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Graefe's Archive For Clinical and... Nov 2022Extraocular muscle enlargement can occur secondary to a range of orbital and systemic diseases. Although the most common cause of extraocular muscle enlargement is... (Review)
Review
Extraocular muscle enlargement can occur secondary to a range of orbital and systemic diseases. Although the most common cause of extraocular muscle enlargement is thyroid eye disease, a range of other inflammatory, infective, neoplastic, and vascular conditions can alter the size and shape of the extraocular muscles. Imaging with computed tomography and magnetic resonance imaging plays an essential role in the workup of these conditions. This article provides an image-rich review of the wide range of pathology that can cause enlargement of the extraocular muscles.
Topics: Humans; Oculomotor Muscles; Tomography, X-Ray Computed; Graves Ophthalmopathy; Magnetic Resonance Imaging; Hypertrophy
PubMed: 35713708
DOI: 10.1007/s00417-022-05727-1 -
Journal of Applied Physiology... Jul 2016We reported, using a unilateral resistance training (RT) model, that training with high or low loads (mass per repetition) resulted in similar muscle hypertrophy and...
We reported, using a unilateral resistance training (RT) model, that training with high or low loads (mass per repetition) resulted in similar muscle hypertrophy and strength improvements in RT-naïve subjects. Here we aimed to determine whether the same was true in men with previous RT experience using a whole-body RT program and whether postexercise systemic hormone concentrations were related to changes in hypertrophy and strength. Forty-nine resistance-trained men (23 ± 1 yr, mean ± SE) performed 12 wk of whole-body RT. Subjects were randomly allocated into a higher-repetition (HR) group who lifted loads of ∼30-50% of their maximal strength (1RM) for 20-25 repetitions/set (n = 24) or a lower-repetition (LR) group (∼75-90% 1RM, 8-12 repetitions/set, n = 25), with all sets being performed to volitional failure. Skeletal muscle biopsies, strength testing, dual-energy X-ray absorptiometry scans, and acute changes in systemic hormone concentrations were examined pretraining and posttraining. In response to RT, 1RM strength increased for all exercises in both groups (P < 0.01), with only the change in bench press being significantly different between groups (HR, 9 ± 1, vs. LR, 14 ± 1 kg, P = 0.012). Fat- and bone-free (lean) body mass and type I and type II muscle fiber cross-sectional area increased following training (P < 0.01) with no significant differences between groups. No significant correlations between the acute postexercise rise in any purported anabolic hormone and the change in strength or hypertrophy were found. In congruence with our previous work, acute postexercise systemic hormonal rises are not related to or in any way indicative of RT-mediated gains in muscle mass or strength. Our data show that in resistance-trained individuals, load, when exercises are performed to volitional failure, does not dictate hypertrophy or, for the most part, strength gains.
Topics: Adult; Exercise; Hormones; Humans; Hypertrophy; Male; Muscle Strength; Muscle, Skeletal; Resistance Training; Weight Lifting; Young Adult
PubMed: 27174923
DOI: 10.1152/japplphysiol.00154.2016 -
Journal of Asian Natural Products... Dec 2022Autophagy plays an important role in the pathogenesis of cardiovascular diseases. Dysregulation of autophagy may have a huge effect on cardiac hypertrophy induced by... (Review)
Review
Autophagy plays an important role in the pathogenesis of cardiovascular diseases. Dysregulation of autophagy may have a huge effect on cardiac hypertrophy induced by overload pressure although reports on autophagy and cardiac hypertrophy have been contradictory. Some studies showed that autophagy activation attenuated cardiac hypertrophy. However, others suggested that inhibition of autophagy would be protective. Different research models or different pathways involved could be responsible for it. Cardiac hypertrophy may be alleviated through regulation of autophagy. This review aims to highlight the pathways and therapeutic targets identified in the prevention and treatment of cardiac hypertrophy by regulating autophagy.
Topics: Animals; Mice; Molecular Structure; Cardiomegaly; Autophagy; Myocytes, Cardiac; Mice, Inbred C57BL
PubMed: 35043747
DOI: 10.1080/10286020.2021.2024810 -
JACC. Cardiovascular Imaging Nov 2019Pathological left ventricular hypertrophy is a common feature of many cardiac diseases. It results from both myocyte hypertrophy and interstitial expansion. Interstitial... (Review)
Review
Pathological left ventricular hypertrophy is a common feature of many cardiac diseases. It results from both myocyte hypertrophy and interstitial expansion. Interstitial expansion is most commonly secondary to the accumulation of mature cross-linked collagen fibers due to dysregulated metabolism, known as interstitial fibrosis. This occurs secondary to a variety of stimuli including ischemic, toxic, metabolic, infective, genetic, and hemodynamic factors. Less commonly, interstitial expansion may occur because of the accumulation of misfolded amyloid protein or interstitial edema. It is now well recognized that the presence and extent of interstitial disease are associated with adverse outcomes. There is therefore interest in the development of novel therapies that target the pathways that drive these disease processes. With the emergence of such therapies, it is becoming increasingly important to be able to characterize the type and extent of interstitial disease to enable the use of such targeted therapies in a personalized manner.
Topics: Biopsy; Extracellular Space; Fibrosis; Humans; Hypertrophy, Left Ventricular; Magnetic Resonance Imaging; Myocardium; Tomography, Emission-Computed; Ventricular Function, Left; Ventricular Remodeling
PubMed: 31542527
DOI: 10.1016/j.jcmg.2019.05.033 -
JCI Insight Aug 2023The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic...
The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum (ER) is largely unknown. Here, we report that the SEL1L-HRD1 ER-associated degradation (ERAD) complex, the primary molecular machinery that degrades misfolded proteins in the ER, is vital to maintain postnatal muscle growth and systemic energy balance. Myocyte-specific SEL1L deletion blunts the hypertrophic phase of muscle growth, resulting in a net zero gain of muscle mass during this developmental period and a 30% reduction in overall body growth. In addition, myocyte-specific SEL1L deletion triggered a systemic reprogramming of metabolism characterized by improved glucose sensitivity, enhanced beigeing of adipocytes, and resistance to diet-induced obesity. These effects were partially mediated by the upregulation of the myokine FGF21. These findings highlight the pivotal role of SEL1L-HRD1 ERAD activity in skeletal myocytes for postnatal muscle growth, and its physiological integration in maintaining whole-body energy balance.
Topics: Humans; Endoplasmic Reticulum-Associated Degradation; Ubiquitin-Protein Ligases; Proteins; Muscles; Energy Metabolism; Hypertrophy
PubMed: 37535424
DOI: 10.1172/jci.insight.170387 -
Singapore Medical Journal Jul 2023Muscle fibres are multinuclear cells, and the cytoplasmic territory where a single myonucleus controls transcriptional activity is called the myonuclear domain (MND).... (Review)
Review
Muscle fibres are multinuclear cells, and the cytoplasmic territory where a single myonucleus controls transcriptional activity is called the myonuclear domain (MND). MND size shows flexibility during muscle hypertrophy. The MND ceiling hypothesis states that hypertrophy results in the expansion of MND size to an upper limit or MND ceiling, beyond which additional myonuclei via activation of satellite cells are required to support further growth. However, the debate about the MND ceiling hypothesis is far from settled, and various studies show conflicting results about the existence or otherwise of MND ceiling in hypertrophy. The aim of this review is to summarise the literature about the MND ceiling in various settings of hypertrophy and discuss the possible factors contributing to a discrepancy in the literature. We conclude by describing the physiological and clinical significance of the MND ceiling limit in the muscle adaptation process in various physiological and pathological conditions.
Topics: Humans; Muscle Fibers, Skeletal; Hypertrophy; Muscle, Skeletal
PubMed: 34544215
DOI: 10.11622/smedj.2021103 -
Journal of Cachexia, Sarcopenia and... Jun 2024Proliferating cancer cells shift their metabolism towards glycolysis, even in the presence of oxygen, to especially generate glycolytic intermediates as substrates for...
BACKGROUND
Proliferating cancer cells shift their metabolism towards glycolysis, even in the presence of oxygen, to especially generate glycolytic intermediates as substrates for anabolic reactions. We hypothesize that a similar metabolic remodelling occurs during skeletal muscle hypertrophy.
METHODS
We used mass spectrometry in hypertrophying C2C12 myotubes in vitro and plantaris mouse muscle in vivo and assessed metabolomic changes and the incorporation of the [U-C]glucose tracer. We performed enzyme inhibition of the key serine synthesis pathway enzyme phosphoglycerate dehydrogenase (Phgdh) for further mechanistic analysis and conducted a systematic review to align any changes in metabolomics during muscle growth with published findings. Finally, the UK Biobank was used to link the findings to population level.
RESULTS
The metabolomics analysis in myotubes revealed insulin-like growth factor-1 (IGF-1)-induced altered metabolite concentrations in anabolic pathways such as pentose phosphate (ribose-5-phosphate/ribulose-5-phosphate: +40%; P = 0.01) and serine synthesis pathway (serine: -36.8%; P = 0.009). Like the hypertrophy stimulation with IGF-1 in myotubes in vitro, the concentration of the dipeptide l-carnosine was decreased by 26.6% (P = 0.001) during skeletal muscle growth in vivo. However, phosphorylated sugar (glucose-6-phosphate, fructose-6-phosphate or glucose-1-phosphate) decreased by 32.2% (P = 0.004) in the overloaded muscle in vivo while increasing in the IGF-1-stimulated myotubes in vitro. The systematic review revealed that 10 metabolites linked to muscle hypertrophy were directly associated with glycolysis and its interconnected anabolic pathways. We demonstrated that labelled carbon from [U-C]glucose is increasingly incorporated by ~13% (P = 0.001) into the non-essential amino acids in hypertrophying myotubes, which is accompanied by an increased depletion of media serine (P = 0.006). The inhibition of Phgdh suppressed muscle protein synthesis in growing myotubes by 58.1% (P < 0.001), highlighting the importance of the serine synthesis pathway for maintaining muscle size. Utilizing data from the UK Biobank (n = 450 243), we then discerned genetic variations linked to the serine synthesis pathway (PHGDH and PSPH) and to its downstream enzyme (SHMT1), revealing their association with appendicular lean mass in humans (P < 5.0e-8).
CONCLUSIONS
Understanding the mechanisms that regulate skeletal muscle mass will help in developing effective treatments for muscle weakness. Our results provide evidence for the metabolic rewiring of glycolytic intermediates into anabolic pathways during muscle growth, such as in serine synthesis.
Topics: Glucose; Muscle, Skeletal; Animals; Mice; Humans; Hypertrophy; Muscle Fibers, Skeletal; Insulin-Like Growth Factor I; Metabolomics
PubMed: 38742477
DOI: 10.1002/jcsm.13468 -
Cellular Physiology and Biochemistry :... 2017Cardiac remodeling occurs after stress to the heart, manifested as pathological processes, including hypertrophy and apoptosis of cardiomyocytes, dysfunction of vascular... (Review)
Review
Cardiac remodeling occurs after stress to the heart, manifested as pathological processes, including hypertrophy and apoptosis of cardiomyocytes, dysfunction of vascular endothelial cells and vascular smooth muscle cells as well as differentiation and proliferation of fibroblasts, ultimately resulting in progression of cardiovascular diseases. Emerging evidence has revealed that long non-coding RNAs (lncRNAs) acted as powerful and dynamic modifiers of cardiac remodeling. LncRNAs including Chaer, Chast, Mhrt, CHRF, ROR, H19, and MIAT have been implicated in cardiac hypertrophy while NRF, H19, APF, CARL, UCA, Mhrt and several other lncRNAs (n379599, n379519, n384640, n380433 and n410105) in cardiomyocyte loss and extracellular matrix remodeling. In addition, MALAT1 and TGFB2-OT1 have been reported to contribute to vascular endothelial cells dysfunction while lincRNA-p21 and lnc-Ang362 to vascular smooth muscle cells proliferation. Thus, manipulation of lncRNA expression levels through either the inhibition of disease-up-regulated lncRNAs or increasing disease-down-regulated lncRNAs represents novel therapeutic strategies for cardiac remodeling.
Topics: Animals; Apoptosis; Cardiomegaly; Cell Differentiation; Cell Proliferation; Endothelial Cells; Humans; Muscle, Smooth, Vascular; Myocytes, Cardiac; Myocytes, Smooth Muscle; RNA, Long Noncoding
PubMed: 28376483
DOI: 10.1159/000471913 -
International Journal of Sports Medicine Jul 2023This study assessed associations between changes in the weekly number of sets performed and the percentage change in muscle thickness of the biceps (MT) and triceps (MT)...
This study assessed associations between changes in the weekly number of sets performed and the percentage change in muscle thickness of the biceps (MT) and triceps (MT) brachii muscles. Through a retrospective analysis, sixty-eight resistance-trained subjects that participated in previous studies had their previous training volumes analyzed and compared to the volume imposed during each individual study. The relationship between variables was determined through correlation and a k-cluster analysis was performed to subdivide the participants into three groups and classified as:<0%; 0-50%, and >50% increase in the number of sets for both muscle groups. Moderate and weak correlations were observed between the alterations in training volume and changes in MT (r=0.44, =0.001) and MT (r=0.35, =0.002), respectively. A significant difference was noted between<0% to >50% for MT and MT (=0.017; =0.042, respectively), while no significant difference was observed between<0% to 0-50% and 0-50% to >50% (both p >0.05) for both muscle groups. In conclusion, muscle hypertrophy of the upper limbs is only weakly to moderately associated with changes in training volume of trained subjects.
Topics: Humans; Muscle Strength; Retrospective Studies; Resistance Training; Muscle, Skeletal; Hypertrophy
PubMed: 37160161
DOI: 10.1055/a-2053-8426 -
Skeletal Muscle Jul 2022Skeletal muscle homeostasis and function are ensured by orchestrated cellular interactions among several types of cells. A noticeable aspect of skeletal muscle biology... (Review)
Review
Skeletal muscle homeostasis and function are ensured by orchestrated cellular interactions among several types of cells. A noticeable aspect of skeletal muscle biology is the drastic cell-cell communication changes that occur in multiple scenarios. The process of recovering from an injury, which is known as regeneration, has been relatively well investigated. However, the cellular interplay that occurs in response to mechanical loading, such as during resistance training, is poorly understood compared to regeneration. During muscle regeneration, muscle satellite cells (MuSCs) rebuild multinuclear myofibers through a stepwise process of proliferation, differentiation, fusion, and maturation, whereas during mechanical loading-dependent muscle hypertrophy, MuSCs do not undergo such stepwise processes (except in rare injuries) because the nuclei of MuSCs become directly incorporated into the mature myonuclei. In this review, six specific examples of such differences in MuSC dynamics between regeneration and hypertrophy processes are discussed.
Topics: Cell Differentiation; Humans; Hypertrophy; Muscle, Skeletal; Myoblasts; Regeneration
PubMed: 35794679
DOI: 10.1186/s13395-022-00300-0