3D microscopy and image analysis provide reliable measurements of length, branching, density, tortuosity and orientation of tubular structures in biological samples. We present a survey of methods for analysis of large samples by measurement of local differences in geometrical characteristics. The methods are demonstrated on the structure of the capillary bed in a rat brain., J. Janáček ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
The purpose of this study was to determine if there is flowmediated vasodilation of the femoral artery in response to progressive increases in flow within a physiological range observed in the in vivo experiments. Femoral artery blood flow was determined in conscious rabbits (n=5) using chronically implanted flowprobes. Resting blood flow was 8.3±0.6 ml/min and increased to 39.9±5.4 ml/min during high intensity exercise. Femoral arteries (n=12, 1705±43 μm outer diameter) harvested from a separate group of rabbits were mounted on cannulas and diameter was continuously monitored by video system. Functional integrity of the endothelium was tested with acetylcholine. The arteries were set at a transmural pressure of 100 mm Hg and preconstricted with phenylephrine to 73±3 % of initial diameter. Using a roller pump with pressure held constant, the arteries were perfused intraluminally with warmed, oxygenated Krebs' solution (pH=7.4) over a physiological range of flows up to 35 ml/min. As flow increased from 5 ml/min to 35 ml/min, diameter decreased significantly (p<0.05) from 1285±58 μm to 1100±49 μm. Thus, in vessels with a functional endothelium, increasing intraluminal flow over a physiological range of flows produced constriction, not dilation. Based on these results, it seems unlikely that flow-mediated vasodilation in the rabbit femoral artery contributes to exercise hyperemia., P. S. Clifford ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
The purpose of the present study was to investigate whether peripheral brain-derived neurotrophic factor (BDNF) treatment induced metabolic adaptations in mouse skeletal muscle. BDNF (20 mg/kg/day) was injected subcutaneously for successive 14 days. BDNF treatment significantly reduced the total food intake and inhibited the weight gain in comparison to the control group. The glucose transporter 4 (GLUT4) protein expression in the gastrocnemius muscle was significantly increased by BDNF treatment in comparison to the control and pair-fed groups. Neither the oxidative nor the glycolytic enzyme activities in the gastrocnemius muscle changed after the BDNF treatment. These results suggest that the peripheral BDNF treatment promotes the skeletal muscle GLUT4 protein expression as well as hypophagia., M. Suwa ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Adipocyte fatty acid binding protein (A-FABP) is a novel adipokine involved in the regulation of lipid and glucose metabolism and inflammation. To evaluate its potential role in the development of postoperative hyperglycemia and insulin resistance we assessed A-FABP serum concentrations and mRNA expression in skeletal and myocardial muscle, subcutan eous and epicardial adipose tissue and peripheral monocytes in 11 diabetic and 20 age- and sex-matched non-diabetic patients undergoing elective cardiac surgery. Baseline serum A-FABP did not differ between the groups (31.1±5.1 vs. 25.9±4.6 ng /ml, p=0.175). Cardiac surgery markedly increased serum A-FABP in both groups with a rapid peak at the end of surgery foll owed by a gradual decrease to baseline values during the next 48 h with no significant difference between the groups at any timepoint. These trends were analogous to postoperative excursions of plasma glucose, insulin and selected proinflammatory markers. Cardiac surgery increased A-FABP mRNA expression in peripheral monocytes, while no effect was observed in adipose tissue or muscle. Our data suggest that circulating A-FABP might be involved in the development of acute perioperative stress response, insulin resistance and hyperglycemia of critically ill irrespectively of the presence of diab etes mellitus., T. Kotulak ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
In this review we present immunohistochemical methods for visualization of capillaries and muscle fibres in thick muscle sections. Special attention is paid to the procedures that preserve good morphology. Applying confocal microscopy and virtual 3D stereological grids, or tracing of capillaries in virtual reality, length of capillaries within a muscle volume or length of capillaries adjacent to a muscle fibre per fibre length, fibre surface area or fibre volume can be evaluated by an unbiased approach. Moreover, 3D models of capillaries and muscle fibres can be produced. Comparison of the developed methods with counting capillary profiles from 2D sections is discussed and the reader is warned that counting capillary profiles from 2D sections can underestimate the capillary length by as much as 75 percent. Application of the described 3D methodology is illustrated by the anatomical remodelling of capillarity during acute denervation and early reinnervation in the ra t soleus and extensor digitorum longus muscles., I. Eržen, J. Janáček, L. Kubínová., and Obsahuje bibliografii a bibliografické odkazy
Chronic hypoxia alters respiratory muscle force and fatigue, effects that could be attributed to hypoxia and/or increased activation due to hyperventilation. We hypothesized that chronic hypoxia is associated with phenotypic change in non-respiratory muscles and therefore we tested the hypothesis that chronic hypobaric hypoxia increases limb muscle force and fatigue. Adult male Wistar rats were exposed to normoxia or hypobaric hypoxia (PB=450 mm Hg) for 6 weeks. At the end of the treatment period, soleus (SOL) and extensor digitorum longus (EDL) muscles were removed under pentobarbitone anaesthesia and strips were mounted for isometric force determination in Krebs solution in standard water-jacketed organ baths at 25 °C. Isometric twitch and tetanic force, contractile kinetics, forcefrequency relationship and fatigue characteristics were determined in response to electrical field stimulation. Chronic hypoxia increased specific force in SOL and EDL compared to age-matched normoxic controls. Furthermore, chronic hypoxia decreased endurance in both limb muscles. We conclude that hypoxia elicits functional plasticity in limb muscles perhaps due to oxidative stress. Our results may have implications for respiratory disorders that are characterized by prolonged hypoxia such as chronic obstructive pulmonary disease (COPD)., R. El-Khoury, A. Bradford, K. D. O´Halloran., and Obsahuje seznam literatury
The use of the herbicide paraquat (1,1'-dimethyl-4,4'-bipyridylium dichloride; PQ) which is widely used in agriculture is known to cause dopaminergic neurotoxicity. However, the mechanisms underlying this effect are not fully understood. This present study investigated the behavioral manifestations, motor coordination, and dopaminergic neurodegeneration following exposure to PQ. Male rats were injected with PQ (10 mg/kg i.p.) daily for three weeks. Rotarod systems were used for measuring locomotor activity and motor coordination. The effects of PQ on dorsiflexor, electrophysiologically-induced muscle contraction were studied. Dopamine concentrations in the ventral mesencephalon were measured by high performance liquid chromatography and the number of dopaminergic neurons in substantia nigra pars compacta was estimated by tyrosine hydroxylase immunohistochemistry. PQ induced difficulty in movement and significant reduction in motor activity and twitch tension at the dorsiflexor skeletal muscle. The number of tyrosine hydroxylase positive neurons was significantly less in the substantia nigra pars compacta and nigral dopamine level was significantly reduced in PQ treated animals (20.4±3.4 pg/mg) when compared with control animals (55.0±2.4 pg/mg wet tissue). Daily treatment of PQ for three weeks induces selective dopaminergic neuronal loss in the substantia nigra and significant behavioral and peripheral motor deficit effects., M. A. Fahim, ... [et al.]., and Obsahuje seznam literatury
Protein levels (Western blot) of the major glucose transporter isoform (GLGT4) were measured in skeletal muscles (quadriceps femoris) of an animal model of human metabolic syndrome X, i.e. the hereditary hypertriglyceridaemic (HTG) insulin-resistant rats fed various diets. The results were compared with the data obtained in normal Wistar rats which underwent the identical protocol. In HTG rats fed the basal diet (B) or high- sucrose diet (HS) (known to induce hypertriglyceridaemia and to impair insulin action), a decrease of GLGT4 protein levels (B: Control 100±3 vs HTG 46±5 %, p<0.005; HS: Control 80±9 vs HTG 49±3 %, p<0.005) was observed. Furthermore, marine Pish oil (FO) rich in n-3 polyunsaturated fatty acids (PGFA), added to the basal diet (30 wt % of n-3 PGFA) reduced the GLGT4 protein levels (B: 100±3 vs B+FO: 42±4 %, p<0.005) in control rats to values similar to those found in HTG rats (B: 46±4 %). However, dietary FO did not have any effect in HTG rats (49±3 %). Feeding the high-sucrose diet supplemented with FO to both the control and HTG rats was followed by a further decrement of GLGT4 protein (Control 15±5 vs HTG 14±4%). In conclusions, a) the hereditary HTG rats had by about 50 % lower GLGT4 protein levels in the quadriceps femoris muscle in comparison to normal Wistar rats; b) high-sucrose diet or raised dietary intake of n-3 PGFA did not further alter the number of glucose carriers in quadriceps femoris muscle in HTG rats and c) feeding the high-sucrose diet with higher proportion of n-3 PGFA was associated with an additional reduction of the GLGT4 protein level in this muscle.
a1_With hypoxic stress, hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) are elevated and their responses are altered in skeletal muscles of plateau animals [China Qinghai-Tibetan plateau pikas (Ochotona curzoniae )] as compared with control animals [normal lowland Sprague-Dawley (SD) rats]. The results indicate that HIF-1α and VEGF are engaged in physiological functions under hypoxic environment. The purpose of the current study was to examine the protein levels of VEGF receptor subtypes (VEGFRs: VEGFR-1, VEGFR-2 and VEGFR-3) in the end organs, namely skeletal muscle, heart and lung in response to hypoxic stress. ELISA and Western blot analysis were employed to determine HIF-1α and the protein expression of VEGFRs in control animals and plateau pikas. We further blocked HIF-1α signal to determine if HIF-1α regulates alternations in VEGFRs in those tissues. We hypothesized that responsiveness of VEGFRs in the major end organs of plateau animals is differential with insult of hypoxic stress and is modulated by low oxygen sensitive HIF-1α. Our results show that hypoxic stress induced by exposure of lower O2 for 6 h significantly increased the levels of VEGFR-2 in skeletal muscle, heart and lung and the increases were amplified in plateau pikas. Our results also demonstrate that hypoxic stress enhanced VEGFR-3 in lungs of plateau animals. Nonetheless, no significant alternations in VEGFR-1 were observed in those tissues with hypoxic stress. Moreover, we observed decreases of VEGFR-2 in skeletal muscle, heart and lung; and decreases of VEGFR-3 in lung following HIF-1α inhibition. Overall, our findings suggest that in plateau animals 1) responsiveness of VEGFRs is different under hypoxic environment; 2) amplified VEGFR-2 response appears in skeletal muscle, heart and lung, and enhanced VEGFR-3 response is mainly observed in lung; 3) HIF-1α plays a regulatory role in the levels of VEGFRs. Our results provide the underlying cellular and molecular mechanisms responsible for hypoxic environment in plateau animals, having an impact on research of physiological and ecological adaptive responses to acute or chronic hypoxic stress in humans who living at high attitude and who live at a normal sea level but suffer from hypoxic disorders., H.-C. Xie, J.-G. Li, J.-P. He., and Obsahuje bibliografii
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.
After 8 weeks of intermittent fasting, mice fed both a standard laboratory diet and a high-fat diet became hyperphagic and showed an increased amount of glycogen storage in the liver. An important effect of the adaptation to intermittent feeding with a high-fat diet seems to be an activation of the oxidation of lipids. Lipid oxidation prevails over lipogenesis so that the protein levels in the liver and skeletal muscle are preserved and maintained constant.
This study aimed to examine how regular aerobic training can affect the muscle hypertrophy induced by overloading. Male C57BL/6J mice were randomly divided into three groups: rest group, low-intensity aerobic exercise group, and high-intensity aerobic exercise group. Mice in the exercise groups were assigned to run at a speed of 10 m/min (low-intensity) or 25 m/min (high-intensity) for 30 min/day, five days/week, for four weeks. Then, the right hind leg gastrocnemius muscles were surgically removed to overload the plantaris and soleus muscles, while the left hind leg was subjected to a sham-operation. Both the plantaris and soleus muscles grew larger in the overloaded legs than those in the sham-operated legs. Muscle growth increased in the plantaris muscles in the low-intensity exercise group compared to that in the rest or high-intensity exercise groups at one and two weeks after overloading. This enhancement was not observed in the soleus muscles. Consistently, we observed changes in the expression of proteins involved in anabolic intracellular signaling, including Akt, mechanistic target of rapamycin (mTOR), and p70S6K, in the plantaris muscles. Our data showed for the first time that chronic low-intensity aerobic exercise precipitates overload-induced muscle growth., Siriguleng, T. Koike, Y. Natsume, S. Iwama, Y. Oshida., and Obsahuje bibliografii
The purpose of this study was to compare the effects of shortterm fasting-induced rapid weight loss with those of slower but equivalent body weight loss induced by daily calorie restriction on muscle protein degradation pathways and muscle protein content. Male Fischer rats were subjected to either 30 % calorie restriction for 2 weeks to slowly decrease body weight (Slow) or 3-day fasting to rapidly decrease body weight by a comparable level of that of the Slow group (Rapid). The final body weights were about 15 % lower in both the Slow and Rapid groups than in the Con group (p<0.001). The total protein content and wet weight of fast-twitch plantaris muscle, but not slow-twitch soleus muscle, were significantly lower in the Rapid group compared with the control rats fed ad libitum. Substantial increases in the expression ratio of autophagosomal membrane proteins (LC3-II/-I ratio) and polyubiquitinated protein concentration, used as biomarkers of autophagy-lysosome and ubiquitinproteasome activities, respectively, were observed in the
plantaris muscle of the Rapid group. Moreover, the LC3-II/-I ratio
and polyubiquitinated protein concentration were negatively correlated with the total protein content and wet weight of plantaris muscle. These results suggest that short-term fastinginduced rapid body weight loss activates autophagy-lysosome and ubiquitin-proteasome systems more strongly than calorie restriction-induced slower weight reduction, resulting in muscular atrophy in fast-twitch muscle.
The skeletal muscles of animals and humans with type 2 diabetes have decreased oxidative capacity. Aerobic exercise can improve muscle oxidative capacity, but no data are available on the amount of exercise required. We investigated the effects of voluntary running exercise and running distance on the skeletal muscle properties of nonobese rats with type 2 diabetes. Six-week-old male diabetic Goto-Kakizaki rats were divided into nonexercised (GK) and exercised (GK-Ex) groups. The rats in the GK-Ex group were permitted voluntary running exercise on wheels for 6 weeks. Age-matched male Wistar rats (WR) were used as nondiabetic controls. Fasting blood glucose and HbA1c levels were higher in the GK and GK-Ex groups than in the WR group and lower in the GK-Ex group than in the GK group. Succinate dehydrogenase (SDH) activity and peroxisome proliferator-activated receptor γ coactivator-1α (Pgc-1α) mRNA levels in the soleus and plantaris muscles were higher in the WR and GK-Ex groups than in the GK group. HbA1c and total cholesterol levels were negatively correlated with running distance and SDH activity and Pgc-1α mRNA levels in the soleus muscle were positively correlated with running distance. The onset and progression of diabetes in nonobese diabetic rats were effectively inhibited by running longer distances.
Obesity is often associated with metabolic impairments in peripheral tissues. Evidence suggests an excess of free fatty acids (FFA) as one factor linking obesity and related pathological conditions and the impact of FFA overload on skeletal muscle metabolism is described herein. Obesity is associated with dysfunctional adipose tissue unable to buffer the flux of dietary lipids. Resulting increased levels and fluxes of plasma FFA lead to ectopic lipid deposition and lipotoxicity. FFA accumulated in skeletal muscle are associated with insulin resistance and overall cellular dysfunction. Mechanisms supposed to be involved in these conditions include the Randle cycle, intracellular accumulation of lipid metabolites, inflammation and mitochondrial dysfunction or mitochondrial stress. These mechanisms are described and discussed in the view of current experimental evidence with an emphasis on conflicting theories of decreased vs. increased mitochondrial fat oxidation associated with lipid overload. Since different types of FFA may induce diverse metabolic responses in skeletal muscle cells, this review also focuses on cellular mechanisms underlying the different action of saturated and unsaturated FFA., J. Tumova, M. Andel, J. Trnka., and Obsahuje bibliografii
Hypoxia-inducible factor-1α (HIF-1α) transcriptionally regulates expression of several target genes in protecting tissues against hypoxia. With hypoxic stress, vascular endothelial growth factor (VEGF) is a signal protein produced by cells and further contributes to improvement of vascular functions and restoring the oxygen supply to tissues. In this current study, we first hypothesized that the protein levels of HIF-1α and VEGF are reduced in skeletal muscles of plateau animals [China Qinghai- Tibetan plateau pikas (ochotona curzoniae)] in response to hypoxia as compared with control animals [normal lowland Sprague-Dawley (SD) rats]. We further hypothesized that HIF-1α plays a role in regulating expression of VEGF in skeletal muscle. Note that HIF-1α and VEGF were determined by using two-site immunoenzymatic assay (ELISA) methods. Our results demonstrated that hypoxic stress induced by exposure of lower O2 (6 h) significantly increased the levels of HIF-1α and VEGF in the oxidative and glycolytic muscles of SD rats and pikas (P<0.05 vs. normoxic conditions). Notably, the increases in HIF-1α and VEGF were significantly less in pikas (P<0.05, vs. SD controls) than in SD rats. In addition, a linear relationship was observed between amplified HIF-1α and VEGF in oxidative muscle (r=0.76 and P<0.01) and glycolytic muscle (r=0.72 and P<0.01) and inhibiting HIF-1α significantly decreased expression of VEGF induced by hypoxic stress in skeletal muscles (P<0.05). Overall, our findings suggest that (1) responsiveness of HIF-1α and VEGF in skeletal muscles to hypoxic stress is blunted in plateau animals, and (2) HIF-1α has a regulatory effect on VEGF under hypoxic environment., H.-C. Xie, J.-P. He, J.-F. Zhu, J.-G. Li., and Obsahuje bibliografii
Rat skeletal muscle myofibrils were incubated in the presence of D-glucose, D-fructose, D-galactose, D-ribose, D-tagatose, D-arabinose, D-xylose, D-mannose, L-sorbose, L-rhamnose or DL-glyceraldehyde and myofibrillar ATPase activity as well as the extent of glycation was measured. The attachment of sugars to proteins during glycation was generally dependent on the percentage of a given sugar present in the open-chain form. Glycation resulted in the decrease of myofibrillar ATPase activity. This decrease was low after incubation of myofibrillar proteins with slowly glycating sugars (e.g. glucose) and high with fast glycating sugars (e.g. ribose or glyceraldehyde). ATPase activity was less reduced in the presence of /3-mercaptoethanol.
M1-muscarinic acetylcholine (ACh) receptors (M1R) were directly demonstrated immunocytochemic ally in electronmicroscopic images of rat diaphragm neuromus cular junctions (NMJ). Specific electron-dense granules were located at presynaptic nerve ending membranes and in the sa rcolemma in the depths of postsynaptic folds. This first visualization of M1R on both sides of the NMJ is in agreement with previous pharmacological data on the regulatory role of M1R in quantal and non-quantal ACh release. and Obsahuje bibliografii a bibliografické odkazy
We studied the changes in seru m fibroblast growth factor-21 (FGF-21) concentrations, its mR NA, and protein expression in skeletal muscle and adipose tissue of 15 patients undergoing cardiac surgery. Blood samples were obtained: prior to initiation of anesthesia, prior to the start of extracorporeal circulation, upon completion of the surger y, and 6, 24, 48, and 96 hours after the end of the surgery. Tissue sampling was performed at the start and end of surgery. The mean baseline serum FGF-21 concentration was 63.1 (43.03-113. 95) pg/ml and it increased during surgery with peak 6 ho urs after its end [385.5 (274.55-761.65) pg/ml, p<0.001], and return ed to baseline value [41.4 (29.15-142.83) pg/ml] 96 hours afte r the end of the surgery. Serum glucose, insulin, CRP, IL-6, IL-8, MCP-1, and TNF-alpha concentrations significantly increased during the surgery. Baseline FGF-21 mRNA expression in skeletal muscle was higher than in both adipose tissue depots and it was not affected by the surgery. Epicardial fat FGF-21 mRNA increased after surgery. Muscle FGF-21 mRNA positively correlated with blood glucose levels at the end of the surgery. Our data suggest a possible role of FGF-21 in the regulation of glucose metabolism and insulin sensitivity in surgery-related stress., T. Kotulák ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Adenosine 5'-triphosphate (ATP), phosphocreatine (PCr), creatine (Cr), inorganic phosphate (Pi), lactate (LAC), pyruvate (PYR) and glycogen as glucose (GLG) were determined and free adenosine 5'-diphosphate (ADP) was calculated from ATP:creatine phosphokinase (CPK) reaction in the gracilis muscle of cold-acclimated rats in vivo, and in completely isolated muscles under medium perfusion and superfusion in vitro, using the freezeclamping method. The mean in vivo levels (wmol/g w.w.) were: ATP 4.8, PCr 12.0, Cr 7.8, Pi 1.6, LAC 1.6, PYR 0.09, GLG 22.9, ADP 0.62 x 10-3. Isolation of the muscle (about 11 min of anoxia followed by perfusion in the air with a high pC>2 medium) decreased macroergic phosphate levels (ATP 3.0 , PCr 8.3). In isolated muscles perfused with a high pC>2 medium (99 kPa O2, perfusion rate 70 /rl/min) and simultaneously superfused with a low p02 medium (6.2 kPa O2, 2.3 ml/min) at 28 °C in vitro the levels of metabolites were (wmol/g w.w.): ATP 3.1, PCr 8.5, Cr 5.6, Pi 0.9, LAC 2.1, PYR 0.19, GLG 6.6, ADP 0.44 x 10-3. The mean steady oxygen uptake of the isolated muscle was 97 nmol O2 x min-1 x g-1 w.w. Thus, the levels of macroergic phosphates and their derivatives are lower after isolation and perfusion of the muscle, but the creatine charge [PCr]/([PCr]-f[Cr]] remains stable (0.61 in vivo versus 0.60 in the isolated muscle). This indicates that the steady-state and high energy status of the isolated perfused-superfused gracilis muscle is maintained.
To test the hypothesis that neonatal GLP-1 exposure may program myosin heavy chain (MyHC) composition in adult skeletal muscle, two-day-old rats were transfected intramuscularly with vacant vector plasmid (VP), or recombinant plasmid expressing secretory GLP-1 at the doses of 60 μg (LG) and 120 μg (HG), respectively. Expression of GLP-1 mRNA was detected in muscles of both LG and HG rats 7 days after transfection, with more abundant GLP-1 transcript seen in LG rats. In accordance with the GLP-1 expression, LG rats demonstrated more significant responses to neonatal GLP-1 exposure. Small yet significant growth retardation was observed in LG rats, which is accompanied with significantly reduced serum insulin concentration at 8 weeks of age compared to VP rats. The responses of skeletal muscle were dependent on muscle type. Significant increase of PGC-1α and GLUT4 mRNA expression was detected in soleus of LG rats, whereas a MyHC type switch from ⅡB to Ⅰ was seen in gastrocnemius. These results indicate that neonatal exposure of healthy pups to ectopic GLP-1 causes growth retardation with decreased serum insulin as well as muscle type-dependent modifications in MyHC type composition and metabolic gene expression in adult rats., L. Wang ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
We investigated the effects of repeated hyperthermic bouts on the heat shock response of heat s hock protein ( HSP ) 72 in skeletal muscle. Rats were assigned to control and hyperthermia groups which were exposed to heated water at 42 °C. The hyperthermia group was further divided into sub -groups: a single bout (H30) or four bouts of hyperthermia for 30 min (H30x4). There was an increase in HSP72 protein content of the H30 groups in both extensor digitorum longus (EDL) and soleus muscles. Moreover, HSP72 protein expression in H30x4 group was significantly higher than in H30 group in both EDL and soleus muscles. The HSP72 mRNA was markedly increased from control levels in the H30 and H30x4 group in both types of muscles . However, HSP72 mRNA of the H30x4 group was lower than that of the H30 group in soleus muscles. Heat shock response of HSP72 is activate d even after repeated bouts of hyperthermia, with a differential regulation between muscle types., J. Lee, K. Himori, D. Tatebayashi, M. Abe, T. Yamada., and Obsahuje bibliografii
This study aimed to compare the effects of three different resistance exercise models on the quadriceps muscle crosssectional area, as well as on mTOR phosphorylation and other pivotal molecules involved in the upstream regulation of mTOR. Twenty-four male Wistar rats were divided into untrained (control), endurance resistance training, strength resistance training, and hypertrophy resistance training (HRT) groups (n=6). After 12 weeks of training, the red portion of the quadriceps was removed for histological and Western blot analyses. The results showed that the quadriceps weight and cross-sectional areas in the exercised groups were higher than those of the untrained rats. However, the HRT group presented better results than the other two experimental groups. This same pattern was observed for mTOR phosphorylation and for the most pivotal molecules involved in the upstream control of mTOR (increase of PKB, 14-3-3, ERK, p38 MAPK, and 4E-BP1 phosphorylation, and reduction of tuberin, sestrin 2, REDD1, and phospho AMPK). In summary, our study showed that HRT leads to high levels of mTOR phosphorylation as well as of other proteins involved in the upstream regulation of mTOR., T. F. Luciano, S. O. Marques, B. L. Pieri, D. R. de Souza, L. V. Araújo, R. T. Nesi, D. L. Scheffer, V. H. Comin, R. A. Pinho, A. P. Muller, C. T. de Souza., and Obsahuje bibliografii
The linear relaxation (LR) was studied in isometric unfused tetanus (UT) of the human flexor digitorum sublimis muscle. With a decrease of the force level, the shoulder on the relaxation curve, as measured from the last stimulus, shifted to the right. The length of the linear portion itself weakly depended on activation level. When steady force changed from 100 to 40-50 % of the maximum, the slope of LR decreased only by 15±4 %. At smaller force levels the slope began to increase. LR can probably also be hidden in the twitch. With increased tetanus duration, LR becomes longer and slower at all force levels. LR was markedly diminished in contraction on the steep part of the exponential relaxation after a smooth tetanus. Its full recovery needed a train of 4-5 pulses (near 1 s) at the new stationary level. The form of the response to the additional pulse given during relaxation remained approximately constant during the most of LR portion and differed markedly before and after it. LR did not have direct relation to fatigue: in the first UT LR was always slower and longer than in subsequent ones.
Myostatin (MSTN), an important negative regulator of skeletal muscle, plays an important role in skeletal muscle health. In previous study, we found that the expression of MSTN was different during skeletal muscle injury repair. Therefore, we explored the expression changes of MSTN at different time points during skeletal muscle injury repair after eccentric exercise. In addition, MSTN is regulated by follistatin (FST) and decorin (DCN) in vivo, so our study examined the time-specific changes of FST, DCN and MSTN in the circulation and skeletal muscle during skeletal muscle injury repair after eccentric exercise, and to explore the reasons for the changes of MSTN in the process of exercise-induced muscle injury repair, to provide a basis for promoting muscle injury repair. The rats performed one-time eccentric exercise. Blood and skeletal muscle were collected at the corresponding time points, respectively immediate after exercise (D0), one day (D1), two days (D2), three days (D3), seven days (W1) and fourteen days (W2) after exercise (n=8). The levels of MSTN, FST, DCN in serum and mRNA and protein expression in muscle were detected. MSTN changes in the blood and changes in DCN and FST showed the opposite trend, except immediately after exercise. The change trends of mRNA and protein of gastrocnemius DCN and MSTN are inconsistent, there is post-transcriptional regulation of MSTN and DCN in gastrocnemius. Acute eccentric exercise might stimulate the secretion of DCN and FST into the circulation and inhibit MSTN. MSTN may be regulated by FST and DCN after acute eccentric exercise.
Rheumatoid arthritis (RA) and its animal model adjuvant arthritis (AA) are inflammatory diseases characterized by chronic inflammation, systemic oxidative stress and disturbed mitochondrial bioenergetics of skeletal muscle. The present study aimed to evaluate the effects of coenzyme Q10 - CoQ10 (100 mg/kg b.w.), omega-3-polyunsaturated fatty acids - ω-3-PUFA (400 mg/kg b.w.) and their combined treatment in AA on impaired skeletal muscle mitochondrial bioenergetics, inflammation and changes in levels CoQ9 and CoQ10 in plasma. Markers of inflammation (C-reactive protein, monocytechemotactic protein-1), antioxidant capacity of plasma, respiratory chain parameters of skeletal muscle mitochondria and concentrations of CoQ9 and CoQ10 in plasma and in muscle tissue were estimated. Treatment of the arthritic rats with CoQ10, ω-3-PUFA alone and in combination partially reduced markers of inflammation and increased antioxidant capacity of plasma, significantly increased concentrations of coenzyme Q in mitochondria and improved mitochondrial function in the skeletal muscle. Combined treatment has similar effect on the mitochondrial function as monotherapies; however, it has affected inflammation and antioxidant status more intensively than monotherapies. Long-term supplementary administration of coenzyme Q10 and ω-3-PUFA and especially their combination is able to restore the impaired mitochondrial bioenergetics and antioxidant status in AA., Jarmila Kucharská, Silvester Poništ, Oľga Vančová, Anna Gvozdjáková, Oľga Uličná, Lukáš Slovák, Mohsen Taghdisiesfejir, Katarína Bauerová., and Obsahuje bibliografii