliminating nonfunctional components and promoting cell survival. Here, we examined the levels of autophagy signaling...
Autophagy plays a vital role in cell homeostasis by eliminating nonfunctional components and promoting cell survival. Here, we examined the levels of autophagy signaling proteins after 7 days of overload hypertrophy in the extensor digitorum longus (EDL) and soleus muscles of control and diabetic rats. We compared control and 3-day streptozotocin-induced diabetic rats, an experimental model for type 1 diabetes mellitus (T1DM). EDL muscles showed increased levels of basal autophagy signaling proteins. The diabetic state did not affect the extent of overload-induced hypertrophy or the levels of autophagy signaling proteins (p-ULK1, Beclin-1, Atg5, Atg12-5, Atg7, Atg3, LC3-I and II, and p62) in either muscle. The p-ULK-1, Beclin-1, and p62 protein expression levels were higher in the EDL muscle than in the soleus before the hypertrophic stimulus. On the contrary, the soleus muscle exhibited increased autophagic signaling after overload-induced hypertrophy, with increases in Beclin-1, Atg5, Atg12-5, Atg7, Atg3, and LC3-I expression in the control and diabetic groups, in addition to p-ULK-1 in the control groups. After hypertrophy, Beclin-1 and Atg5 levels increased in the EDL muscle of both groups, while p-ULK1 and LC3-I increased in the control group. In conclusion, the baseline EDL muscle exhibited higher autophagy than the soleus muscle. Although TDM1 promotes skeletal muscle mass loss and strength reduction, it did not significantly alter the extent of overload-induced hypertrophy and autophagy signaling proteins in EDL and soleus muscles, with the two groups exhibiting different patterns of autophagy activation.
Topics: Rats; Animals; Beclin-1; Diabetes Mellitus, Experimental; Muscle, Skeletal; Hypertrophy; Autophagy
PubMed: 37470707
DOI: 10.1002/2211-5463.13677 -
Poultry Science Jul 2023In chickens, muscle development during embryonic growth is predominantly by myofiber hyperplasia. Following hatch, muscle growth primarily occurs via hypertrophy of the...
In chickens, muscle development during embryonic growth is predominantly by myofiber hyperplasia. Following hatch, muscle growth primarily occurs via hypertrophy of the existing myofibers. Since myofiber number is set at hatch, production of more muscle fibers during embryonic growth would provide a greater myofiber number at hatch and potential for posthatch muscle growth by hypertrophy. Therefore, to improve performance in broilers, this study investigated the effect of in ovo spray application of probiotics on overall morphometry and muscle development in broiler embryos. For the study, fertile Ross 308 eggs were sprayed with different probiotics; Lactobacillus paracasei DUP 13076 (LP) and L. rhamnosus NRRL B 442 (LR) prior to and during incubation. The embryos were sacrificed on d 7, 10, 14, and 18 for embryo morphometry and pectoralis major muscle (PMM) sampling. Muscle sections were stained and imaged to quantify muscle fiber density (MFD), myofiber cross-sectional area (CSA), and nuclei density. Additionally, gene expression assays were performed to elucidate the effect of probiotics on myogenic genes. In ovo probiotic supplementation was found to significantly improve embryo weight, breast weight, and leg weight (P < 0.05). Further, histological analysis of PMM revealed a significant increase in MFD and nuclei number in the probiotic-treated embryos when compared to the control (P < 0.05). In 18-day-old broiler embryos, myofibers in the treatment group had a significantly smaller CSA (LP: 95.27 ± 3.28 μm, LR: 178.84 ± 15.1 μm) when compared to the control (211.41 ± 15.67 μm). This decrease in CSA was found to be associated with a concomitant increase in MFD (fibers/mm) in the LP (13,647 ± 482.15) and LR (13,957 ± 463.13) group when compared to the control (7,680 ± 406.78). Additionally, this increase in myofibrillar hyperplasia in the treatment groups was associated with upregulation in the expression of key genes regulating muscle growth including MYF5, MYOD, MYOG, and IGF-1. In summary, in ovo spray application of probiotics promoted overall embryo growth and muscle development in broilers.
Topics: Animals; Chickens; Hyperplasia; Ovum; Pectoralis Muscles; Probiotics; Hypertrophy; Growth and Development; Muscle Development
PubMed: 37216887
DOI: 10.1016/j.psj.2023.102744