Changes In Muscle Cells Research Articles

Clinical and morphological features of scar tissue of the uterus.

One of the key issues for increase uterine scars is the rapid and unwarranted Caesarean sections (CS) as in the world same in Ukraine. One of the way to reduce CS is delivery truth vaginal births in women with previous surgical intervention on the uterus or after CS. The ability of scar on the uterus is the main criterion for an attempt to vaginal birth. Objectivе — to analyze the structural changes of the scar tissue of the uterus. Pathomorphological examination was fragments of uterus scar. The material was fixed in a 10% solution of neutral colored formalin (pH 7.4) carried out according to the standard procedure, poured into paraffin. From the paraffin blocks on the rotary microtome of HM 325, serial histological sections were made in a thickness of 4–5 microns, which were stained with hematoxylin and eosin. Scar tissue was additionally stained for Van Gieson, according to Masson. Fragments of scar tissue were subjected to an immunohistochemical study (IGHS) using monoclonal antibodies (MATs) to CD31 to assess the degree of vascularization vascular component and α-SMA for assessing the condition smooth muscle tissue. Having conducted a comprehensive pathomorphological study in two groups, one can state that in group 1 the pathomorphological picture of the changes in the scar was minimal and confirmed by the retained proportions between the fibrous tissue and the smooth muscle fibers, as well as their characteristic location. Muscle fibers with minimal pathological changes, developed by compensatory changes from the side of the vascular complex. These data were confirmed by conducting IGHS from MAT to CD31, which gives a pronounced positive response in the endothelial layer of the vascular wall, forming continuous cell chains. IGHS from MAT to α-SMA exhibits pronounced homogeneous intensive expression, indicating minimal pathological changes in muscle fibers. These figures make it possible to talk about the ability of uterine scar in 61% in group 1, as opposed to in group 2, this result was only 41%. As a result of a comprehensive clinical and morphological study, it was found that the majority of women in group 1, according to the morphological and histological characteristics, had a capable scar on the uterus, that is, potentially could be considered as a reserve for vaginal birth in women with uterine scar after the previous CS. In the second group, a significant proportion of women confirmed the correlation of regenerative and degenerative changes in the tissues of postoperative scar, indicating prevalence of fibro-sclerotic changes and insufficient vascularization, that is, it states the validity of operational resolution.

Alteration of T-Tubular Architecture and Capacitance Changes in Huntington's Disease

Huntington's disease (HD) is an inherited disorder with debilitating motor, cognitive, and psychiatric dysfunction. Motor symptoms, including chorea, rigidity, dystonia, and weakness, have principally been attributed to central neurodegeneration, but recent work suggests that primary skeletal muscle defects may also contribute to the motor symptoms. Electrophysiology studies in our lab have revealed a marked decrease in specific capacitance in HD muscle fibers from R6/2 transgenic mice compared with controls. This reduced capacitance is greater than expected when accounting for the smaller size of HD fibers. Because the transverse tubular system (TTS) in skeletal muscle makes up a significant proportion of total cell membrane, we hypothesized that structural changes in the TTS were responsible for reduced capacitance in the disease state. A loss or disruption of membrane in the TTS could directly contribute to weakness in HD. Decreased t-tubule diameters in HD fibers without changes in overall cellular TTS density were confirmed using quantitative electron and confocal microscopy. Here, we present results of calculations based on a cylindrical model of skeletal muscle incorporating these changes in muscle fiber and TTS architecture that account for reduced specific capacitance in HD. These results may help our understanding of muscle function in HD and provide a foundation for modeling electrical activity in disease and normal skeletal muscle.

Histological and Cytoskeletal Age-Related Changes of Rabbit Skeletal Muscle Fibers and the Preventive Role of Vitamin E

Histological and Cytoskeletal Age-Related Changes of Rabbit Skeletal Muscle Fibers and the Preventive Role of Vitamin E

Anti-inflammatory and antioxidant effect of melatonin on recovery from muscular trauma induced in rats

In recent decades, the number of people who practice sports has grown exponentially, increasing the number of muscular injuries. Trauma injury occurs when the muscle is exposed to a sudden compression force. Melatonin (MLT) has often been cited in the literature as a potent antioxidant and anti-inflammatory agent. This study was designed to evaluate MLT action on muscle tissue in Wistar rats in an experimental model of muscle trauma. Twenty-eight Wistar rats were used, divided into four groups: CO (Control), CO + MLT (Control + Melatonin), T (Trauma) and T + MLT (Trauma + Melatonin). MLT (20 mg/kg) was administered (ip) daily at dusk until day 7. The trauma occurred on day 1, 2 h before the first MLT application. On day 8, muscle tissue was collected for histological analysis (HE), immunohistochemistry (TNF-α and NFκB), evaluation of oxidative stress through analysis of lipoperoxidation by TBARS and activity of SOD and GPx enzymes, and analysis of nitrites and nitrates. In the evaluation of TBARS and SOD, we observed a significant increase in the T group and a significant decrease in the T + MLT group. In the evaluation of GPx, there was a significant increase in the T group and a significant decrease in the T + MLT group. The histological analysis of muscle tissue revealed structural changes of muscle fibers and inflammatory infiltrate in the T group but a decrease in this damage in the T + MLT group. In the immunohistochemical evaluation, increased expression of TNFα and NFκB proteins in the T group was observed and a significant decrease of this expression in the T + MLT group. MLT was shown to attenuate oxidative damage and to diminish the expression of inflammatory proteins and tissue damage in this experimental model.

Phenotypic Modulation of Skeletal Muscle Fibers in LPIN1-Deficient Lipodystrophic ( fld) Mice.

Lipin-1 ( Lpin1)-deficient lipodystrophic mice have scant and immature adipocytes and develop transient fatty liver early in life. Unlike normal mice, these mice cannot rely on stored triglycerides to generate adenosine triphosphate (ATP) from the β-oxidation of fatty acids during periods of fasting. To compensate, these mice store much higher amounts of glycogen in skeletal muscle and liver than wild-type mice in order to support energy needs during periods of fasting. Our studies demonstrated that there are phenotypic changes in skeletal muscle fibers that reflect an adaptation to this unique metabolic situation. The phenotype of skeletal muscle (soleus, gastrocnemius, plantaris, and extensor digitorum longus [EDL]) from Lpin1-/- was evaluated using various methods including immunohistochemistry for myosin heavy chains (Myh) 1, 2, 2a, 2b, and 2x; enzyme histochemistry for myosin ATPase, cytochrome-c oxidase (COX), and succinyl dehydrogenase (SDH); periodic acid-Schiff; and transmission electron microscopy. Fiber-type changes in the soleus muscle of Lpin1-/- mice were prominent and included decreased Myh1 expression with concomitant increases in Myh2 expression and myosin-ATPase activity; this change was associated with an increase in the presence of Myh1/2a or Myh1/2x hybrid fibers. Alterations in mitochondrial enzyme activity (COX and SDH) were apparent in the myofibers in the soleus, gastrocnemius, plantaris, and EDL muscles. Electron microscopy revealed increases in the subsarcolemmal mitochondrial mass in the muscles of Lpin1-/- mice. These data demonstrate that lipin-1 deficiency results in phenotypic fiber-specific modulation of skeletal muscle necessary for compensatory fuel utilization adaptations in lipodystrophy.

WITHDRAWN: Histological difference of Soleus Muscle fibers due to Sciatic Nerve Transection in Rats

ABSTRACT The structural integrity and activity of the skeletal muscle fibers is dependent on their sound innervations. Degeneration and atrophy of skeletal muscle fibers occurs after denervation. The present study aimed to investigate and assess the structural changes of soleus muscle fibers after severance of sciatic nerve at different periods of time. 25 rats were used and allocated into three groups: control (N = 5), sham operation (N = 5) and the sciatic nerve transection group (n = 15). The later was further subdivided into 3 subgroups (n = 5) where tissues samples from each soleus muscles were taken for histological examination at 2, 4 and 8 weeks- after severance of the sciatic nerve. The soleus muscle of control and sham operations exhibited normal muscular pattern while at two weeks post-transection, scattered necrotic muscular areas of variable size, extensive inflammatory cell infiltration, and wide perimysium, reduction of the muscle fiber size and loss of fiber striations were seen. Reduction of the inflammatory infiltration and increased fibrous tissue formation with wide perimysium were observed at four weeks while at eight weeks post-transection, normal perimysium, loss of striations and thin muscle fibers were seen. The present study indicated that degenerative changes of muscular tissues were noticeable at two and four week’s post-transection of its motor nerve supply, with subsequent minimal improvement afterwards.

P-258 - Monitoring intracellular hydrogen peroxide changes in skeletal muscle fibres by HyPer, a genetically encoded hydrogen peroxide biosensor

Numerous pathophysiological processes are driven by cellular signalling pathways where hydrogen peroxide (H2O2) seems to play an important role as a molecular signal. We have used a genetically encoded hydrogen peroxide biosensor, HyPer, in order to monitor and quantify intracellular H2O2 changes. We combined different approaches, based in direct microinjection of HyPer DNA construct in the flexor digitorum brevis muscle following by application of electroporation in this muscle, and achieved the expression of biosensor HyPer in isolated single skeletal muscle fibres. Using live cell fluorescence microscopy image analysis, we monitored intracellular flow of H2O2 in fibres that expressed HyPer. This is due to HyPer fluorescence properties, mainly the increase of HyPer fluorescence when this reacts with H2O2. Different experimental conditions were examined: i) H2O2 extracellular exposure, ii) exposure to an enzymatic system that generates H2O2, glucose oxidase (GOX), and iii) exposure to a reducing agent, dithiothreitol. Changes of extracellular H2O2 concentration were reflected in changes of fluorescence emitted by HyPer intracellularly. This reveal that there is a H2O2 flux across cellular membrane and HyPer biosensor is a suitable tool to detect and register this H2O2 flux.

Muscle Fiber and Performance Changes after Fast Eccentric Complex Training.

The purpose of this study was to examine the effects of a short-term fast eccentric and ballistic complex training program on muscle power, rate of force development (RFD), muscle fiber composition, and cross-sectional area (CSA). Sixteen male physical education students were randomly assigned to either a training group (TG, n = 8) or a control group (n = 8). The TG followed a 6-wk low volume training program, including fast eccentric squat training with an individually optimized load of 74% ± 7% of maximal half-squat strength (1RM) twice per week and a ballistic training session with loaded (30% 1RM) and unloaded jump squats, once per week, all combined with unloaded plyometric jumps. Half squat 1RM was increased in the TG from 1.87 ± 0.28 to 2.14 ± 0.31 kg per kilogram body mass (14.4% ± 9.3%, P = 0.01). The percentage of types I, IIA, and IIX fibers were similar in the two groups at pretesting and did not change after the intervention period (P = 0.53-0.89). Muscle fiber CSA increased in all fiber types by 8.3% to 11.6% (P = 0.02 to 0.001) in TG only. Countermovement jump height and peak power measured at five different external loads (0%-65% of 1RM) only increased in the TG by approximately 20% to 36% (P < 0.01) and approximately 16% to 22% (P < 0.01), respectively. Peak ground reaction force during jump squats remained unchanged in both groups, whereas RFD increased in the TG only (40%-107%, P = 0.001). A combination of low-volume fast eccentric and ballistic jump squat training with plyometric jumps in a strength-power potentiation complex format, induced substantial increases in peak leg muscle power, RFD, and maximal strength, accompanied by gains in CSA of all muscle fiber types, without a reduction in fast twitch fiber composition.

Fasting/Refeeding Cycles Prevent Myocardial Dysfunction and Morphology Damage in the Spontaneously Hypertensive Rats.

BackgroundCaloric restriction is known to impair the cardiac function and morphology in hypertrophied hearts of spontaneously hypertensive rats (SHR); however, the influence of fasting/refeeding (RF) is unknown.ObjectiveTo investigate the fasting/refeeding approach on myocardial remodeling and function. In addition, the current study was designed to bring information regarding the mechanisms underlying the participation of Ca2+ handling and β-adrenergic system.MethodsSixty-day-old male SHR rats were submitted to food ad libitum (C), 50% food restriction (R50) or RF cycles for 90 days. Cardiac remodeling was assessed by ultrastructure analysis and isolated papillary muscle function. The level of significance considered was 5% (α = 0.05).ResultsThe RF rats presented lower cardiac atrophy than R50 in relation to C rats. The C rats increased weight gain, R50 maintained their initial body weight and RF rats increased and decreased weight during RF. The RF did not cause functional impairment because the isotonic and isometric parameters showed similar behavior to those of C. The isotonic and isometric cardiac parameters were significantly elevated in RF rats compared to R50 rats. In addition, the R50 rats had cardiac damage in relation to C for isotonic and isometric variables. While the R50 rats showed focal changes in many muscle fibers, the RF rats displayed mild alterations, such as loss or disorganization of myofibrils.ConclusionFasting/refeeding promotes cardiac beneficial effects and attenuates myocardial injury caused by caloric restriction in SHR rats, contributing to reduce the cardiovascular risk profile and morphological injuries. Furthermore, RF promotes mild improvement in Ca2+ handling and β-adrenergic system.

Ultrasonographic evaluation of changes in the muscle architecture of the gastrocnemius with botulinum toxin treatment for lower extremity spasticity in children with cerebral palsy.

Botulinum toxin A treatment involves injecting botulinum toxin A to relax muscle spasticity. Using ultrasonography, this study examined changes in the muscle architecture before and after treatment to evaluate the influence of botulinum toxin A injection on muscles. The participants included 18 children (mean age, 6.2 years) with cerebral palsy who were treated with botulinum toxin A for lower extremity spasticity and 27 healthy children (mean age, 6.4 years) as a control group. In all cases, botulinum toxin A was injected into the gastrocnemius muscle. The muscle length, muscle width, and pennation angle (which indicates the degree of muscle fiber tone), were measured using B-mode ultrasonography before and 12 weeks after injection. The muscle length and muscle width were shorter in the cerebral palsy group than in the control group. The pennation angle in the cerebral palsy group significantly decreased after injection from 28.2±3.6° to 25.8±2.5° in the resting position of the ankle and from 18.6±2.8° to 15.9±1.7° in the maximum dorsiflexion position of the ankle. In the control group, the pennation angle was 25.9±3.2° in the resting position of the ankle and 15.1±2.5° in the maximum dorsiflexion position of the ankle. The rate of increase of fascicle length during passive movement from the resting position of the ankle to the maximum dorsiflexion position was 143.9% in the cerebral palsy group, which was significantly less than the value of 157.7% in the control group. After botulinum toxin A treatment, the rate of increase of fascicle length in the cerebral palsy group increased to 155.1%. The decrease in the pennation angle after botulinum toxin A treatment is considered to be the result of a reduction of spasticity and subsequent structural changes in flaccid muscle fibers.

Hysto-ultrastructure of the facial nerve and mimic muscles in the norm and in the conditions of eхperimental neuropathy

We studied the structural components of the facial nerve in the norm and with cold neuropathy, indicating morphological changes in neuromuscular endings and muscle fibers at 10, 15, 30 and 60 days from the beginning of the simulation of experimental neuropathy, which was caused by local supercooling of the projection portions of the extracranial parts of the facial nerve on the background of the preliminary introduction of Freud’s complete adjuvant. We established that the pathomorphological changes in the endonevral microcirculatory bed have a phase character: the initial spasm (up to 10 days) changes in paralytic vasodilation, and its residual effects remain until the end of the experiment (60 days). Changes in hemomicrocirculation conditions lead to marked disturbances in the structure of myelinic nerve fibers, which have the character of segmental demyelination with signs of delay in axonal transport and reactive restructuring of neuromuscular endings. The change in the metric composition of myelinated nerve fibers is due to an increase in the number of nerve fibers of medium and large diameters (up to 30 days) and small diameter (after 30 days). In different periods of the experiment, a decrease in the branching area of the terminal branches of the motor axon is observed in the nerve cells, local edema of the endonevria, degenerative changes in a part of the nerve fibers develop. Due to the fine-grained decay of the final nerve branches, degeneration of the motor endings took place two weeks after the start of the experiment. Neuropathy for 30 days caused a pronounced inhibition of spotting in the peripheral parts of the motor nerve fibers. After 60 days of experiment, a large number of muscle fibers underwent destructive changes. The size of a significant part of the neuromuscular endings was reduced. In all terms of cold neuropathy, neurolematocytes reacted in the same way: cytoplasm was swollen, argyrophilic grains appeared in the nuclei, fine-grained decay of individual nuclei occurred.

Mechanism of changes of peripheral neuro-muscle endings of the tongues of rats with experimental streptozotocyn diabetes mellitus

The paper presents the characteric of dynamics of morphological changes of neuromuscular endings of the tongues of rats with experimentally induced streptozotocin diabetes mellitus. The hysto-ultrastructural research showed pathomorphologic changes in the experimental diabetes mellitus at different time periods. Their regulations indicate the relation of neuromuscular endings and elements of muscular tissues. During experimental streptozotocin diabetes mellitus, there occured interconnected structural changes of muscle fibers, myelin nerve fibers and the microcirculatory channel of the tongue with damage to the neuromuscular endings. In the dynamics of the diabetic process, three phases were distinguished: the phase of reactive-dystrophic changes with maximum severity two weeks after the beginning of the experimental modeling of streptozotocin diabetes mellitus; the phase of destructive-dystrophic processes, which began after the fourth week from the beginning of the modeling experimental streptozotocin diabetes; degenerative-destructive phase, which developed after the sixth week of the experiment. The dynamics of changes in the neuromuscular endings are also related to the duration of diabetes mellitus, they occur in two stages: in the first stage (up to 4 weeks) reactive processes were observed , in the second (6–8 weeks) – dystrophic processes. The uneven degree of their manifestation is related to the reaction of the microcirculatory channel of neuromuscular endings and composition of the tongue muscles. The greatest sensitivity to hyperglycemia was observed in muscle fibers of the intermediate type.

Exogenous GDF11 induces cardiac and skeletal muscle dysfunction and wasting.

Growth differentiation factor 11 (GDF11), a TGF-beta superfamily member, is highly homologous to myostatin and essential for embryonic patterning and organogenesis. Reports of GDF11 effects on adult tissues are conflicting, with some describing anti-aging and pro-regenerative activities on the heart and skeletal muscle while others opposite or no effects. Herein, we sought to determine the in vivo cardiac and skeletal muscle effects of excess GDF11. Mice were injected with GDF11 secreting cells, an identical model to that used to initially identify the in vivo effects of myostatin. GDF11 exposure in mice induced whole body wasting and profound loss of function in cardiac and skeletal muscle over a 14-day period. Loss of cardiac mass preceded skeletal muscle loss. Cardiac histologic and echocardiographic evaluation demonstrated loss of ventricular muscle wall thickness, decreased cardiomyocyte size, and decreased cardiac function 10days following initiation of GDF11 exposure. Changes in skeletal muscle after GDF11 exposure were manifest at day 13 and wereassociated with wasting, decreased fiber size, and reduced strength. Changes in cardiomyocytes and skeletal muscle fibers were associated with activation of SMAD2, the ubiquitin-proteasome pathway and autophagy. Thus,GDF11 over administration in vivo results in cardiac and skeletal muscle loss, dysfunction, and death. Here, serum levels of GDF11 by Western blotting were 1.5-fold increased over controls. Although GDF11 effects in vivo are likely dose, route, and duration dependent, its physiologic changes are similar to myostatin and other Activin receptors ligands. These data support that GDF11, like its other closely related TGF-beta family members, induces loss of cardiac and skeletal muscle mass and function.

Abnormal spontaneous activity in primary myopathic disorders.

Reproducible non-insertional spontaneous activity (SA), with the exception of endplate activity, is an unequivocal sign of abnormality and is one of the most useful findings obtained on electromyography. In this retrospective study we analyzed occurrence and distribution of abnormal SA in 151 patients with genetically confirmed myopathies. Complex repetitive discharges (CRDs) occurred more frequently than fibrillation potentials (fibs) and positive sharp waves (PSWs) in centronuclear myopathy (CNM) and limb-girdle muscular dystrophy type 2A (LGMD-2A), whereas fibs/PSWs were observed more often in desminopathy and facioscapulohumeral dystrophy (FSHD). Abnormal SA was commonly found in CNM (66.7%) and desminopathy (61.5%), occasionally in Duchenne (DMD) and Becker muscular dystrophy (BMD) (45.2% and 27.6%, respectively), but rarely in FSHD (14.9%) and LGMD-2A (12.0%). Abnormal SA probably occurs more frequently in disorders associated with structural changes in muscle fibers. Screening for SA may be a valuable tool for diagnosis of non-myotonic myopathies. Muscle Nerve 56: 427-432, 2017.

Increase in carbon dioxide accelerates the performance of endurance exercise in rats.

Endurance exercise generates CO2 via aerobic metabolism; however, its role remains unclear. Exogenous CO2 by transcutaneous delivery promotes muscle fibre-type switching to increase endurance power in skeletal muscles. Here we determined the performance of rats running in activity wheels with/without transcutaneous CO2 exposure to clarify its effect on endurance exercise and recovery from muscle fatigue. Rats were randomised to control, training and CO2 groups. Endurance exercise included activity-wheel running with/without transcutaneous CO2 delivery. Running performance was measured after exercise initiation. We also analysed changes in muscle weight and muscle fibres in the tibialis anterior muscle. Running performance improved over the treatment period in the CO2 group, with a concomitant switch in muscle fibres to slow-type. The mitochondrial DNA content and capillary density in the CO2 group increased. CO2 was beneficial for performance and muscle development during endurance exercise: it may enhance recovery from fatigue and support anabolic metabolism in skeletal muscles.

The Contribution of Neuromuscular Stimulation in Elucidating Muscle Plasticity Revisited.

Studies carried out during the past 45 years on the effects of chronic low-frequency stimulation on skeletal muscle have revealed a multiplicity of adaptive changes of muscle fibres in response to increased activity. As reflected by induced changes in the metabolic properties, protein profiles of the contractile machinery and elements of the Ca2+-regulatory system, all essential components of the muscle fibre undergo pronounced changes in their properties that ultimately lead to their reversible transformation from fast-to-slow phenotype. The chronic low-frequency stimulation experiment thus allows exploring many aspects of the plasticity of mammalian skeletal muscle. Moreover it offers the possibility of elucidating molecular mechanisms that remodel phenotypic properties of a differentiated post-mitotic cell during adaptation to altered functional demands. The understanding of the adaptive potential of muscle can be taken advantage of for repairing muscle damage in various muscle diseases. In addition it can be used to prevent muscle wasting during inactivity and aging. Indeed, pioneering studies are still the sound grounds for the many current applications of Functional Electrical Stimulation and for the related research activities that are still proposed and funded.

English

The prevalence of cardiovascular changes markedly increases with deterioration of patient&#39;s renal function and can stack up 65 to 70% in end-stage renal disease. A rapid fall in renal function is often associated with uncontrolled congestive heart failure. Beyond their lipid-lowering effect, statins have been shown to protect the heart in different diseases. Liraglutide is a glucagon-like peptide-1 (GLP-1) analogue, used to control diabetes. It improves cardiac dysfunction in non-diabetics, but underlying mechanisms remain to some extent, unclear. Fifty two male Sprague-Dawley rats weighing 200 to 250 g were grouped into negative control, positive control, liraglutide treated group (0.3 mg/kg), atorvastatin treated group (10 mg/kg), liraglutide and atorvastatin treated group (0.3 and 10 mg/kg, respectively), liraglutide and atorvastatin treated group (0.15 and 5 mg/kg, respectively). Combination of both drugs significantly reduce creatine phosphokinase isoenzyme (CK-MB) in both doses (p&lt;0.008, p &lt;0.002) and lactate dehydrognase (LDH) (p&lt;0.04, p&lt;0.01). Liraglutide alone or in combination with atorvastatin in both doses (p&lt;0.02, p&lt;0.01 and p&lt;0.01) significantly increased superoxide dismutase (SOD). Atorvastatin alone (p&lt;0.02) or in combination with liraglutide in both doses (p&lt;0.001, p&lt;0.001) induced a significant decrease of malondialdehyde (MDA). Atorvastatin alone (p&lt;0.01) or in combination with liraglutide in both doses induced a significant amelioration of nitric oxide (NO) and cholesterol (p&lt;0.01 and p&lt;0.02). Significant improvements in blood urea nitrogen (BUN) and glucose profile were seen with all tested drugs either single or in combination. Combined implementation of both drugs improves histopathological changes of cardiac muscle fibres. Liraglutide has promising effects on cardiovascular changes in adenine induced chronic nephropathy through modulation of LDH, CK-MB and improvement of NO and SOD. Also, it can mitigate fibrosis and cardiac tissue changes. Its effects markedly increase in conjunction with atorvastatin. Combined administration of liraglutide and atorvastatin in a high dose has a reliable effect on improving outcome in biochemical and histopthological cardiac muscle fibers changes. Key word: Atorvastatin, liraglutide, adenine, renal failure.

How does passive lengthening change the architecture of the human medial gastrocnemius muscle?

There are few comprehensive investigations of the changes in muscle architecture that accompany muscle contraction or change in muscle length in vivo. For this study, we measured changes in the three-dimensional architecture of the human medial gastrocnemius at the whole muscle level, the fascicle level and the fiber level using anatomical MRI and diffusion tensor imaging (DTI). Data were obtained from eight subjects under relaxed conditions at three muscle lengths. At the whole muscle level, a 5.1% increase in muscle belly length resulted in a reduction in both muscle width (mean change -2.5%) and depth (-4.8%). At the fascicle level, muscle architecture measurements obtained at 3,000 locations per muscle showed that for every millimeter increase in muscle-tendon length above the slack length, average fascicle length increased by 0.46 mm, pennation angle decreased by 0.27° (0.17° in the superficial part and 0.37° in the deep part), and fascicle curvature decreased by 0.18 m-1 There was no evidence of systematic variation in architecture along the muscle's long axis at any muscle length. At the fiber level, analysis of the diffusion signal showed that passive lengthening of the muscle increased diffusion along fibers and decreased diffusion across fibers. Using these measurements across scales, we show that the complex shape changes that muscle fibers, whole muscles, and aponeuroses of the medial gastrocnemius undergo in vivo cannot be captured by simple geometrical models. This justifies the need for more complex models that link microstructural changes in muscle fibers to macroscopic changes in architecture.NEW & NOTEWORTHY Novel MRI and DTI techniques revealed changes in three-dimensional architecture of the human medial gastrocnemius during passive lengthening. Whole muscle belly width and depth decreased when the muscle lengthened. Fascicle length, pennation, and curvature changed uniformly or near uniformly along the muscle during passive lengthening. Diffusion of water molecules in muscle changes in the same direction as fascicle strains.

Mechanical ventilation leads to remodeling of diaphragma and soleus in rats

To investigate the structural response of diaphragm and soleus of the rat after mechanical ventilation (MV), and to explore the specific mechanism of the dysfunction of both muscles. Sixteen male Sprague-Dawley (SD) rats were randomly divided into control group and MV group, with 8 rats in each group. Rats in MV group were treated with controlled ventilation and maintained anesthesia, and those in control group were only anesthetized without MV and maintained anesthesia. The diaphragm and soleus were harvested after MV for 18 hours, and the morphology changes were observed with light microscope. The cross section of muscle fiber was observed by immunofluorescence technique analysis, and the cross-sectional area of muscle fiber was calculated. The ultra structural changes in muscle fibers were observed under transmission electron microscope. (1) Observed under light microscope, the cross section of the diaphragm and soleus muscle in the control group was regular, the nucleus was normal and the cytoplasm was homogeneous. The fibers in the diaphragm-biopsy specimens from MV subjects were smaller than those from control subjects, whereas these signs were not found in soleus. But fiber atrophy in MV specimens was not accompanied by an inflammatory-cell infiltrate. (2) Under the fluorescence microscope, the control group had a smaller cross-section of the slow-twitch muscle in diaphragm, while the fast-twitch muscle fibers were larger. As compared with diaphragm-biopsy specimens from control, specimens from MV subjects showed decreased cross-sectional areas of slow-twitch and fast-twitch fibers, respectively (μm2: 1 069.00±155.24 vs. 1 297.12±331.15, 2 279.66±442.31 vs. 3 031.80±596.11, both P < 0.05). The disproportionate decrease in fast-twitch fibers cross-sectional areas [(70.42±3.61)% vs. (75.63±2.48)%] resulted in an increase in the percentage of total area occupied by the slow-twitch fibers [(29.58±3.61)% vs. (24.35±2.48)%, both P < 0.01]. There were no significant differences in cross-sectional areas of slow-twitch and fast-twitch fibers in soleus between control group and MV group (μm2: 3 193.80±559.36 vs. 3 008.84±559.22, 3 392.86±514.56 vs. 3 594.35±651.67, both P > 0.05). (3) In the control group, the muscle fibers of the diaphragm and soleus were arranged orderly, the boundary of the light and dark bands and the "Z-line" were clear, and there was no autophagy in the visual field. The outer membrane of the mitochondria was complete, and the cristae were in the shape of clapboard. The signs of misalignment of myofibrils, disruption of "Z-line" and vacuolar mitochondria were found in diaphragm from MV group, whereas these signs were not found in soleus. Diaphragm from MV group exhibited an increase in autophagic vesicles visualized by transmission electron microscopy as compared with control group. Controlled MV for 18 hours resulted in diaphragmatic inactivity and promoted muscle injury and atrophy, while autophagy and mitochondrial dysfunction were enhanced. Soleus immobilization for 18 hours was not associated with muscle atrophy. These facts suggest that the signaling associated with diaphragm atrophy during MV may involve different mechanisms compared with other models of muscle atrophy. Diaphragm appeared to be more susceptible to MV.

Effect of the bendiocarb on the ultrastructure of rabbit skeletal muscle

Bendiocarb belongs to the group of carbamate insecticides that inhibit acetylcholinesterase. In agriculture, it is used to control a variety of insects, therefore it is important to examine every potential aspect of its toxicology. The aim of this study was to observe the effect of bendiocarb on the ultrastructure of the skeletal muscle in rabbits. Rabbits in all experimental groups received capsules of bendiocarb (96% Bendiocarb, Bayer, Germany) per os daily at a dose of 5 mg/kg body weight. Samples of skeletal muscles were collected on days 10 and 20. On day 10 of the experiment, muscle fibres were not affected consistently. The observed changes were moderate and focal. Electron microscopy revealed dilatation of sarcoplasmic reticulum, and myofilament disorganization. On day 20 of the experiment, the ultrastructural changes in muscle fibres were more intense and more frequent. The most important alteration was the disruption of the sarcomeres due to the lysis of both thick and thin myofilaments. However, in the unchanged regions of muscle fibres a prominent mitochondrial swelling was observed. Many mitochondria lacked cristae and thus appeared as large membrane-bound cytoplasmic vesicles. The results presented in this study indicate that bendiocarb affects the ultrastructure of skeletal muscles. The intensity of damage (dissolution of myofilaments and disruption of sarcomeres) was related to the duration of administration of bendiocarb.