Much research has been done in sports nutrition in recent years as the demand for performance-enhancing substances increases. Higher intake of nitrates from the diet can increase the bioavailability of nitric oxide (NO) via the nitrate-nitrite-NO pathway. Nevertheless, the increased availability of NO does not always lead to improved performance in some individuals. This review aims to evaluate the relationship between the athlete's training status and the change in time trial performance after increased dietary nitrate intake. Articles indexed by Scopus and PubMed published from 2015 to 2019 were reviewed. Thirteen articles met the eligibility criteria: clinical trial studies on healthy participants with different training status (according to VO2max), conducting time trial tests after dietary nitrate supplementation. The PRISMA guidelines were followed to process the review. We found a statistically significant relationship between VO2max and ergogenicity in time trial performance using one-way ANOVA (p = 0.001) in less-trained athletes (VO2 < 55 mL/kg/min). A strong positive correlation was observed in experimental situations using a chronic supplementation protocol but not in acute protocol situations. In the context of our results and recent histological observations of muscle fibres, there might be a fibre-type specific role in nitric oxide production and, therefore, supplement of ergogenicity.

• MeSH
• časové faktory MeSH
• databáze faktografické MeSH
• dusičnany farmakologie   MeSH
• fyzická vytrvalost účinky léků   MeSH
• kosterní svalová vlákna účinky léků   MeSH
• látky zvyšující výkon farmakologie   MeSH
• lidé MeSH
• oxid dusnatý farmakologie   MeSH
• potravní doplňky MeSH
• sportovci * MeSH
• sportovní výkon MeSH
• spotřeba kyslíku MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• systematický přehled MeSH

Cold exposure depolarizes cells in insects due to a reduced electrogenic ion transport and a gradual increase in extracellular K+ concentration ([K+]). Cold-induced depolarization is linked to cold injury in chill-susceptible insects, and the locust, Locusta migratoria, has been shown to improve cold tolerance following cold acclimation through depolarization resistance. Here we investigate how cold acclimation influences depolarization resistance and how this resistance relates to improved cold tolerance. To address this question, we investigated if cold acclimation affects the electrogenic transport capacity and/or the relative K+ permeability during cold exposure by measuring membrane potentials of warm- and cold-acclimated locusts in the presence and absence of ouabain (Na+-K+ pump blocker) or 4-aminopyridine (4-AP; voltage-gated K+ channel blocker). In addition, we compared the membrane lipid composition of muscle tissue from warm- and cold-acclimated locust and the abundance of a range transcripts related to ion transport and cell injury accumulation. We found that cold-acclimated locusts are depolarization resistant due to an elevated K+ permeability, facilitated by opening of 4-AP-sensitive K+ channels. In accordance, cold acclimation was associated with an increased abundance of Shaker transcripts (gene encoding 4-AP-sensitive voltage-gated K+ channels). Furthermore, we found that cold acclimation improved muscle cell viability following exposure to cold and hyperkalemia even when muscles were depolarized substantially. Thus cold acclimation confers resistance to depolarization by altering the relative ion permeability, but cold-acclimated locusts are also more tolerant to depolarization.

• MeSH
• 4-aminopyridin farmakologie   MeSH
• aklimatizace účinky léků   fyziologie   MeSH
• kosterní svalová vlákna účinky léků   fyziologie   MeSH
• Locusta migratoria fyziologie   MeSH
• membránové potenciály účinky léků   fyziologie   MeSH
• nízká teplota * MeSH
• ouabain farmakologie   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Typically, mammalian and avian models have been used to examine the effects of ammonia on skeletal muscle. Hyperammonemia causes sarcopenia or muscle wasting, in mammals and has been linked to sarcopenia in liver disease patients. Avian models of skeletal muscle have responded positively to hyperammonemia, differing from the mammalian response. Fish skeletal muscle has not been examined as extensively as mammalian and avian muscle. Fish skeletal muscle shares similarities with avian and mammalian muscle but has notable differences in growth, fiber distribution, and response to the environment. The wide array of body sizes and locomotion needs of fish also leads to greater diversity in muscle fiber distribution and growth between different fish species. The response of fish muscle to high levels of ammonia is important for aquaculture and quality food production but has not been extensively studied to date. Understanding the differences between fish, mammalian and avian species' myogenic response to hyperammonemia could lead to new therapies for muscle wasting due to a greater understanding of the mechanisms behind skeletal muscle regulation and how ammonia effects these mechanisms. This paper provides an overview of fish skeletal muscle and ammonia excretion and toxicity in fish, as well as a comparison to avian and mammalian species.

• MeSH
• amoniak farmakologie   toxicita   MeSH
• hyperamonemie etiologie   MeSH
• jaterní cirhóza etiologie   MeSH
• kosterní svalová vlákna účinky léků   MeSH
• kosterní svaly účinky léků   metabolismus   MeSH
• ptáci MeSH
• ryby MeSH
• sarkopenie etiologie   MeSH
• savci MeSH
• svalová atrofie metabolismus   patofyziologie   MeSH
• vývoj svalů účinky léků   fyziologie   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

OBJECTIVES: Propofol may adversely affect the function of mitochondria and the clinical features of propofol infusion syndrome suggest that this may be linked to propofol-related bioenergetic failure. We aimed to assess the effect of therapeutic propofol concentrations on energy metabolism in human skeletal muscle cells. DESIGN: In vitro study on human skeletal muscle cells. SETTINGS: University research laboratories. SUBJECTS: Patients undergoing hip surgery and healthy volunteers. INTERVENTIONS: Vastus lateralis biopsies were processed to obtain cultured myotubes, which were exposed to a range of 1-10 μg/mL propofol for 96 hours. MEASUREMENTS AND MAIN RESULTS: Extracellular flux analysis was used to measure global mitochondrial functional indices, glycolysis, fatty acid oxidation, and the functional capacities of individual complexes of electron transfer chain. In addition, we used [1-C]palmitate to measure fatty acid oxidation and spectrophotometry to assess activities of individual electron transfer chain complexes II-IV. Although cell survival and basal oxygen consumption rate were only affected by 10 μg/mL of propofol, concentrations as low as 1 μg/mL reduced spare electron transfer chain capacity. Uncoupling effects of propofol were mild, and not dependent on concentration. There was no inhibition of any respiratory complexes with low dose propofol, but we found a profound inhibition of fatty acid oxidation. Addition of extra fatty acids into the media counteracted the propofol effects on electron transfer chain, suggesting inhibition of fatty acid oxidation as the causative mechanism of reduced spare electron transfer chain capacity. Whether these metabolic in vitro changes are observable in other organs and at the whole-body level remains to be investigated. CONCLUSIONS: Concentrations of propofol seen in plasma of sedated patients in ICU cause a significant inhibition of fatty acid oxidation in human skeletal muscle cells and reduce spare capacity of electron transfer chain in mitochondria.

• MeSH
• energetický metabolismus MeSH
• hypnotika a sedativa škodlivé účinky   farmakologie   MeSH
• kosterní svalová vlákna účinky léků   metabolismus   MeSH
• kosterní svaly cytologie   účinky léků   metabolismus   MeSH
• kultivované buňky MeSH
• lidé MeSH
• propofol škodlivé účinky   farmakologie   MeSH
• senioři MeSH
• spotřeba kyslíku účinky léků   MeSH
• svalové mitochondrie účinky léků   metabolismus   MeSH
• techniky in vitro MeSH
• Check Tag
• lidé MeSH
• senioři MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

The cancerogen 1,2-dimethylhydrazine (DMH), widely used in the experimental animal model of carcinogenesis, affects various organs, but its effect on muscle fibers is unknown. To evaluate the effect of 15-week DMH treatment on the fiber size and myosin heavy chain (MyHC) isoforms, which substantially determine fiber types and their contractile characteristics, pure and hybrid fiber types were immunohistochemically determined according to the MyHC isoform expression in soleus, extensor digitorum longus, gastrocnemius medialis and lateralis muscles of DMH-treated and control male Wistar rats. Whereas the size of fibers was mostly unaffected, the MyHC isoform expression was partially affected in both gastrocnemius samples, but not in the soleus and extensor digitorum longus of DMH-treated rats. The lower proportions of hybrid fiber types and especially that of type 1/2x in most gastrocnemius samples of DMH-treated rats resulted in a shift towards a single MyHC isoform expression, but the extent and pattern of the MyHC isoform shift varied across the different gastrocnemius samples. Such variable response to DMH treatment across muscles indicates that each muscle possesses its own adaptive range. These findings are essential for an accurate evaluation of skeletal muscle characteristics in DMH animal model.

• MeSH
• 1,2-dimethylhydrazin toxicita   MeSH
• karcinogeny toxicita   MeSH
• kosterní svalová vlákna účinky léků   metabolismus   patologie   MeSH
• krysa rodu rattus MeSH
• potkani Wistar MeSH
• svalová vlákna typu I účinky léků   metabolismus   patologie   MeSH
• svalová vlákna typu II účinky léků   metabolismus   patologie   MeSH
• těžké řetězce myosinu biosyntéza   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

BACKGROUND: Glutamine has been considered essential for rapidly dividing cells, but its effect on mitochondrial function is unknown. MATERIALS AND METHODS: Human myoblasts were isolated from skeletal muscle biopsy samples (n = 9) and exposed for 20 days to 6 different glutamine concentrations (0, 100, 200, 300, 500, and 5000 µM). Cells were trypsinized and manually counted every 5 days. Seven days before the end of exposure, half of these cells were allowed to differentiate to myotubes. Afterward, energy metabolism in both myotubes and myoblasts was assessed by extracellular flux analysis (Seahorse Biosciences, Billerica, MA). The protocol for myoblasts was optimized in preliminary experiments. To account for different mitochondrial density or cell count, data were normalized to citrate synthase activity. RESULTS: Fastest myoblast proliferation was observed at 300 µM glutamine, with a significant reduction at 0 and 100 µM. Glutamine did not influence basal oxygen consumption, anaerobic glycolysis or respiratory chain capacity. Glutamine significantly (P = .015) influenced the leak through the inner mitochondrial membrane. Efficiency of respiratory chain was highest at 200-300 µM glutamine (~90% of oxygen used for adenosine triphosphate synthesis). Increased glutamine concentration to 500 or 5000 µM caused mitochondrial uncoupling in myoblasts and myotubes, decreasing the efficiency of the respiratory chain to ~70%. CONCLUSION: Glutamine concentrations, consistent with moderate clinical hypoglutaminemia (300 µM), bring about an optimal condition of myoblast proliferation and for efficiency of aerobic phosphorylation in an in vitro model of human skeletal muscle. These data support the hypothesis of hypoglutaminemia as an adaptive phenomenon in conditions leading to bioenergetic failure (eg, critical illness).

• MeSH
• biopsie MeSH
• energetický metabolismus účinky léků   MeSH
• fosforylace účinky léků   MeSH
• glutamin metabolismus   farmakologie   MeSH
• kosterní svalová vlákna cytologie   účinky léků   MeSH
• kosterní svaly cytologie   MeSH
• lidé MeSH
• mitochondrie účinky léků   metabolismus   MeSH
• myoblasty kosterní cytologie   účinky léků   MeSH
• proliferace buněk účinky léků   MeSH
• spotřeba kyslíku účinky léků   MeSH
• techniky in vitro MeSH
• transport elektronů účinky léků   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH

Organophosphorus nerve agents inhibit acetylcholinesterase (AChE) which causes the breakdown of the transmitter acetylcholine (ACh) in the synaptic cleft. Overstimulation of cholinergic receptors (muscarinic and nicotinic) by excessive amounts of ACh causes several health problems and may even cause death. Reversible AChE inhibitors play an important role in prophylaxis against nerve agents. The presented study investigated whether 7-methoxytacrine (7-MEOTA) and 7-MEOTA-donepezil derivatives can act as central and peripheral reversible AChE inhibitors and simultaneously antagonize muscarinic and nicotinic receptors. The possible mechanism of action was studied on cell cultures (patch clamp technique, calcium mobilization assay) and on isolated smooth muscle tissue (contraction study). Furthermore, the kinetics of the compounds were also examined. CNS availability was predicted by determining the passive blood-brain barrier penetration estimated via a modified PAMPA assay. In conclusion, this study provides promising evidence that the new synthesized 7-MEOTA-donepezil derivatives have the desired anticholinergic effect; they can inhibit AChE, and nicotinic and muscarinic receptors in the micromolar range. Furthermore, they seem to penetrate readily into the CNS. However, their real potency and benefit must be verified by in vivo experiments.

• MeSH
• antagonisté muskarinových receptorů aplikace a dávkování   MeSH
• cholinergní antagonisté aplikace a dávkování   MeSH
• indany aplikace a dávkování   MeSH
• kosterní svalová vlákna účinky léků   metabolismus   MeSH
• krysa rodu rattus MeSH
• kultivované buňky MeSH
• nikotinoví antagonisté aplikace a dávkování   MeSH
• piperidiny aplikace a dávkování   MeSH
• potkani Wistar MeSH
• takrin aplikace a dávkování   analogy a deriváty   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Insulin resistance, the key defect in type 2 diabetes (T2D), is associated with a low capacity to adapt fuel oxidation to fuel availability, i.e., metabolic inflexibility. This, in turn, contributes to a further damage of insulin signaling. Effectiveness of T2D treatment depends in large part on the improvement of insulin sensitivity and metabolic adaptability of the muscle, the main site of whole-body glucose utilization. We have shown previously in mice fed an obesogenic high-fat diet that a combined use of n-3 long-chain polyunsaturated fatty acids (n-3 LC-PUFA) and thiazolidinediones (TZDs), anti-diabetic drugs, preserved metabolic health and synergistically improved muscle insulin sensitivity. We investigated here whether n-3 LC-PUFA could elicit additive beneficial effects on metabolic flexibility when combined with a TZD drug rosiglitazone. Adult male C57BL/6N mice were fed an obesogenic corn oil-based high-fat diet (cHF) for 8 weeks, or randomly assigned to various interventions: cHF with n-3 LC-PUFA concentrate replacing 15% of dietary lipids (cHF+F), cHF with 10 mg rosiglitazone/kg diet (cHF+ROSI), cHF+F+ROSI, or chow-fed. Indirect calorimetry demonstrated superior preservation of metabolic flexibility to carbohydrates in response to the combined intervention. Metabolomic and gene expression analyses in the muscle suggested distinct and complementary effects of the interventions, with n-3 LC-PUFA supporting complete oxidation of fatty acids in mitochondria and the combination with n-3 LC-PUFA and rosiglitazone augmenting insulin sensitivity by the modulation of branched-chain amino acid metabolism. These beneficial metabolic effects were associated with the activation of the switch between glycolytic and oxidative muscle fibers, especially in the cHF+F+ROSI mice. Our results further support the idea that the combined use of n-3 LC-PUFA and TZDs could improve the efficacy of the therapy of obese and diabetic patients.

• MeSH
• dieta s vysokým obsahem tuků škodlivé účinky   MeSH
• glykolýza účinky léků   MeSH
• kosterní svalová vlákna účinky léků   metabolismus   MeSH
• kosterní svaly účinky léků   metabolismus   MeSH
• kyseliny mastné omega-3 farmakologie   MeSH
• metabolomika MeSH
• myši inbrední C57BL MeSH
• myši MeSH
• obezita etiologie   metabolismus   MeSH
• oxidace-redukce účinky léků   MeSH
• regulace genové exprese účinky léků   MeSH
• synergismus léků MeSH
• thiazolidindiony farmakologie   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

OBJECTIVES: The S100A4 protein is known as a metastasis promoting factor; however, its involvement in non-malignant diseases such as RA and psoriasis has been recently described. The aim of this study was to investigate the expression and possible role of S100A4 in idiopathic inflammatory myopathies. METHODS: S100A4 protein expression was detected by immunohistochemistry in muscle tissue from control individuals (n = 11) and patients with PM and DM (n = 8/6). IF staining was used to co-localize S100A4 with selected cells. Cytokine expression and protein synthesis in S100A4-treated cells were analysed by RT-PCR and ELISA. RESULTS: S100A4 protein was significantly up-regulated in muscle tissue of patients with inflammatory myopathies compared with control individuals and was associated particularly with the presence of mononuclear infiltrates. Only few regenerating muscle fibres in PM/DM expressed S100A4. Then we analysed the effect of S100A4 on human myocytes and peripheral blood mononuclear cells (PBMCs). Although S100A4 did not affect myocytes, stimulation of PBMCs with S100A4 significantly induced the expression and synthesis of TNF-α, IL-1β and IL-6, but not of IFN-α. We showed that S100A4 is not directly involved in perforin/granzyme B-induced apoptosis and that it does not modulate the expression of Bax and Bcl2 mRNA in myocytes and PBMCs. CONCLUSION: Increased expression of S100A4 in inflamed muscle tissue highlights its potential role in the pathogenesis of inflammatory myopathies. S100A4 may act as a cytokine-like factor indirectly promoting muscle fibre damage by stimulating mononuclear cells to increase the synthesis of pro-inflammatory cytokines.

• MeSH
• biologické markery metabolismus   MeSH
• cytokiny genetika   metabolismus   MeSH
• dermatomyozitida genetika   metabolismus   patologie   MeSH
• dospělí MeSH
• exprese genu MeSH
• kosterní svalová vlákna účinky léků   metabolismus   patologie   MeSH
• kosterní svaly metabolismus   patologie   MeSH
• leukocyty mononukleární účinky léků   metabolismus   MeSH
• lidé středního věku MeSH
• lidé MeSH
• lipopolysacharidy farmakologie   MeSH
• messenger RNA metabolismus   MeSH
• polymyozitida genetika   metabolismus   patologie   MeSH
• proteiny S100 genetika   metabolismus   farmakologie   MeSH
• rekombinantní proteiny farmakologie   MeSH
• senioři MeSH
• upregulace účinky léků   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Ve svalové tkáni při myasthenii gravis (MG) byly už dříve popsány histologické změny (lymfocytární infiltráty, atrofie vláken II. typu). Patogeneze těchto změn však zůstala nejasná. V naší studii jsme provedli systematickou analýzu svalových biopsií pacientů s MG s cílem zmapovat histopatologické změny mimo nervosvalovou ploténku, objasnit spojitost těchto změn s vlastní MG a stanovit jejich případný prognostický význam. Soubor a metodika: Biopsiem. sternothyroideus 207 pacientů s MG odebrané během thymektomie byly analyzovány histopatologicky, histochemicky a morfometricky. Výsledky byly korelovány s klinickými a laboratorními parametry onemocnění. Výsledky: U 143 pacientů jsme v svalové tkáni nezaznamenali žádné histopatologické změny.Ve 20 případech jsme v intersticiu svalové tkáně nalezli infiltraci lymfocyty; na rozdíl od polymyozitidy se však jednalo o zralé naivní CR45RA+ T lymfocyty. Lymfocytární infiltrace měla vztah k onemocnění thymu. Ve 35 případech jsme morfometricky zjistili atrofii vláken II. typu, korelující s léčbou kortikosteroidy. Tito pacienti dosáhli remise onemocnění po delší době než pacienti bez atrofie. Ve 12 biopsiích jsme nalezli nevýrazné známky porušeného mitochondriálního metabolizmu, ve 34 případech byla přítomna angulární atrofická vlákna; pro žádnou z těchto změn jsme neprokázali prognostický význam. Závěry: Strukturální změny svalové tkáně při MG mimo nervosvalovou ploténku většinou nejsou odrazem vlastní MG; spíše se jedná o důsledek onemocnění thymu nebo dlouhodobé terapie kortikosteroidy. K diskuzi zůstává otázka, zda má smysl u pacientů s MG svalovou biopsii během thymektomie nadále provádět, přínos získaných informací je spíše sporný.

Surprisingly, structural changes outside the neuromuscular junctions were reported in limited series of myasthenia gravis (MG) muscles previously - mainly small collection of interstitial lymphocytes and atrophy of type II muscle fibers. However, the pathophysiological mechanisms remained unclear. We performed a systematic study on MG muscle biopsies to contribute to understanding of the association to MG and to demonstrate possible prognostic value. Methods: Sternothyroid muscle biopsies from 207 MG patients taken during thymectomy were analyzed histopathologically and by histochemistry and morphometry and correlated to the clinical features and the outcome of MG patients. Results: In 143 MG patients, no obvious pathological changes were observed in muscle biopsies. In 20 patients we observed an interstitial infiltration by mature naive CD45RA+lymphocytes. The lymphocytic infiltration associated with the thymus pathology, mainly with thymoma. The morphometry disclosed selective atrophy of type II muscle fibers in 35 cases. The atrophy of type II muscle fibers was related to long-term corticosteroid treatment and the potential prognostic value could be demonstrated for its detection: the MG patients with type II fibers atrophy presented slower tendency to reach remission. Further, in 12 cases we demonstrated mild changes in mitochondrial metabolism, in 34 cases we disclosed angular atrophic fibers; no prognostic value was demonstrated for these changes. Conclusions: The previously reported histopathological changes in MG muscle are rare and mostly do not represent a feature of the MG, rather a consequence of the thymic disorder or of the long-term steroid therapy. The value of muscle biopsy performed during thymectomy for the particular MG patient remains controversial.

• MeSH
• biopsie metody   využití   MeSH
• financování organizované MeSH
• hormony kůry nadledvin škodlivé účinky   terapeutické užití   MeSH
• klinické laboratorní techniky metody   využití   MeSH
• kosterní svalová vlákna patologie   účinky léků   MeSH
• lidé MeSH
• mitochondriální myopatie diagnóza   MeSH
• myasthenia gravis diagnóza   chirurgie   komplikace   MeSH
• polymyozitida diagnóza   MeSH
• statistika jako téma metody   MeSH
• svalové atrofie diagnóza   etiologie   komplikace   MeSH
• thymektomie metody   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• hodnotící studie MeSH