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Reumatologia Clinica 2017Calf pseudohypertrophy due to radiculopathy is an exceptional phenomenon rarely described. We report a 67 year old woman with a previous history of lumbar disc surgery...
Calf pseudohypertrophy due to radiculopathy is an exceptional phenomenon rarely described. We report a 67 year old woman with a previous history of lumbar disc surgery consulting by progressive increase for more than a year of evolution painless right calf associated loss of strength. Electromyographic findings showed chronic S1 radiculopathy and radiologically was appreciated in the medial gastrocnemius and soleus rights substitution of normal muscle tissue by adipose tissue without evidence of myopathy or sarcomatous degeneration.
Topics: Aged; Female; Humans; Hypertrophy; Leg; Magnetic Resonance Imaging; Muscle, Skeletal; Muscular Diseases; Radiculopathy
PubMed: 27101742
DOI: 10.1016/j.reuma.2016.02.012 -
Physiological Reports Sep 2020This study aimed to review the effects of ladder-based resistance training (LRT) on muscle hypertrophy and strength in rodents through a systematic review with... (Meta-Analysis)
Meta-Analysis
This study aimed to review the effects of ladder-based resistance training (LRT) on muscle hypertrophy and strength in rodents through a systematic review with meta-analysis. We systematically searched PubMed/Medline, SportDiscuss, Scopus, Google Scholar, Science Direct, and Scielo database on May 18, 2020. Thirty-four studies were included measuring total (mCSA) or mean muscle fibers cross-sectional area (fCSA) or maximum load-carrying capacity (MLCC) or muscle mass (MM). About the main results, LRT provides sufficient mechanical stimulation to increase mCSA and fCSA. Meta-analysis showed a significant overall effect on the fCSA (SMD 1.89, 95% CI [1.18, 2.61], p < .00001, I = 85%); however, subgroup analysis showed that some muscle types might not be hypertrophied through the LRT. Meta-analysis showed a significant training effect on the MM (SMD 0.92, 95% CI [0.52, 1.32], p < .00001, I = 72%). Sub-group analysis revealed that soleus (SMD 1.32, 95% CI [0.11, 2.54], p = .03, I = 86%) and FHL (SMD 1.92, 95% CI [1.00, 2.85], p < .0001, I = 71%) presented significant training effects, despite moderate heterogeneity levels (I = 72%). MLCC increases considerably after a period of LRT, regardless of its duration and the characteristics of the protocols (SMD 12.37, 95% CI [9.36, 15.37], p < .00001, I = 90%). Through these results, we reach the following conclusions: (a) LRT is efficient to induce muscle hypertrophy, although this effect varies between different types of skeletal muscles, and; (b) the ability of rodents to carry load increases regardless of the type and duration of the protocol used.
Topics: Animals; Hypertrophy; Mice; Muscle Strength; Muscle, Skeletal; Physical Conditioning, Animal; Rats
PubMed: 32889774
DOI: 10.14814/phy2.14502 -
American Journal of Physiology. Heart... May 2022
Topics: Cardiomegaly; Humans; Myocytes, Cardiac
PubMed: 35394856
DOI: 10.1152/ajpheart.00162.2022 -
BMJ Case Reports Dec 2010A 4-year-old male child presented with severe growth failure and developmental delay. He had hypertrophy of calf muscles and the thyroid profile showed low levels of T3,...
A 4-year-old male child presented with severe growth failure and developmental delay. He had hypertrophy of calf muscles and the thyroid profile showed low levels of T3, T4 and markedly elevated level of thyroid-stimulating hormone thus confirming the presence of hypothyroidism. This combination of hypothyroidism and hypertrophy of muscles is classically described as Kocher-Debré-Semelaigne syndrome. This child was started on 50 µg of levothyroxine.
Topics: Child, Preschool; Congenital Hypothyroidism; Humans; Hypertrophy; Male; Muscle, Skeletal; Muscular Diseases; Phenotype
PubMed: 22802324
DOI: 10.1136/bcr.04.2010.2877 -
Scientific Reports Sep 2023The heart depends on a functional vasculature for oxygenation and transport of nutrients, and it is of interest to learn how primary impairment of the vasculature can...
The heart depends on a functional vasculature for oxygenation and transport of nutrients, and it is of interest to learn how primary impairment of the vasculature can indirectly affect cardiac function and heart morphology. Notch3-deficiency causes vascular smooth muscle cell (VSMC) loss in the vasculature but the consequences for the heart remain largely elusive. Here, we demonstrate that Notch3 mice have enlarged hearts with left ventricular hypertrophy and mild fibrosis. Cardiomyocytes were hypertrophic but not hyperproliferative, and the expression of several cardiomyocyte markers, including Tnt2, Myh6, Myh7 and Actn2, was altered. Furthermore, expression of genes regulating the metabolic status of the heart was affected: both Pdk4 and Cd36 were downregulated, indicating a metabolic switch from fatty acid oxidation to glucose consumption. Notch3 mice furthermore showed lower liver lipid content. Notch3 was expressed in heart VSMC and pericytes but not in cardiomyocytes, suggesting that a perturbation of Notch signalling in VSMC and pericytes indirectly impairs the cardiomyocytes. In keeping with this, Pdgfb mice, characterized by reduced numbers of VSMC and pericytes, showed left ventricular and cardiomyocyte hypertrophy. In conclusion, we demonstrate that reduced Notch3 or PDGFB signalling in vascular mural cells leads to cardiomyocyte dysfunction.
Topics: Animals; Mice; Becaplermin; Cardiomegaly; Hypertrophy, Left Ventricular; Lipid Metabolism; Myocytes, Cardiac; Proto-Oncogene Proteins c-sis
PubMed: 37699967
DOI: 10.1038/s41598-023-42010-7 -
Physiology (Bethesda, Md.) Jun 2008Muscle performance is influenced by turnover of contractile proteins. Production of new myofibrils and degradation of existing proteins is a delicate balance, which,... (Review)
Review
Muscle performance is influenced by turnover of contractile proteins. Production of new myofibrils and degradation of existing proteins is a delicate balance, which, depending on the condition, can promote muscle growth or loss. Protein synthesis and protein degradation are coordinately regulated by pathways that are influenced by mechanical stress, physical activity, availability of nutrients, and growth factors. Understanding the signaling that regulates muscle mass may provide potential therapeutic targets for the prevention and treatment of muscle wasting in metabolic and neuromuscular diseases.
Topics: Animals; Contractile Proteins; Humans; Hypertrophy; Muscle Contraction; Muscle, Skeletal; Muscular Atrophy; Signal Transduction
PubMed: 18556469
DOI: 10.1152/physiol.00041.2007 -
International Journal of Molecular... Nov 2022Oxidative stress and inflammation are associated with skeletal muscle function decline with ageing or disease or inadequate exercise and/or poor diet. Paradoxically,... (Review)
Review
Oxidative stress and inflammation are associated with skeletal muscle function decline with ageing or disease or inadequate exercise and/or poor diet. Paradoxically, reactive oxygen species and inflammatory cytokines are key for mounting the muscular and systemic adaptive responses to endurance and resistance exercise. Both ageing and lifestyle-related metabolic dysfunction are strongly linked to exercise redox and hypertrophic insensitivity. The adaptive inability and consequent exercise intolerance may discourage people from physical training resulting in a vicious cycle of under-exercising, energy surplus, chronic mitochondrial stress, accelerated functional decline and increased susceptibility to serious diseases. Skeletal muscles are malleable and dynamic organs, rewiring their metabolism depending on the metabolic or mechanical stress resulting in a specific phenotype. Endogenous RNA silencing molecules, microRNAs, are regulators of these metabolic/phenotypic shifts in skeletal muscles. Skeletal muscle microRNA profiles at baseline and in response to exercise have been observed to differ between adult and older people, as well as trained vs. sedentary individuals. Likewise, the circulating microRNA blueprint varies based on age and training status. Therefore, microRNAs emerge as key regulators of metabolic health/capacity and hormetic adaptability. In this narrative review, we summarise the literature exploring the links between microRNAs and skeletal muscle, as well as systemic adaptation to exercise. We expand a mathematical model of microRNA burst during adaptation to exercise through supporting data from the literature. We describe a potential link between the microRNA-dependent regulation of redox-signalling sensitivity and the ability to mount a hypertrophic response to exercise or nutritional cues. We propose a hypothetical model of endurance exercise-induced microRNA "memory cloud" responsible for establishing a landscape conducive to aerobic as well as anabolic adaptation. We suggest that regular aerobic exercise, complimented by a healthy diet, in addition to promoting mitochondrial health and hypertrophic/insulin sensitivity, may also suppress the glycolytic phenotype and mTOR signalling through miRNAs which in turn promote systemic metabolic health.
Topics: Humans; MicroRNAs; Muscle, Skeletal; Exercise; Circulating MicroRNA; Signal Transduction; Hypertrophy
PubMed: 36499053
DOI: 10.3390/ijms232314716 -
Matrix Biology : Journal of the... Feb 2022The regulation of skeletal muscle growth following pro-hypertrophic stimuli requires a coordinated response by different cell types that leads to extracellular matrix...
The regulation of skeletal muscle growth following pro-hypertrophic stimuli requires a coordinated response by different cell types that leads to extracellular matrix (ECM) remodeling and increases in muscle cross-sectional area. Indeed, matricellular proteins serve a key role as communication vehicles that facilitate the propagation of signaling stimuli required for muscle adaptation to environmental challenges. We found that the matricellular protein cellular communication network factor 2 (CCN2), also known as connective tissue growth factor (CTGF), is induced during a time course of overload-driven skeletal muscle hypertrophy in mice. To elucidate the role of CCN2 in mediating the hypertrophic response, we utilized genetically engineered mouse models for myofiber-specific CCN2 gain- and loss-of-function and then examined their response to mechanical stimuli through muscle overload. Interestingly, myofiber-specific deletion of CCN2 blunted muscle's hypertrophic response to overload without interfering with ECM deposition. On the other hand, when in excess through transgenic CCN2 overexpression, CCN2 was efficient in promoting overload-induced aberrant ECM accumulation without affecting myofiber growth. Altogether, our genetic approaches highlighted independent ECM and myofiber stress adaptation responses, and positioned CCN2 as a central mediator of both. Mechanistically, CCN2 acts by regulating focal adhesion kinase (FAK) mediated transduction of overload-induced extracellular signals, including interleukin 6 (IL6), and their regulatory impact on global protein synthesis in skeletal muscle. Overall, our study highlights the contribution of muscle-derived extracellular matrix factor CCN2 for proper hypertrophic muscle growth.
Topics: Animals; Connective Tissue Growth Factor; Extracellular Matrix; Hypertrophy; Mice; Muscle, Skeletal; Signal Transduction
PubMed: 35045313
DOI: 10.1016/j.matbio.2022.01.003 -
Cell Stem Cell Feb 2022Adaptation to mechanical load, leading to enhanced force and power output, is a characteristic feature of skeletal muscle. Formation of new myonuclei required for...
Adaptation to mechanical load, leading to enhanced force and power output, is a characteristic feature of skeletal muscle. Formation of new myonuclei required for efficient muscle hypertrophy relies on prior activation and proliferation of muscle stem cells (MuSCs). However, the mechanisms controlling MuSC expansion under conditions of increased load are not fully understood. Here we demonstrate that interstitial mesenchymal progenitors respond to mechanical load and stimulate MuSC proliferation in a surgical mouse model of increased muscle load. Mechanistically, transcriptional activation of Yes-associated protein 1 (Yap1)/transcriptional coactivator with PDZ-binding motif (Taz) in mesenchymal progenitors results in local production of thrombospondin-1 (Thbs1), which, in turn, drives MuSC proliferation through CD47 signaling. Under homeostatic conditions, however, CD47 signaling is insufficient to promote MuSC proliferation and instead depends on prior downregulation of the Calcitonin receptor. Our results suggest that relayed signaling between mesenchymal progenitors and MuSCs through a Yap1/Taz-Thbs1-CD47 pathway is critical to establish the supply of MuSCs during muscle hypertrophy.
Topics: Animals; CD47 Antigen; Hypertrophy; Mice; Muscle, Skeletal; Myoblasts; Stem Cells
PubMed: 34856120
DOI: 10.1016/j.stem.2021.11.003 -
European Review For Medical and... 2016The association of bilateral hypertrophy of temporalis and masseteric muscles is a rare clinical entity. The origin of the condition is unclear, causing cosmetic... (Review)
Review
OBJECTIVE
The association of bilateral hypertrophy of temporalis and masseteric muscles is a rare clinical entity. The origin of the condition is unclear, causing cosmetic problems, pain, and functional impairment.
PATIENTS AND METHODS
In this paper we analyzed 15 patients treated at the Department of Maxillo-Facial Surgery of the University of Naples Federico II, from 2000 to 2013, for temporalis and/or masseteric muscle hypertrophy, and in particular, a rare case of a patient with a marked bilateral swelling of the temporalis and masseteric region, in conjunction with a review of the literature.
RESULTS
Fourteen patients have not any kind of postoperatively problems. The last patient had been aware of the swelling for many years and complained of recurrent headaches. We adopted a new protocol fort this patients and the patient was very pleased with the treatment results, and reported a reduction in headaches and a continuation of his well-being, in addition to greater self-confidence. The last follow-up was performed three years after the first treatment, and the patient showed a complete resolution of his symptoms, and just a small increase of the swelling.
CONCLUSIONS
The treatment of temporalis and masseteric hypertrophy with Botulin toxin could be an effective option compared to conservative treatment or surgical intervention, although the review of the literature shows that this is only a temporary treatment. In fact, surgery still remains the best option. The treatment must be repeated every 4/6 months for 2-3 consecutive years before having stable benefits. To overcome this problem, an association with a bite treatment allowed us to achieve more lasting and more stable results over time without a recurrence of symptoms between the treatments. Furthermore, this association has enabled us to obtain a more rapid reduction of the hypertrophy.
Topics: Adult; Aged; Botulinum Toxins, Type A; Female; Humans; Hypertrophy; Injections, Intramuscular; Male; Masseter Muscle; Middle Aged; Neuromuscular Agents; Temporal Muscle; Treatment Outcome
PubMed: 26813447
DOI: No ID Found