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1.
Methods Mol Biol ; 2822: 13-24, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38907908

RESUMO

RNA extraction and analyses from tissues using bulk RNA-Sequencing (RNA-Seq) provide a more accurate picture of the gene expression compared to other molecular biology techniques for RNA quantification. Challenges associated with high-quality RNA extraction from skeletal muscles require a modification of standard protocols. Here, we describe a procedure for high-quality RNA isolation from intrinsic laryngeal muscles transferable to skeletal muscles with comparable technical and biological difficulties. Standard protocols for RNA isolation were optimized by maximizing the pooling strategy, determining the sample weight, applying cryogenic muscle disruption, and incorporating RNase-inhibiting reagents during the tissue preparation steps.


Assuntos
Sequenciamento de Nucleotídeos em Larga Escala , Músculo Esquelético , RNA , Análise de Sequência de RNA , Músculo Esquelético/metabolismo , Sequenciamento de Nucleotídeos em Larga Escala/métodos , Animais , RNA/isolamento & purificação , RNA/genética , Análise de Sequência de RNA/métodos , Perfilação da Expressão Gênica/métodos , Camundongos
2.
Heart Lung ; 68: 81-91, 2024 Jun 27.
Artigo em Inglês | MEDLINE | ID: mdl-38941771

RESUMO

BACKGROUND: Progressive exercise intolerance is a hallmark of pulmonary hypertension (pH), severely impacting patients' independence and quality of life (QoL). Accumulating evidence over the last decade shows that combined abnormalities in peripheral reflexes and target organs contribute to disease progression and exercise intolerance. OBJECTIVE: The aim of this study was to review the literature of the last decade on the contribution of the cardiovascular, respiratory, and musculoskeletal systems to pathophysiology and exercise intolerance in pH. METHODS: A systematic literature search was conducted using specific terms in PubMed, SciELO, and the Cochrane Library databases for original pre-clinical or clinical studies published between 2013 and 2023. Studies followed randomized controlled/non-randomized controlled and pre-post designs. RESULTS: The systematic review identified 25 articles reporting functional or structural changes in the respiratory, cardiovascular, and musculoskeletal systems in pH. Moreover, altered biomarkers in these systems, lower cardiac baroreflex, and heightened peripheral chemoreflex activity seemed to contribute to functional changes associated with poor prognosis and exercise intolerance in pH. Potential therapeutic strategies acutely explored involved manipulating the baroreflex and peripheral chemoreflex, improving cardiovascular autonomic control via cardiac vagal control, and targeting specific pathways such as GPER1, GDF-15, miR-126, and the JMJD1C gene. CONCLUSION: Information published in the last 10 years advances the notion that pH pathophysiology involves functional and structural changes in the respiratory, cardiovascular, and musculoskeletal systems and their integration with peripheral reflexes. These findings suggest potential therapeutic targets, yet unexplored in clinical trials, that could assist in improving exercise tolerance and QoL in patients with pH.

3.
Front Physiol ; 15: 1371839, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38694209

RESUMO

Scientific evidence regarding the effect of different ladder-based resistance training (LRT) protocols on the morphology of the neuromuscular system is scarce. Therefore, the present study aimed to compare the morphological response induced by different LRT protocols in the ultrastructure of the tibial nerve and morphology of the motor endplate and muscle fibers of the soleus and plantaris muscles of young adult Wistar rats. Rats were divided into groups: sedentary control (control, n = 9), a predetermined number of climbs and progressive submaximal intensity (fixed, n = 9), high-intensity and high-volume pyramidal system with a predetermined number of climbs (Pyramid, n = 9) and lrt with a high-intensity pyramidal system to exhaustion (failure, n = 9). myelinated fibers and myelin sheath thickness were statistically larger in pyramid, fixed, and failure. myelinated axons were statistically larger in pyramid than in control. schwann cell nuclei were statistically larger in pyramid, fixed, and failure. microtubules and neurofilaments were greater in pyramid than in control. morphological analysis of the postsynaptic component of the plantar and soleus muscles did not indicate any significant difference. for plantaris, the type i myofibers were statistically larger in the pyramid and fixed compared to control. the pyramid, fixed, and failure groups for type ii myofibers had larger csa than control. for soleus, the type i myofibers were statistically larger in the pyramid than in control. pyramid and fixed had larger csa for type ii myofibers than control and failure. the pyramid and fixed groups showed greater mass progression delta than the failure. We concluded that the LRT protocols with greater volume and progression of accumulated mass elicit more significant changes in the ultrastructure of the tibial nerve and muscle hypertrophy without endplate changes.

4.
J Physiol ; 602(12): 2823-2838, 2024 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-38748778

RESUMO

Skeletal muscle dysfunction is a major problem in critically ill patients suffering from sepsis. This condition is associated with mitochondrial dysfunction and increased autophagy in skeletal muscles. Autophagy is a proteolytic mechanism involved in eliminating dysfunctional cellular components, including mitochondria. The latter process, referred to as mitophagy, is essential for maintaining mitochondrial quality and skeletal muscle health. Recently, a fluorescent reporter system called mito-QC (i.e. mitochondrial quality control) was developed to specifically quantify mitophagy levels. In the present study, we used mito-QC transgenic mice and confocal microscopy to morphologically monitor mitophagy levels during sepsis. To induce sepsis, Mito-QC mice received Escherichia coli lipopolysaccharide (10 mg kg-1 i.p.) or phosphate-buffered saline and skeletal muscles (hindlimb and diaphragm) were excised 48 h later. In control groups, there was a negative correlation between the basal mitophagy level and overall muscle mitochondrial content. Sepsis increased general autophagy in both limb muscles and diaphragm but had no effect on mitophagy levels. Sepsis was associated with a downregulation of certain mitophagy receptors (Fundc1, Bcl2L13, Fkbp8 and Phbb2). The present study suggests that general autophagy and mitophagy can be dissociated from one another, and that the characteristic accumulation of damaged mitochondria in skeletal muscles under the condition of sepsis may reflect a failure of adequate compensatory mitophagy. KEY POINTS: There was a negative correlation between the basal level of skeletal muscle mitophagy and the mitochondrial content of individual muscles. Mitophagy levels in limb muscles and the diaphragm were unaffected by lipopolysaccharide (LPS)-induced sepsis. With the exception of BNIP3 in sepsis, LPS administration induced either no change or a downregulation of mitophagy receptors in skeletal muscles.


Assuntos
Camundongos Transgênicos , Mitofagia , Músculo Esquelético , Sepse , Animais , Sepse/metabolismo , Músculo Esquelético/metabolismo , Músculo Esquelético/patologia , Camundongos , Lipopolissacarídeos/farmacologia , Camundongos Endogâmicos C57BL , Masculino , Mitocôndrias Musculares/metabolismo , Autofagia/fisiologia
5.
Biol Trace Elem Res ; 2024 May 06.
Artigo em Inglês | MEDLINE | ID: mdl-38709369

RESUMO

Neuromuscular excitability is a vital body function, and Mg2+ is an essential regulatory cation for the function of excitable membranes. Loss of Mg2+ homeostasis disturbs fluxes of other cations across cell membranes, leading to pathophysiological electrogenesis, which can eventually cause vital threat to the patient. Chronic subclinical Mg2+ deficiency is an increasingly prevalent condition in the general population. It is associated with an elevated risk of cardiovascular, respiratory and neurological conditions and an increased mortality. Magnesium favours bronchodilation (by antagonizing Ca2+ channels on airway smooth muscle and inhibiting the release of endogenous bronchoconstrictors). Magnesium exerts antihypertensive effects by reducing peripheral vascular resistance (increasing endothelial NO and PgI2 release and inhibiting Ca2+ influx into vascular smooth muscle). Magnesium deficiency disturbs heart impulse generation and propagation by prolonging cell depolarization (due to Na+/K+ pump and Kir channel dysfunction) and dysregulating cardiac gap junctions, causing arrhythmias, while prolonged diastolic Ca2+ release (through leaky RyRs) disturbs cardiac excitation-contraction coupling, compromising diastolic relaxation and systolic contraction. In the brain, Mg2+ regulates the function of ion channels and neurotransmitters (blocks voltage-gated Ca2+ channel-mediated transmitter release, antagonizes NMDARs, activates GABAARs, suppresses nAChR ion current and modulates gap junction channels) and blocks ACh release at neuromuscular junctions. Magnesium exerts multiple therapeutic neuroactive effects (antiepileptic, antimigraine, analgesic, neuroprotective, antidepressant, anxiolytic, etc.). This review focuses on the effects of Mg2+ on excitable tissues in health and disease. As a natural membrane stabilizer, Mg2+ opposes the development of many conditions of hyperexcitability. Its beneficial recompensation and supplementation help treat hyperexcitability and should therefore be considered wherever needed.

6.
Indian J Nucl Med ; 39(1): 61-62, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38817722

RESUMO

Exertion and exercise increase glucose metabolism within the skeletal muscles causing increased fludeoxyglucose (FDG) uptake on 18F-FDG positron emission tomography/computed tomography (PET/CT). Here, we present findings of 18F-FDG PET/CT in a patient with acute viral hepatitis A-induced liver failure with multiple foci of pyoderma and incessant itching resulting in increased FDG uptake in the muscles of the bilateral forearm, producing the "bilateral hot forearm sign."

7.
Cureus ; 16(3): e55981, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38606215

RESUMO

Hypokalemic periodic paralysis (HPP) is an uncommon condition resulting from channelopathy, impacting skeletal muscles. It is distinguished by episodes of sudden and temporary muscle weakness alongside low potassium levels. The normalization of potassium resolves the associated paralysis. Most of these cases are hereditary. Few cases are acquired and are associated with an etiology related to endocrine disorders (e.g., thyrotoxicosis, hyperaldosteronism, and hypercortisolism). It is characterized by acute flaccid paralysis, usually of the ascending type, affecting the proximal region more than the distal region. Herein, we report the case of a 29-year-old male who instead of the ascending type presented with descending-type acute flaccid paralysis. Potassium level at presentation was 1.7 mEq/L. The patient was managed with parenteral and oral potassium supplementation, after which the weakness was completely resolved.

8.
Aging (Albany NY) ; 16(8): 7141-7152, 2024 04 18.
Artigo em Inglês | MEDLINE | ID: mdl-38643465

RESUMO

Disrupted mitochondrial dynamics and mitophagy contribute to functional deterioration of skeletal muscle (SM) during aging, but the regulatory mechanisms are poorly understood. Our previous study demonstrated that the expression of thyroid hormone receptor α (TRα) decreased significantly in aged mice, suggesting that the alteration of thyroidal elements, especially the decreased TRα, might attenuate local THs action thus to cause the degeneration of SM with aging, while the underlying mechanism remains to be further explored. In this study, decreased expression of myogenic regulators Myf5, MyoD1, mitophagy markers Pink1, LC3II/I, p62, as well as mitochondrial dynamic factors Mfn1 and Opa1, accompanied by increased reactive oxygen species (ROS), showed concomitant changes with reduced TRα expression in aged mice. Further TRα loss- and gain-of-function studies in C2C12 revealed that silencing of TRα not only down-regulated the expression of above-mentioned myogenic regulators, mitophagy markers and mitochondrial dynamic factors, but also led to a significant decrease in mitochondrial activity and maximum respiratory capacity, as well as more mitochondrial ROS and damaged mitochondria. Notedly, overexpression of TRα could up-regulate the expression of those myogenic regulators, mitophagy markers and mitochondrial dynamic factors, meanwhile also led to an increase in mitochondrial activity and number. These results confirmed that TRα could concertedly regulate mitochondrial dynamics, autophagy, and activity, and myogenic regulators rhythmically altered with TRα expression. Summarily, these results suggested that the decline of TRα might cause the degeneration of SM with aging by regulating mitochondrial dynamics, mitophagy and myogenesis.


Assuntos
Mitocôndrias , Músculo Esquelético , Sarcopenia , Receptores alfa dos Hormônios Tireóideos , Animais , Camundongos , Envelhecimento/metabolismo , Linhagem Celular , Mitocôndrias/metabolismo , Mitocôndrias/patologia , Mitocôndrias Musculares/metabolismo , Mitocôndrias Musculares/patologia , Dinâmica Mitocondrial , Mitofagia , Músculo Esquelético/metabolismo , Músculo Esquelético/patologia , Espécies Reativas de Oxigênio/metabolismo , Sarcopenia/metabolismo , Sarcopenia/patologia , Receptores alfa dos Hormônios Tireóideos/genética , Receptores alfa dos Hormônios Tireóideos/metabolismo
9.
Biochem Biophys Res Commun ; 715: 150001, 2024 Jun 30.
Artigo em Inglês | MEDLINE | ID: mdl-38676996

RESUMO

The skeletal muscle is a pivotal organ involved in the regulation of both energy metabolism and exercise capacity. There is no doubt that exercise contributes to a healthy life through the consumption of excessive energy or the release of myokines. Skeletal muscles exhibit insulin sensitivity and can rapidly uptake blood glucose. In addition, they can undergo non-shivering thermogenesis through actions of both the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) and small peptide, sarcolipin, resulting in systemic energy metabolism. Accordingly, the maintenance of skeletal muscles is important for both metabolism and exercise. Prolyl isomerase Pin1 is an enzyme that converts the cis-trans form of proline residues and controls substrate function. We have previously reported that Pin1 plays important roles in insulin release, thermogenesis, and lipolysis. However, the roles of Pin1 in skeletal muscles remains unknown. To clarify this issue, we generated skeletal muscle-specific Pin1 knockout mice. Pin1 deficiency had no effects on muscle weights, morphology and ratio of fiber types. However, they showed exacerbated obesity or insulin resistance when fed with a high-fat diet. They also showed a lower ability to exercise than wild type mice did. We also found that Pin1 interacted with SERCA and elevated its activity, resulting in the upregulation of oxygen consumption. Overall, our study reveals that Pin1 in skeletal muscles contributes to both systemic energy metabolism and exercise capacity.


Assuntos
Metabolismo Energético , Músculo Esquelético , Peptidilprolil Isomerase de Interação com NIMA , Condicionamento Físico Animal , ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático , Animais , Masculino , Camundongos , Dieta Hiperlipídica , Metabolismo Energético/genética , Resistência à Insulina , Camundongos Endogâmicos C57BL , Camundongos Knockout , Músculo Esquelético/metabolismo , Peptidilprolil Isomerase de Interação com NIMA/metabolismo , Peptidilprolil Isomerase de Interação com NIMA/genética , ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/metabolismo , ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/genética
10.
Anim Biosci ; 37(8): 1345-1354, 2024 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-38575126

RESUMO

OBJECTIVE: The objective of this study was to identify candidate genes that play important roles in skeletal muscle development in ducks. METHODS: In this study, we investigated the transcriptional sequencing of embryonic pectoral muscles from two specialized lines: Liancheng white ducks (female) and Cherry valley ducks (male) hybrid Line A (LCA) and Line C (LCC) ducks. In addition, prediction of target genes for the differentially expressed mRNAs was conducted and the enriched gene ontology (GO) terms and Kyoto encyclopedia of genes and genomes signaling pathways were further analyzed. Finally, a protein-to-protein interaction network was analyzed by using the target genes to gain insights into their potential functional association. RESULTS: A total of 1,428 differentially expressed genes (DEGs) with 762 being up-regulated genes and 666 being down-regulated genes in pectoral muscle of LCA and LCC ducks identified by RNA-seq (p<0.05). Meanwhile, 23 GO terms in the down-regulated genes and 75 GO terms in up-regulated genes were significantly enriched (p<0.05). Furthermore, the top 5 most enriched pathways were ECM-receptor interaction, fatty acid degradation, pyruvate degradation, PPAR signaling pathway, and glycolysis/gluconeogenesis. Finally, the candidate genes including integrin b3 (Itgb3), pyruvate kinase M1/2 (Pkm), insulinlike growth factor 1 (Igf1), glucose-6-phosphate isomerase (Gpi), GABA type A receptorassociated protein-like 1 (Gabarapl1), and thyroid hormone receptor beta (Thrb) showed the most expression difference, and then were selected to verification by quantitative realtime polymerase chain reaction (qRT-PCR). The result of qRT-PCR was consistent with that of transcriptome sequencing. CONCLUSION: This study provided information of molecular mechanisms underlying the developmental differences in skeletal muscles between specialized duck lines.

11.
Mar Drugs ; 22(3)2024 Feb 28.
Artigo em Inglês | MEDLINE | ID: mdl-38535454

RESUMO

Muscle atrophy is a detrimental and injurious condition that leads to reduced skeletal muscle mass and disruption of protein metabolism. Oyster (Crassostrea nippona) is a famous and commonly consumed shellfish in East Asia and has become a popular dietary choice worldwide. The current investigation evaluated the efficacy of C. nippona against muscle atrophy, which has become a severe health issue. Mammalian skeletal muscles are primarily responsible for efficient metabolism, energy consumption, and body movements. The proteins that regulate muscle hypertrophy and atrophy are involved in muscle growth. C. nippona extracts were enzymatically hydrolyzed using alcalase (AOH), flavourzyme (FOH), and protamex (POH) to evaluate their efficacy in mitigating dexamethasone-induced muscle damage in C2C12 cells in vitro. AOH exhibited notable cell proliferative abilities, promoting dose-dependent myotube formation. These results were further solidified by protein expression analysis. Western blot and gene expression analysis via RT-qPCR demonstrated that AOH downregulated MuRF-1, Atrogin, Smad 2/3, and Foxo-3a, while upregulating myogenin, MyoD, myosin heavy chain expression, and mTOR, key components of the ubiquitin-proteasome and mTOR signaling pathways. Finally, this study suggests that AOH holds promise for alleviating dexamethasone-induced muscle atrophy in C2C12 cells in vitro, offering insights for developing functional foods targeting conditions akin to sarcopenia.


Assuntos
Crassostrea , Animais , Atrofia Muscular , Suplementos Nutricionais , Serina-Treonina Quinases TOR , Dexametasona , Mamíferos
12.
Toxicol Res (Camb) ; 13(2): tfae047, 2024 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-38529200

RESUMO

Trichinellosis is a parasite zoonosis that is spread through ingesting raw or undercooked meat that contains the Trichinella spiralis (T. spiralis) infective larvae. It has three clinical phases: intestinal, migratory, and muscular. Kuth root, also known as Costus (Saussurea lappa) roots, is used in many traditional medical systems all over the world to treat a variety of illnesses, such as dyspepsia, diarrhoea, vomiting, and inflammation. Current study assessed the therapeutic Potential of costus roots extract (CRE) treatment on experimental trichinellosis induce changes in DNA damage, oxidative stress and Proliferating cell nuclear antigen (PCNA) expression in muscle fibers in male rats. A total of 60 male Sprague Dawley rats were divided into 6 groups (Gps) [Gp1, Negative control; Gp2, Costus (CRE); Gp3, Positive control or Infected rats with T. spiralis, Gp4; Pre-treated infection with CRE; Gp5 & Gp6, Post treated infection with CRE for one and two weeks respectively]. Current results revealed that; Trichinella spiralis experimentally infection induced significant elevation in tissue malondialdehyde (MDA), DNA damage, PCNA expression and significant depletion in tissue glutathione (GSH), superoxide dismutase (SOD) and catalase (Cat) activities. Pre or/and post CRE treated infected rats with T. spiralis (Gp4-Gp6) induced improvements and depletion in DNA damage, PCNA expression, MDA and elevation in GSH, SOD, catalase as compared to infected rats with T. spiralis (Gp3) with best results for the pretreatments (Gp4). Trichinella spiralis experimental infection induced DNA damage and oxidative stress in rat skeletal muscles and treatments with costus roots extract modulates these changes.

13.
Postgrad Med J ; 100(1185): 488-495, 2024 Jun 28.
Artigo em Inglês | MEDLINE | ID: mdl-38449066

RESUMO

BACKGROUND: The diagnosis of myasthenia gravis (MG) in children remains difficult. Circulating small extracellular vesicle (sEV)-derived miRNAs (sEV-miRNAs) have been recognized as biomarkers of various diseases and can be excreted by different cell types. These biomarker candidates also play a vital role in autoimmune diseases via intercellular communication. METHODS: In the present study, we used sEV isolation and purification methods to extract the plasma-derived sEV-miRNAs from children with MG and healthy controls. A small RNA sequencing analysis confirmed the miRNA expression features in plasma-derived sEVs from MG patients. The miRNA expression analysis in vitro was determined using microarray analysis. The enrichment and network analyses of altered sEV-miRNAs were performed using miRNA databases and Database for Annotation, Visualization, and Integrated Discovery website. Quantitative real-time polymerase chain reaction was performed for validation of sEV-miRNA. The diagnostic power of altered sEV-miRNAs was evaluated using receiver operating characteristic curve analyses. RESULTS: Twenty-four sEV-miRNAs with altered expression level were identified between groups by DESeq2 method. The miRNAs were extracted from the sEVs, which were isolated from human primary skeletal muscle cell culture treated with mAb198. The target genes and enriched pathways of sEV-miRNAs partially overlapped between cell supernatant and plasma samples. The significantly downregulated miR-143-3p was validated in quantitative real-time polymerase chain reaction analysis. CONCLUSIONS: For the first time, we report that plasma-derived sEV-miRNAs may act as novel circulating biomarkers and therapeutic targets in pediatric MG.


Assuntos
Biomarcadores , Vesículas Extracelulares , MicroRNAs , Músculo Esquelético , Miastenia Gravis , Humanos , Miastenia Gravis/genética , Miastenia Gravis/sangue , Miastenia Gravis/diagnóstico , Vesículas Extracelulares/metabolismo , Criança , MicroRNAs/sangue , Masculino , Feminino , Biomarcadores/sangue , Músculo Esquelético/metabolismo , Estudos de Casos e Controles , Adolescente , Reação em Cadeia da Polimerase em Tempo Real , MicroRNA Circulante/sangue
14.
Respir Care ; 69(6): 640-650, 2024 May 28.
Artigo em Inglês | MEDLINE | ID: mdl-38503465

RESUMO

Exercise limitation is a characteristic feature of chronic respiratory diseases such as COPD and is associated with poor outcomes including decreased functional status and health-related quality of life and increased mortality. The mechanisms responsible for exercise limitation are complex and include ventilatory limitation, cardiovascular impairment, and skeletal muscle dysfunction. In addition, comorbidities such as cardiovascular disease are common in this population and can further impact exercise capacity. Exercise training, a core component of pulmonary rehabilitation, improves exercise capacity by addressing many of these mechanisms that, in turn, can potentially slow the decline of lung function, reduce the frequency of exacerbations, and decrease mortality. This article will discuss the mechanisms of exercise limitation in individuals with chronic respiratory disease, primarily focusing on COPD, and provide an overview of exercise training and its benefits in this patient population.


Assuntos
Terapia por Exercício , Tolerância ao Exercício , Doença Pulmonar Obstrutiva Crônica , Qualidade de Vida , Humanos , Doença Pulmonar Obstrutiva Crônica/reabilitação , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Terapia por Exercício/métodos , Tolerância ao Exercício/fisiologia , Exercício Físico/fisiologia , Músculo Esquelético/fisiopatologia
15.
Acta Physiol (Oxf) ; 240(5): e14129, 2024 05.
Artigo em Inglês | MEDLINE | ID: mdl-38459757

RESUMO

AIM: The influence on acute skeletal muscle transcriptomics of neuromuscular electrical stimulation (NMES), as compared to established exercises, is poorly understood. We aimed to investigate the effects on global mRNA-expression in the quadriceps muscle early after a single NMES-session, compared to the effects of voluntary knee extension exercise (EX), and to explore the discomfort level. METHODS: Global vastus lateralis muscle gene expression was assessed (RNA-sequencing) in 30 healthy participants, before and 3 h after a 30-min session of NMES and/or EX. The NMES-treatment was applied using textile electrodes integrated in pants and set to 20% of each participant's pre-tested MVC mean (±SD) 200 (±80) Nm. Discomfort was assessed using Visual Analogue Scale (VAS, 0-10). The EX-protocol was performed at 80% of 1-repetition-maximum. RESULTS: NMES at 20% of MVC resulted in VAS below 4 and induced 4448 differentially expressed genes (DEGs) with 80%-overlap of the 2571 DEGs of EX. Genes well-known to be up-regulated following exercise, for example, PPARGC1A, ABRA, VEGFA, and GDNF, were also up-regulated by NMES. Gene set enrichment analysis demonstrated many common pathways after EX and NMES. Also, some pathways were exclusive to either EX, for example, muscle tissue proliferation, or to NMES, for example, neurite outgrowth and connective tissue proliferation. CONCLUSION: A 30-min NMES-session at 20% of MVC with NMES-pants, which can be applied with an acceptable level of discomfort, induces over 4000 DEGs, of which 80%-overlap with DEGs of EX. NMES can induce exercise-like molecular effects, that potentially can lead to health and performance benefits in individuals who are unable to perform resistance exercise.


Assuntos
Estimulação Elétrica , Músculo Esquelético , Transcriptoma , Humanos , Masculino , Adulto , Músculo Esquelético/metabolismo , Músculo Esquelético/fisiologia , Estimulação Elétrica/métodos , Feminino , Músculo Quadríceps/metabolismo , Músculo Quadríceps/fisiologia , Adulto Jovem , Exercício Físico/fisiologia
16.
BMC Vet Res ; 20(1): 73, 2024 Feb 24.
Artigo em Inglês | MEDLINE | ID: mdl-38402164

RESUMO

BACKGROUND: Telocytes are modified interstitial cells that communicate with other types of cells, including stem cells. Stemness properties render them more susceptible to environmental conditions. The current morphological investigation examined the reactions of telocytes to salt stress in relation to stem cells and myoblasts. The common carp are subjected to salinity levels of 0.2, 6, and 10 ppt. The gill samples were preserved and prepared for TEM. RESULTS: The present study observed that telocytes undergo morphological change and exhibit enhanced secretory activities in response to changes in salinity. TEM can identify typical telocytes. This research gives evidence for the communication of telocytes with stem cells, myoblasts, and skeletal muscles. Telocytes surround stem cells. Telopodes made planar contact with the cell membrane of the stem cell. Telocytes and their telopodes surrounded the skeletal myoblast. These findings show that telocytes may act as nurse cells for skeletal stem cells and myoblasts, which undergo fibrillogenesis. Not only telocytes undergo morphological alternations, but also skeletal muscles become hypertrophied, which receive telocyte secretory vesicles in intercellular compartments. CONCLUSION: In conclusion, the activation of telocytes is what causes stress adaptation. They might act as important players in intercellular communication between cells. It is also possible that reciprocal interaction occurs between telocytes and other cells to adapt to changing environmental conditions.


Assuntos
Carpas , Telócitos , Animais , Salinidade , Telócitos/metabolismo , Microscopia Eletrônica de Transmissão/veterinária , Músculo Esquelético , Células-Tronco , Mioblastos
17.
Gene ; 904: 148216, 2024 Apr 30.
Artigo em Inglês | MEDLINE | ID: mdl-38307219

RESUMO

Multiple post-receptor intracellular alterations such as impaired glucose transfer, glucose phosphorylation, decreased glucose oxidation, and glycogen production contribute to insulin resistance (IR) in skeletal muscle, manifested by diminished insulin-stimulated glucose uptake. Type-2 diabetes mellites (T2DM) has caused by IR, which is also seen in obese patients and those with metabolic syndrome. The Vitamin-D receptor (VDR) and poly unsaturated fatty acids (PUFAs) roles in skeletal muscle growth, shapes, and function for combating type-2 diabetes have been clarified throughout this research. VDR and PUFAs appears to show a variety of effects on skeletal muscle, in addition it shows a promising role on bone and mineral homeostasis. Individuals having T2DM are reported to suffer from severe muscular weakness and alterations in shape of the muscle. Several studies have investigated the effect on VDR on muscular strength and mass, which leads to Vitamin-D deficiency (VDD) in individuals, in which most commonly seen in elderly. VDR has been shown to affect skeletal cellular proliferation, intracellular calcium handling, as well as genomic activity in a variety of different ways such as muscle metabolism, insulin sensitivity, which is the major characteristic pathogenesis for IR in combating T2DM. The identified VDR gene polymorphisms are ApaI, TaqI, FokI, and BsmI that are associated with T2DM. This review collates informations on the mechanisms by which VDR activation takes place in skeletal muscles. Despite the significant breakthroughs made in recent decades, various studies show that IR affects VDR and PUFAs metabolism in skeletal muscle. Therefore, this review collates the data to show the role of VDR and PUFAs in the skeletal muscles to combat T2DM.


Assuntos
Diabetes Mellitus Tipo 2 , Resistência à Insulina , Humanos , Idoso , Vitamina D , Diabetes Mellitus Tipo 2/metabolismo , Receptores de Calcitriol/genética , Resistência à Insulina/genética , Vitaminas , Músculo Esquelético/metabolismo , Glucose
18.
J Allergy Clin Immunol Pract ; 12(5): 1254-1262.e1, 2024 May.
Artigo em Inglês | MEDLINE | ID: mdl-38316184

RESUMO

BACKGROUND: People with asthma may have skeletal muscle dysfunction but data describing core function in severe asthma are limited. OBJECTIVE: To compare core function between people with severe asthma and healthy controls and to determine the difference between males and females. Furthermore, we aimed to investigate the association between core function and breathing symptoms. METHOD: Adults with a diagnosis of severe asthma and healthy controls undertook an assessment that included 3 core function tests: partial sit-up, Biering-Sorensen, and side bridge. Breathing symptoms were assessed by the modified Medical Research Council dyspnea scale, modified Borg scale, and Nijmegen questionnaire. RESULTS: People with severe asthma (n = 136) (38% male, age median [Q1-Q3] 59 y [45-68], body mass index 30 kg/m2 [26-37]) were compared with 66 people without respiratory disease (47% male, age 55 y [34-65], body mass index 25 kg/m2 [22-28]). There was no difference between groups in the partial sit-up (P = .09). However, participants with severe asthma performed worse with the Biering-Sorensen (P < .001), and the left and right side bridge test (P < .001 for both) than the healthy comparison group. Similar results were found when comparing males and females separately. Males with severe asthma had increased function compared with their female counterparts in the left side bridge test. Core function tests correlated with the breathing symptom measures, the modified Medical Research Council, modified Borg scale, and Nijmegen questionnaire (-0.51 > r > -0.19; P ≤ .03). CONCLUSIONS: Adults with severe asthma have worse core function than their control counterparts, independent of sex. Furthermore, as core function decreases, breathing symptoms increase.


Assuntos
Asma , Índice de Gravidade de Doença , Humanos , Asma/fisiopatologia , Asma/diagnóstico , Masculino , Feminino , Pessoa de Meia-Idade , Adulto , Idoso , Inquéritos e Questionários , Dispneia/fisiopatologia , Respiração , Fatores Sexuais , Testes de Função Respiratória , Índice de Massa Corporal
19.
J Am Heart Assoc ; 13(2): e031085, 2024 Jan 16.
Artigo em Inglês | MEDLINE | ID: mdl-38214271

RESUMO

BACKGROUND: Skeletal muscles are postulated to be a potent regulator of systemic nitric oxide homeostasis. In this study, we aimed to evaluate the impact of physical training on the heart and skeletal muscle nitric oxide bioavailability (judged on the basis of intramuscular nitrite and nitrate) in rats. METHODS AND RESULTS: Rats were trained on a treadmill for 8 weeks, performing mainly endurance running sessions with some sprinting runs. Muscle nitrite (NO2-) and nitrate (NO3-) concentrations were measured using a high-performance liquid chromatography-based method, while amino acids, pyruvate, lactate, and reduced and oxidized glutathione were determined using a liquid chromatography coupled with tandem mass spectrometry technique. The content of muscle nitrite reductases (electron transport chain proteins, myoglobin, and xanthine oxidase) was assessed by western immunoblotting. We found that 8 weeks of endurance training decreased basal NO2- in the locomotory muscles and in the heart, without changes in the basal NO3-. In the slow-twitch oxidative soleus muscle, the decrease in NO2- was already present after the first week of training, and the content of nitrite reductases remained unchanged throughout the entire period of training, except for the electron transport chain protein content, which increased no sooner than after 8 weeks of training. CONCLUSIONS: Muscle NO2- level, opposed to NO3-, decreases in the time course of training. This effect is rapid and already visible in the slow-oxidative soleus after the first week of training. The underlying mechanisms of training-induced muscle NO2- decrease may involve an increase in the oxidative stress, as well as metabolite changes related to an increased muscle anaerobic glycolytic activity contributing to (1) direct chemical reduction of NO2- or (2) activation of muscle nitrite reductases.


Assuntos
Nitratos , Condicionamento Físico Animal , Ratos , Animais , Nitratos/metabolismo , Nitritos , Óxido Nítrico/metabolismo , Dióxido de Nitrogênio/metabolismo , Músculo Esquelético/metabolismo , Exercício Físico , Nitrito Redutases/metabolismo
20.
Arch Biochem Biophys ; 752: 109881, 2024 02.
Artigo em Inglês | MEDLINE | ID: mdl-38185233

RESUMO

Tropomyosin (Tpm) is a regulatory actin-binding protein involved in Ca2+ activation of contraction of striated muscle. In human slow skeletal muscles, two distinct Tpm isoforms, γ and ß, are present. They interact to form three types of dimeric Tpm molecules: γγ-homodimers, γß-heterodimers, or ßß-homodimers, and a majority of the molecules are present as γß-Tpm heterodimers. Point mutation R91P within the TPM3 gene encoding γ-Tpm is linked to the condition known as congenital fiber-type disproportion (CFTD), which is characterized by severe muscle weakness. Here, we investigated the influence of the R91P mutation in the γ-chain on the properties of the γß-Tpm heterodimer. We found that the R91P mutation impairs the functional properties of γß-Tpm heterodimer more severely than those of earlier studied γγ-Tpm homodimer carrying this mutation in both γ-chains. Since a significant part of Tpm molecules in slow skeletal muscle is present as γß-heterodimers, our results explain why this mutation leads to muscle weakness in CFTD.


Assuntos
Doenças Musculares , Tropomiosina , Humanos , Tropomiosina/química , Músculo Esquelético/metabolismo , Doenças Musculares/genética , Mutação , Debilidade Muscular/metabolismo , Actinas/genética , Actinas/metabolismo
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