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Muscle Contraction (muscle + contraction)
Kinds of Muscle Contraction Selected AbstractsMyosin Light Chain Kinase as a Multifunctional Regulatory Protein of Smooth Muscle ContractionIUBMB LIFE, Issue 6 2001Ying Gao Abstract Myosin light chain kinase (MLCK) is a regulatory protein for smooth muscle contraction, which acts by phosphorylating 20-kDa myosin light chain (MLC20) to activate the myosin ATPase activity. Although this mode of action is well-established, there are numerous reports of smooth muscle contraction that is not associated with MLC20 phosphorylation. The kinase activity for the phosphorylation is localized at the central part of MLCK, which is also furnished with actin-binding activity at its N terminal and myosin-binding activity at its C terminal. This article overviews as to how such multifunctional properties of MLCK modify the actin-myosin interaction and presents our observations that the phosphorylation is not obligatory in induction of smooth muscle contraction. [source] The Effect of Fatigue on the Timing of Electrical Stimulation-Evoked Muscle Contractions in People with Spinal Cord InjuryNEUROMODULATION, Issue 3 2004Peter J. Sinclair PhD Abstract This study investigated the activation dynamics of electrical stimulation-evoked muscle contractions performed by individuals with spinal cord injury (SCI). The purpose was to determine whether electrical stimulation (ES) firing patterns during cycling exercise should be altered in response to fatigue-induced changes in the time taken for force to rise and fall with ES. Seven individuals with SCI performed isometric contractions and pedaled a motorized cycle ergometer with stimulation applied to the quadriceps muscles. Both exercise conditions were performed for five minutes while the patterns of torque production were recorded. ES-evoked knee extension torque fell by 75% under isometric conditions, and the rate of force rise and decline decreased in proportion to torque (r = 0.91, r = 0.94, respectively). There was no change in the time for torque to rise to 50% of maximum levels. The time for torque to decline did increase slightly, but only during the first minute of exercise. Cycling power output fell approximately 50% during the five minutes of exercise, however, there was no change in the time taken for torque to rise or fall. The magnitude of ES-evoked muscle torques decline substantially with fatigue, however, the overall pattern of torque production remained relatively unchanged. These results suggest there is no need to alter stimulation firing patterns to accommodate fatigue during ES-evoked exercise. [source] Coronary Blood Flow Produced by Muscle Contractions Induced by Intracardiac Electrical CPR during Ventricular FibrillationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2009HAO WANG M.D. It has been reported that transthoracic electrical cardiopulmonary resuscitation (ECPR) generates coronary perfusion pressures (CPP) similar to manual chest compressions (MCC). We hypothesized that intracardiac ECPR produces similar CPP. Methods: ECPR pulse train protocols were applied for 20 seconds in a porcine model following 10 seconds of ventricular fibrillation (VF), using a defibrillator housing electrode and a right ventricular coil (IC-ECPR). Each protocol consisted of 200-ms electrical pulse trains applied at a rate of 100 pulse trains/min. The protocols were grouped in skeletal-based versus cardiac-based stimulation measurements. CPP was recorded and compared to historical MCC values generated by a similar experimental design. CPP > 15 mm Hg at 30 seconds of VF following the application of an IC-ECPR protocol was defined as successful. Results: Mean CPP for all intracardiac ECPR pulse train protocols at 30 seconds of VF was 14.8 ± 3.8 mm Hg (n = 39). Mean CPP in seven successful skeletal-based IC-ECPR protocols was 19.4 ± 3.2 mm Hg, and mean CPP in 10 successful cardiac-based IC-ECPR protocols was 17.4 ± 2.1 mm Hg. Reported CPP for 15 MCC experiments at 30 seconds of VF was 22.9 ± 9.4 mm Hg (P = 0.35 compared to skeletal-based IC-ECPR, P = 0.08 compared to cardiac-based IC-ECPR). Conclusions: Intracardiac applied electrical CPR produced observable skeletal muscle contractions, measurable pressure pulses, and coronary perfusion pressures similar to MCC during a brief episode of untreated VF. [source] Time series analysis of jaw muscle contraction and tissue deformation during mastication in miniature pigsJOURNAL OF ORAL REHABILITATION, Issue 1 2004Z. J. Liu summary, Masticatory muscle contraction causes both jaw movement and tissue deformation during function. Natural chewing data from 25 adult miniature pigs were studied by means of time series analysis. The data set included simultaneous recordings of electromyography (EMG) from bilateral masseter (MA), zygomaticomandibularis (ZM) and lateral pterygoid muscles, bone surface strains from the left squamosal bone (SQ), condylar neck (CD) and mandibular corpus (MD), and linear deformation of the capsule of the jaw joint measured bilaterally using differential variable reluctance transducers. Pairwise comparisons were examined by calculating the cross-correlation functions. Jaw-adductor muscle activity of MA and ZM was found to be highly cross-correlated with CD and SQ strains and weakly with MD strain. No muscle's activity was strongly linked to capsular deformation of the jaw joint, nor were bone strains and capsular deformation tightly linked. Homologous muscle pairs showed the greatest synchronization of signals, but the signals themselves were not significantly more correlated than those of non-homologous muscle pairs. These results suggested that bone strains and capsular deformation are driven by different mechanical regimes. Muscle contraction and ensuing reaction forces are probably responsible for bone strains, whereas capsular deformation is more likely a product of movement. [source] Signaling mechanisms in skeletal muscle: Acute responses and chronic adaptations to exerciseIUBMB LIFE, Issue 3 2008Katja S.C. Röckl Abstract Physical activity elicits physiological responses in skeletal muscle that result in a number of health benefits, in particular in disease states, such as type 2 diabetes. An acute bout of exercise/muscle contraction improves glucose homeostasis by increasing skeletal muscle glucose uptake, while chronic exercise training induces alterations in the expression of metabolic genes, such as those involved in muscle fiber type, mitochondrial biogenesis, or glucose transporter 4 (GLUT4) protein levels. A primary goal of exercise research is to elucidate the mechanisms that regulate these important metabolic and transcriptional events in skeletal muscle. In this review, we briefly summarize the current literature describing the molecular signals underlying skeletal muscle responses to acute and chronic exercise. The search for possible exercise/contraction-stimulated signaling proteins involved in glucose transport, muscle fiber type, and mitochondrial biogenesis is ongoing. Further research is needed because full elucidation of exercise-mediated signaling pathways would represent a significant step toward the development of new pharmacological targets for the treatment of metabolic diseases such as type 2 diabetes. © 2008 IUBMB IUBMB Life, 60(3): 145,153, 2008 [source] Fat as a fuel: emerging understanding of the adipose tissue,skeletal muscle axisACTA PHYSIOLOGICA, Issue 4 2010K. N. Frayn Abstract The early pioneers in the field of metabolism during exercise such as Lindhard and Krogh understood the importance of fat as a fuel for muscle contraction. But they could not have understood the details of the pathways involved, as neither the metabolic role of adipose tissue nor the transport role of non-esterified fatty acids (NEFA) in the plasma was clearly understood at the time. We now recognize that the onset of muscular contraction coincides with an increase in the delivery of NEFA from adipose tissue, probably coordinated by the sympatho-adrenal system. During light exercise, adipose tissue-derived NEFA make up the majority of the oxidative fuel used by muscle. As exercise is prolonged, the importance of NEFA increases. The onset of exercise is marked by an increased proportion of NEFAs entering ,-oxidation rather than re-esterification and recycling. At moderate intensities of exercise, other sources of fat, potentially plasma- and intramyocellular-triacylglycerol, supplement the supply of plasma NEFA. The delivery of NEFA is augmented by increased adipose tissue blood flow and by other stimuli such as atrial natriuretic peptide. Only during high-intensity exercise is there a failure of adipose tissue to deliver sufficient fatty acids for muscle (which is coupled with an inability of muscle to use them, even when fatty acids are supplied artificially). This limitation of adipose tissue NEFA delivery may reflect some feedback inhibition of lipolysis, perhaps via lactate, or possibly ,-adrenergic inhibition of lipolysis at very high catecholamine concentrations. [source] Changes in presumed motor cortical activity during fatiguing muscle contraction in humansACTA PHYSIOLOGICA, Issue 3 2010T. Seifert Abstract Aim:, Changes in sensory information from active muscles accompany fatiguing exercise and the force-generating capacity deteriorates. The central motor commands therefore must adjust depending on the task performed. Muscle potentials evoked by transcranial magnetic stimulation (TMS) change during the course of fatiguing muscle activity, which demonstrates activity changes in cortical or spinal networks during fatiguing exercise. Here, we investigate cortical mechanisms that are actively involved in driving the contracting muscles. Methods:, During a sustained submaximal contraction (30% of maximal voluntary contraction) of the elbow flexor muscles we applied TMS over the motor cortex. At an intensity below motor threshold, TMS reduced the ongoing muscle activity in biceps brachii. This reduction appears as a suppression at short latency of the stimulus-triggered average of rectified electromyographic (EMG) activity. The magnitude of the suppression was evaluated relative to the mean EMG activity during the 50 ms prior to the cortical stimulus. Results:, During the first 2 min of the fatiguing muscle contraction the suppression was 10 ± 0.9% of the ongoing EMG activity. At 2 min prior to task failure the suppression had reached 16 ± 2.1%. In control experiments without fatigue we did not find a similar increase in suppression with increasing levels of ongoing EMG activity. Conclusion:, Using a form of TMS which reduces cortical output to motor neurones (and disfacilitates them), this study suggests that neuromuscular fatigue increases this disfacilitatory effect. This finding is consistent with an increase in the excitability of inhibitory circuits controlling corticospinal output. [source] Regulation of glucose transporter 4 traffic by energy deprivation from mitochondrial compromiseACTA PHYSIOLOGICA, Issue 1 2009A. Klip Abstract Skeletal muscle is the major store and consumer of fatty acids and glucose. Glucose enters muscle through glucose transporter 4 (GLUT4). Upon insufficient oxygen availability or energy compromise, aerobic metabolism of glucose and fatty aids cannot proceed, and muscle cells rely on anaerobic metabolism of glucose to restore cellular energy status. An increase in glucose uptake into muscle is a key response to stimuli requiring rapid energy supply. This chapter analyses the mechanisms of the adaptive regulation of glucose transport that rescue muscle cells from mitochondrial uncoupling. Under these conditions, the initial drop in ATP recovers rapidly, through a compensatory increase in glucose uptake. This adaptive response involves AMPK activation by the initial ATP drop, which elevates cell surface GLUT4 and glucose uptake. The gain in surface GLUT4 involves different signals and routes of intracellular traffic compared with those engaged by insulin. The hormone increases GLUT4 exocytosis through phosphatidylinositol 3-kinase and Akt, whereas energy stress retards GLUT4 endocytosis through AMPK and calcium inputs. Given that energy stress is a component of muscle contraction, and that contraction activates AMPK and raises cytosolic calcium, we hypothesize that the increase in glucose uptake during contraction may also involve a reduction in GLUT4 endocytosis. [source] Lithium and KB-R7943 effects on mechanics and energetics of rat heart muscleACTA PHYSIOLOGICA, Issue 1 2002P. Bonazzola ABSTRACT The role of calcium influx on energy expenditure during cardiac contraction was studied. For this purpose, the described ability of lithium and KB-R 7943 (KBR) to diminish Ca entry through Na,Ca exchanger (Ponce-Hornos & Langer, J Mol Cell Cardiol 1980, 12, 1367, Satoh et al., Circulation 2000, 101, 1441) were used. In isolated contractions (contractions elicited after at least 5 min of rest) LiCl 45 mmol L,1 decreased pressure developed and pressure,time integral from 42.3 ± 2.7 and 14.5 ± 1.2 to 32.1 ± 3.4 mN mm,2 and 8.3 ± 0.9 mN mm,2 s, respectively. A similar effect was observed in regular contractions (at 0.16 Hz stimulation). The presence of KBR (5 ,mol L,1) in the perfusate induced a slight but not significant decrease in pressure developed and pressure,time integral in steady-state contractions. As it was previously described, the heat involved in a heart muscle contraction can be decomposed into several components (H1, H2, H3 and H4), but only one (H3) was associated with force generation. While H3 decreased with lithium in both types of contractions, H3/PtI ratio remained unaltered, indicating that the economy for pressure maintenance was unaffected. To further investigate the role of Ca entry on force development, a condition in which the contraction is mainly dependent on extracellular calcium was studied. An ,extra' stimulus applied 200 ms after the regular one in a muscle stimulated at 0.16 Hz induces a contraction with this characteristic (Marengo et al., Am J Physiol 1999, 276, H309). Lithium induced a strong decrease in pressure,time integral and H3 associated with this contraction (43 and 45%, respectively) with no change in H3/PtI ratio. Lithium also reduced (53%) an energy component (H2) associated with Ca cycling. The use of KBR showed qualitatively similar results [i.e. a 33% reduction in pressure,time integral associated with the extrasystole (ES) with no changes in H3/PtI ratio and a 30% reduction in the H2 component]. Li and KBR effects appear to be additive and in the presence of 45 mmol L,1 Li and 5 ,mol L,1 KBR the extrasystole was abolished in 77%. Lithium and KBR effects particularly for the extrasystole can be explained through the inhibition of Ca entry via Na,Ca exchange giving support to the participation of the Na,Ca exchanger in the Ca influx from the extracellular space. In addition, the results also suggest the possibility of an effect of Li on an additional Ca sensitive locus (different than the Na,Ca exchanger). In this connection, in isolated contractions lithium decreased the energy release fraction related to mitochondrial processes (H4) increasing the economy of the overall cardiac contraction. [source] Mitogen-activated protein kinase signal transduction in skeletal muscle: effects of exercise and muscle contractionACTA PHYSIOLOGICA, Issue 3 2001U. Widegren Exercise has numerous growth and metabolic effects in skeletal muscle, including changes in glycogen metabolism, glucose and amino acid uptake, protein synthesis and gene transcription. However, the mechanism(s) by which exercise regulates intracellular signal transduction to the transcriptional machinery in the nucleus, thus modulating gene expression, is largely unknown. This review will provide insight on potential intracellular signalling mechanisms by which muscle contraction/exercise leads to changes in gene expression. Mitogen-activated protein kinase (MAPK) cascades are associated with increased transcriptional activity. The MAPK family members can be separated into distinct parallel pathways including the extracellular signal-regulated kinase (ERK) 1/2, the stress-activated protein kinase cascades (SAPK1/JNK and SAPK2/p38) and the extracellular signal-regulated kinase 5 (ERK5). Acute exercise elicits signal transduction via MAPK cascades in direct response to muscle contraction. Thus, MAPK pathways appear to be potential physiological mechanisms involved in the exercise-induced regulation of gene expression in skeletal muscle. [source] Two different unique cardiac isoforms of protein 4.1R in zebrafish, Danio rerio, and insights into their cardiac functions as related to their unique structuresDEVELOPMENT GROWTH & DIFFERENTIATION, Issue 7 2010Kenji Murata Protein 4.1R (4.1R) has been identified as the major component of the human erythrocyte membrane skeleton. The members of the protein 4.1 gene family are expressed in a tissue-specific alternative splicing manner that increases their functions in each tissue; however, the exact roles of cardiac 4.1R in the developing myocardium are poorly understood. In zebrafish (ZF), we identified two heart-specific 4.1R isoforms, ZF4.1RH2 and ZF4.1RH3, encoding N-terminal 30 kDa (FERM) domain and spectrin-actin binding domain (SABD) and C-terminal domain (CTD), separately. Applying immunohistochemistry using specific antibodies for 30 kDa domain and CTD separately, the gene product of ZF4.1RH2 and ZF4.1RH3 appeared only in the ventricle and in the atrium, respectively, in mature hearts. During embryogenesis, both gene expressions are expressed starting 24 h post-fertilization (hpf). Following whole-mount in situ hybridization, ZF4.1RH3 gene expression was detected in the atrium of 37 hpf embryos. These results indicate that the gene product of ZF4.1RH3 is essential for normal morphological shape of the developing heart and to support the repetitive cycles of its muscle contraction and relaxation. [source] Developmental expression and comparative genomic analysis of Xenopus cardiac myosin heavy chain genesDEVELOPMENTAL DYNAMICS, Issue 4 2005Robert J. Garriock Abstract Myosin heavy chains (MHC) are cytoskeletal motor proteins essential to the process of muscle contraction. We have determined the complete sequences of the Xenopus cardiac MHC genes, ,-MHC and ventricular MHC (vMHC), and have characterized their developmental expression profiles. Whereas ,-MHC is expressed from the earliest stages of cardiac differentiation, vMHC transcripts are not detected until the heart has undergone chamber formation. Early expression of vMHC appears to mark the cardiac conduction system, but expression expands to include the ventricle and outflow tract myocardium during subsequent development. Sequence comparisons, transgenic expression analysis, and comparative genomic studies indicate that Xenopus ,-MHC is the true orthologue of the mammalian ,-MHC gene. On the other hand, we show that the Xenopus vMHC gene is most closely related to chicken ventricular MHC (vMHC1) not the mammalian ,-MHC. Comparative genomic analysis has allowed the detection of a mammalian MHC gene (MyH15) that appears to be the orthologue of vMHC, but evidence suggests that this gene is no longer active. Developmental Dynamics 233:1287,1293, 2005. © 2005 Wiley-Liss, Inc. [source] Review article: Emergency department implications of the TASEREMERGENCY MEDICINE AUSTRALASIA, Issue 4 2009Megan Robb Abstract The TASER is a conducted electricity device currently being introduced to the Australian and New Zealand police forces as an alternative to firearms in dealing with violent and dangerous individuals. It incapacitates the subject by delivering rapid pulses of electricity causing involuntary muscle contraction and pain. The use of this device might lead to cardiovascular, respiratory, biochemical, obstetric, ocular and traumatic sequelae. This article will summarize the current literature and propose assessment and management recommendations to guide emergency physicians who will be required to review these patients. [source] The nitric oxide/cyclic guanosine monophosphate pathway modulates the inspiratory-related activity of hypoglossal motoneurons in the adult ratEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2008Fernando Montero Abstract Motoneurons integrate interneuronal activity into commands for skeletal muscle contraction and relaxation to perform motor actions. Hypoglossal motoneurons (HMNs) are involved in essential motor functions such as breathing, mastication, swallowing and phonation. We have investigated the role of the gaseous molecule nitric oxide (NO) in the regulation of the inspiratory-related activity of HMNs in order to further understand how neural activity is transformed into motor activity. In adult rats, we observed nitrergic fibers and bouton-like structures in close proximity to motoneurons, which normally lack the molecular machinery to synthesize NO. In addition, immunohistochemistry studies demonstrated that perfusion of animals with a NO donor resulted in an increase in the levels of cyclic guanosine monophosphate (cGMP) in motoneurons, which express the soluble guanylyl cyclase (sGC) in the hypoglossal nucleus. Modulators of the NO/cGMP pathway were micro-iontophoretically applied while performing single-unit extracellular recordings in the adult decerebrated rat. Application of a NO synthase inhibitor or a sGC inhibitor induced a statistically significant reduction in the inspiratory-related activity of HMNs. However, excitatory effects were observed by ejection of a NO donor or a cell-permeable analogue of cGMP. In slice preparations, application to the bath of a NO donor evoked membrane depolarization and a decrease in rheobase, which were prevented by co-addition to the bath of a sGC inhibitor. These effects were not prevented by reduction of the spontaneous synaptic activity. We conclude that NO from afferent fibers anterogradely modulates the inspiratory-related activity of HMNs by a cGMP-dependent mechanism in physiological conditions. [source] AMPA/kainate and NMDA-like glutamate receptors at the chromatophore neuromuscular junction of the squid: role in synaptic transmission and skin patterningEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2003Pedro A. Lima Abstract Glutamate receptor types were examined at the chromatophore synapses of the squids Alloteuthis subulata and Loligo vulgaris, where nerve-induced muscle contraction causes chromatophore expansion. Immunoblotting with antibody raised against a squid AMPA receptor (sGluR) demonstrated that AMPA/kainate receptors are present in squid skin. Application of l -glutamate evoked chromatophore muscle contractions in both ventral and dorsal skins, while NMDA was only active on a subpopulation of dorsal chromatophores. In dorsal skin, neurotransmission was partly blocked by either AMPA/kainate receptor antagonists (CNQX and DNQX) or NMDA receptor antagonists (AP-5 and MK-801) or completely blocked by simultaneous application of both classes of antagonists. In isolated muscle fibres, ionophoretic application of l -glutamate evoked fast inward CNQX- and DNQX-sensitive currents with reversal potentials around +14 mV and a high conductance to Na+. In fibres from dorsal skin only, a slower outward glutamate-sensitive current appeared at positive holding potentials. At negative potentials, currents were potentiated by glycine or by removing external Mg2+ and were blocked by AP-5 and MK-801. Glutamate caused a fast, followed by a slow, transient increase in cytoplasmic Ca2+. The slow component was increased in amplitude and duration by glycine or by lowering external Mg2+ and decreased by AP-5 and MK-801. In cells from ventral skin, no ,NMDA-like responses' were detected. Thus, while AMPA/kainate receptors mediated fast excitatory synaptic transmission and rapid colour change over the whole skin, activation of both AMPA/kainate and NMDA-like receptors in a subpopulation of dorsal chromatophores prolonged the postsynaptically evoked Ca2+ elevation causing temporally extended colour displays with behavioural significance. [source] Modularity of the rodent mandible: Integrating bones, muscles, and teethEVOLUTION AND DEVELOPMENT, Issue 6 2008Miriam Leah Zelditch Summary Several models explain how a complex integrated system like the rodent mandible can arise from multiple developmental modules. The models propose various integrating mechanisms, including epigenetic effects of muscles on bones. We test five for their ability to predict correlations found in the individual (symmetric) and fluctuating asymmetric (FA) components of shape variation. We also use exploratory methods to discern patterns unanticipated by any model. Two models fit observed correlation matrices from both components: (1) parts originating in same mesenchymal condensation are integrated, (2) parts developmentally dependent on the same muscle form an integrated complex as do those dependent on teeth. Another fits the correlations observed in FA: each muscle insertion site is an integrated unit. However, no model fits well, and none predicts the complex structure found in the exploratory analyses, best described as a reticulated network. Furthermore, no model predicts the correlation between proximal parts of the condyloid and coronoid, which can exceed the correlations between proximal and distal parts of the same process. Additionally, no model predicts the correlation between molar alveolus and ramus and/or angular process, one of the highest correlations found in the FA component. That correlation contradicts the basic premise of all five developmental models, yet it should be anticipated from the epigenetic effects of mastication, possibly the primary morphogenetic process integrating the jaw coupling forces generated by muscle contraction with those experienced at teeth. [source] Quantification of myoglobin deoxygenation and intracellular partial pressure of O2 during muscle contraction during haemoglobin-free medium perfusionEXPERIMENTAL PHYSIOLOGY, Issue 5 2010Hisashi Takakura Although the O2 gradient regulates O2 flux from the capillary into the myocyte to meet the energy demands of contracting muscle, intracellular O2 dynamics during muscle contraction remain unclear. Our hindlimb perfusion model allows the determination of intracellular myoglobin (Mb) saturation () and intracellular oxygen tension of myoglobin () in contracting muscle using near infrared spectroscopy (NIRS). The hindlimb of male Wistar rats was perfused from the abdominal aorta with a well-oxygenated haemoglobin-free Krebs,Henseleit buffer. The deoxygenated Mb (,[deoxy-Mb]) signal was monitored by NIRS. Based on the value of ,[deoxy-Mb],,,and,,were calculated, and the time course was evaluated by an exponential function model. Both,,and,,started to decrease immediately after the onset of contraction. The steady-state values of,,and,,progressively decreased with relative work intensity or muscle oxygen consumption. At the maximal twitch rate,,,and,,were 49% and 2.4 mmHg, respectively. Moreover, the rate of release of O2 from Mb at the onset of contraction increased with muscle oxygen consumption. These results suggest that at the onset of muscle contraction, Mb supplies O2 during the steep decline in,, which expands the O2 gradient to increase the O2 flux to meet the increased energy demands. [source] Chronic effects of type 2 diabetes mellitus on cardiac muscle contraction in the Goto-Kakizaki ratEXPERIMENTAL PHYSIOLOGY, Issue 6 2007F. C. Howarth Type 2 diabetes mellitus accounts for more than 90% of all cases of diabetes mellitus, and cardiovascular complications are the major cause of mortality and death in diabetic patients. The chronic effects of type 2 diabetes mellitus on heart function have been investigated in the Goto-Kakizaki (GK) rat. Experiments were performed in GK rats and age-matched Wistar control rats at 18 months of age. The progressive effects of diabetes on glucose metabolism were monitored periodically by application of the glucose tolerance test. Ventricular action potentials were measured in isolated, perfused heart. Shortening and intracellular Ca2+ were measured in electrically stimulated ventricular myocytes. The GK rats displayed mild fasting hyperglycaemia and progressively worsening glucose tolerance. At 18 months of age and 180 min after intraperitoneal injection of glucose (2 g (kg body weight),1), blood glucose was 436 ± 47 mg dl,1 in GK rats compared with 153 ± 18 mg dl,1 in control animals. Heart weight to body weight ratio was significantly increased in GK rats (4.10 ± 0.09 mg g,1, n= 5) compared with control animals (3.36 ± 0.22 mg g,1, n= 4). Spontaneous heart rate was slightly reduced in GK rats compared with control rats. Although the amplitude of shortening was not altered, the amplitude of the Ca2+ transient was significantly increased in myocytes from GK rats (0.78 ± 0.11 ratio units) compared with control rats (0.50 ± 0.06 ratio units). Despite progressively worsening glucose metabolism, at 18 months of age the contractile function of the heart appears to be well preserved. [source] Comparative studies on the functional roles of N- and C-terminal regions of molluskan and vertebrate troponin-IFEBS JOURNAL, Issue 17 2005Hiroyuki Tanaka Vertebrate troponin regulates muscle contraction through alternative binding of the C-terminal region of the inhibitory subunit, troponin-I (TnI), to actin or troponin-C (TnC) in a Ca2+ -dependent manner. To elucidate the molecular mechanisms of this regulation by molluskan troponin, we compared the functional properties of the recombinant fragments of Akazara scallop TnI and rabbit fast skeletal TnI. The C-terminal fragment of Akazara scallop TnI (ATnI232,292), which contains the inhibitory region (residues 104,115 of rabbit TnI) and the regulatory TnC-binding site (residues 116,131), bound actin-tropomyosin and inhibited actomyosin-tropomyosin Mg-ATPase. However, it did not interact with TnC, even in the presence of Ca2+. These results indicated that the mechanism involved in the alternative binding of this region was not observed in molluskan troponin. On the other hand, ATnI130,252, which contains the structural TnC-binding site (residues 1,30 of rabbit TnI) and the inhibitory region, bound strongly to both actin and TnC. Moreover, the ternary complex consisting of this fragment, troponin-T, and TnC activated the ATPase in a Ca2+ -dependent manner almost as effectively as intact Akazara scallop troponin. Therefore, Akazara scallop troponin regulates the contraction through the activating mechanisms that involve the region spanning from the structural TnC-binding site to the inhibitory region of TnI. Together with the observation that corresponding rabbit TnI-fragment (RTnI1,116) shows similar activating effects, these findings suggest the importance of the TnI N-terminal region not only for maintaining the structural integrity of troponin complex but also for Ca2+ -dependent activation. [source] Cloning and characterization of novel snake venom proteins that block smooth muscle contractionFEBS JOURNAL, Issue 11 2002Yasuo Yamazaki In this study, we isolated a 25-kDa novel snake venom protein, designated ablomin, from the venom of the Japanese Mamushi snake (Agkistrodon blomhoffi). The amino-acid sequence of this protein was determined by peptide sequencing and cDNA cloning. The deduced sequence showed high similarity to helothermine from the Mexican beaded lizard (Heloderma horridum horridum), which blocks voltage-gated calcium and potassium channels, and ryanodine receptors. Ablomin blocked contraction of rat tail arterial smooth muscle elicited by high K+ -induced depolarization in the 0.1,1 µm range, but did not block caffeine-stimulated contraction. Furthermore, we isolated three other proteins from snake venoms that are homologous to ablomin and cloned the corresponding cDNAs. Two of these homologous proteins, triflin and latisemin, also inhibited high K+ -induced contraction of the artery. These results indicate that several snake venoms contain novel proteins with neurotoxin-like activity. [source] Deficiency of Myo18B in mice results in embryonic lethality with cardiac myofibrillar aberrationsGENES TO CELLS, Issue 10 2008Rieko Ajima Myo18B is an unconventional myosin family protein expressed predominantly in muscle cells. Although conventional myosins are known to be localized on the A-bands and function as a molecular motor for muscle contraction, Myo18B protein was localized on the Z-lines of myofibrils in striated muscles. Like Myo18A, another 18th class of myosin, the N-terminal unique domain of the protein and not the motor domain and the coiled-coil tail is critical for its localization to F-actin in myocytes. Myo18B expression was induced by myogenic differentiation through the binding of myocyte-specific enhancer factor-2 to its promoter. Deficiency of Myo18B caused an embryonic lethality in mice accompanied by disruption of myofibrillar structures in cardiac myocytes at embryonic day 10.5. Thus, Myo18B is a unique unconventional myosin that is predominantly expressed in myocytes and whose expression is essential for the development and/or maintenance of myofibrillar structure. [source] Trigger Points in the Suboccipital Muscles and Forward Head Posture in Tension-Type HeadacheHEADACHE, Issue 3 2006César Fernández-de-las-Peńas PT Objective.,To assess the presence of trigger points (TrPs) in the suboccipital muscles and forward head posture (FHP) in subjects with chronic tension-type headache (CTTH) and in healthy subjects, and to evaluate the relationship of TrPs and FHP with headache intensity, duration, and frequency. Background.,Tension-type headache (TTH) is a prototypical headache in which myofascial TrPs in the cervical and pericranial musculature can play an important role. Design.,A blinded, controlled pilot study. Methods.,Twenty CTTH subjects and 20 matched controls without headache participated. TrPs were identified by eliciting referred pain with palpation, and increased referred pain with muscle contraction. Side-view pictures of each subject were taken in sitting and standing positions, in order to assess FHP by measuring the craniovertebral angle. Both measures were taken by a blinded assessor. A headache diary was kept for 4 weeks in order to assess headache intensity, frequency, and duration. Results.,Sixty-five percent (13/20) CTTH subjects showed active TrPs and 35% (7/20) had latent TrPs in the suboccipital muscles. Six (30%) controls also had latent TrPs. Differences in the presence of suboccipital muscle TrPs between both the groups were significant for active TrPs (P < .001) but not for latent TrPs (P > .5). CTTH subjects with active TrPs reported a greater headache intensity and frequency than those with latent TrPs (P < .05). The degree of FHP was greater in CTTH subjects than in controls in both sitting and standing positions (P < .01). Within the CTTH group, there was a negative correlation between the craniovertebral angle and the frequency of headache (rs=,0.6, P < .01, in sitting position; rs=,0.5, P < .05, in standing position). CTTH subjects with active TrPs had a greater FHP than those with latent TrPs, though this difference was not significant. Conclusions.,Suboccipital active TrPs and FHP were associated with CTTH. CCTH subjects with active TrPs reported a greater headache intensity and frequency than those with latent TrPs. The degree of FHP correlated positively with headache duration, headache frequency, and the presence of suboccipital active TrPs. [source] Botulinum Neurotoxin for the Treatment of Migraine and Other Primary Headache Disorders: From Bench to BedsideHEADACHE, Issue 2003David W. Dodick MD Botulinum toxin type A, a neurotoxin, is effective for treating a variety of disorders of involuntary muscle contraction including cervical dystonia, blepharospasm, and hemifacial spasm. It inhibits neuromuscular signaling by blocking the release of acetylcholine at the neuromuscular junction. The biological effects of the toxin are transient, with normal neuronal signaling returning within approximately 3 to 6 months postinjection. Recent clinical findings suggest that botulinum toxin type A may inhibit pain associated with migraine and other types of headache. However, the mechanism by which this toxin inhibits pain is not fully understood and is under investigation. Research findings suggest that botulinum toxin type A inhibits the release of neurotransmitters from nociceptive nerve terminals and, in this way, may possess an analgesic effect. A number of retrospective open-label chart reviews and 3 double-blind, placebo-controlled trials have demonstrated that localized injections of botulinum toxin type A significantly reduce the frequency, severity, and disability associated with migraine headaches. Although the majority of patients in these studies experienced no botulinum toxin type A-mediated side effects, a small percentage of patients did report transient minor side effects including blepharoptosis, diplopia, and injection-site weakness. Currently, 4 randomized, placebo-controlled, clinical trials are being conducted to evaluate the efficacy, optimal dosing, and side-effect profile of botulinum toxin type A as a novel treatment for migraine and other types of headache. These studies may provide further evidence that botulinum toxin type A is an effective option for the preventive treatment of migraine. [source] Improving functional magnetic resonance imaging motor studies through simultaneous electromyography recordingsHUMAN BRAIN MAPPING, Issue 9 2007Bradley J. MacIntosh Abstract Specially designed optoelectronic and data postprocessing methods are described that permit electromyography (EMG) of muscle activity simultaneous with functional MRI (fMRI). Hardware characterization and validation included simultaneous EMG and event-related fMRI in 17 healthy participants during either ankle (n = 12), index finger (n = 3), or wrist (n = 2) contractions cued by visual stimuli. Principal component analysis (PCA) and independent component analysis (ICA) were evaluated for their ability to remove residual fMRI gradient-induced signal contamination in EMG data. Contractions of ankle tibialis anterior and index finger abductor were clearly distinguishable, although observing contractions from the wrist flexors proved more challenging. To demonstrate the potential utility of simultaneous EMG and fMRI, data from the ankle experiments were analyzed using two approaches: 1) assuming contractions coincided precisely with visual cues, and 2) using EMG to time the onset and offset of muscle contraction precisely for each participant. Both methods produced complementary activation maps, although the EMG-guided approach recovered more active brain voxels and revealed activity better in the basal ganglia and cerebellum. Furthermore, numerical simulations confirmed that precise knowledge of behavioral responses, such as those provided by EMG, are much more important for event-related experimental designs compared to block designs. This simultaneous EMG and fMRI methodology has important applications where the amplitude or timing of motor output is impaired, such as after stroke. Hum Brain Mapp 2006. © 2006 Wiley-Liss, Inc. [source] Skeletal muscle glucose uptake during exercise: A focus on reactive oxygen species and nitric oxide signalingIUBMB LIFE, Issue 5 2009Troy L. Merry Abstract Like insulin, muscle contraction (in vitro or in situ) and exercise increase glucose uptake into skeletal muscle. However, the contraction/exercise pathway of glucose uptake in skeletal muscle is an independent pathway to that of insulin. Indeed, skeletal muscle glucose uptake is normal during exercise in those who suffer from insulin resistance and diabetes. Thus, the pathway of contraction-mediated glucose uptake into skeletal muscle provides an attractive potential target for pharmaceutical treatment and prevention of such conditions, especially as skeletal muscle is the major site of impaired glucose disposal in insulin resistance. The mechanisms regulating skeletal muscle glucose uptake during contraction have not been fully elucidated. Potential regulators include Ca2+ (via CaMK's and/or CaMKK), AMPK, ROS, and NO signaling, with some redundancy likely to be evident within the system. In this review, we attempt to briefly synthesize current evidence regarding the potential mechanisms involved in regulating skeletal muscle glucose uptake during contraction, focusing on ROS and NO signaling. While reading this review, it will become clear that this is an evolving field of research and that much more work is required to elucidate the mechanism(s) regulating skeletal muscle glucose uptake during contraction. © 2009 IUBMB IUBMB Life 61(5): 479,484, 2009 [source] Myosin Light Chain Kinase as a Multifunctional Regulatory Protein of Smooth Muscle ContractionIUBMB LIFE, Issue 6 2001Ying Gao Abstract Myosin light chain kinase (MLCK) is a regulatory protein for smooth muscle contraction, which acts by phosphorylating 20-kDa myosin light chain (MLC20) to activate the myosin ATPase activity. Although this mode of action is well-established, there are numerous reports of smooth muscle contraction that is not associated with MLC20 phosphorylation. The kinase activity for the phosphorylation is localized at the central part of MLCK, which is also furnished with actin-binding activity at its N terminal and myosin-binding activity at its C terminal. This article overviews as to how such multifunctional properties of MLCK modify the actin-myosin interaction and presents our observations that the phosphorylation is not obligatory in induction of smooth muscle contraction. [source] Close relation of arterial ICC-like cells to the contractile phenotype of vascular smooth muscle cellJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 4 2007Vladimír Pucovský Abstract This work aimed to establish the lineage of cells similar to the interstitial cells of Cajal (ICC), the arterial ICC-like (AIL) cells, which have recently been described in resistance arteries, and to study their location in the artery wall. Segments of guinea-pig mesenteric arteries and single AIL cells freshly isolated from them were used. Confocal imaging of immunostained cells or segments and electron microscopy of artery segments were used to test for the presence and cellular localization of selected markers, and to localize AIL cells in intact artery segments. AIL cells were negative for PGP9.5, a neural marker, and for von Willebrand factor (vWF), an endothelial cell marker. They were positive for smooth muscle ,-actin and smooth muscle myosin heavy chain (SM-MHC), but expressed only a small amount of smoothelin, a marker of contractile smooth muscle cells (SMC), and of myosin light chain kinase (MLCK), a critical enzyme in the regulation of smooth muscle contraction. Cell isolation in the presence of latrunculin B, an actin polymerization inhibitor, did not cause the disappearance of AIL cells from cell suspension. The fluorescence of basal lamina protein collagen IV was comparable between the AIL cells and the vascular SMCs and the fluorescence of laminin was higher in AIL cells compared to vascular SMCs. Moreover, cells with thin processes were found in the tunica media of small resistance arteries using transmis-sion electron microscopy. The results suggest that AIL cells are immature or phenotypically modulated vascular SMCs constitutively present in resistance arteries. [source] Molecular and immunohistochemical analyses of cardiac troponin T during cardiac development in the Mexican axolotl, Ambystoma mexicanumJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 1 2007C. Zhang Abstract The Mexican axolotl, Ambystoma mexicanum, is an excellent animal model for studying heart development because it carries a naturally occurring recessive genetic mutation, designated gene c, for cardiac nonfunction. The double recessive mutants (c/c) fail to form organized myofibrils in the cardiac myoblasts resulting in hearts that fail to beat. Tropomyosin expression patterns have been studied in detail and show dramatically decreased expression in the hearts of homozygous mutant embryos. Because of the direct interaction between tropomyosin and troponin T (TnT), and the crucial functions of TnT in the regulation of striated muscle contraction, we have expanded our studies on this animal model to characterize the expression of the TnT gene in cardiac muscle throughout normal axolotl development as well as in mutant axolotls. In addition, we have succeeded in cloning the full-length cardiac troponin T (cTnT) cDNA from axolotl hearts. Confocal microscopy has shown a substantial, but reduced, expression of TnT protein in the mutant hearts when compared to normal during embryonic development. J. Cell. Biochem. 100: 1,15, 2007. © 2006 Wiley-Liss, Inc. [source] Development and physiology of gastric dilation air sacculitis in Chinook salmon, Oncorhynchus tshawytscha (Walbaum)JOURNAL OF FISH DISEASES, Issue 8 2007L G Forgan Abstract The syndrome known as gastric dilation air sacculitis (GDAS) has previously been shown to affect Chinook salmon, Oncorhynchus tshawytscha, in seawater (SW) aquaculture. Feed and osmoregulatory stress have been implicated as potential epidemiological co-factors. The development and physiology of GDAS was investigated in SW and freshwater (FW) adapted smolts. Diet A (low-cohesion pellets) and diet B (high-cohesion pellets) were fed to both FW- and SW-adapted fish. GDAS was induced only in the SW trial on feeding diet A. Stimulated gastro-intestinal (GI) smooth muscle contractility, and fluid transport by the pyloric caeca were different in GDAS-affected fish, which also showed osmoregulatory dysfunction. Cardiac stomach (CS) smooth muscle contractility in response to acetylcholine and potassium chloride (KCl) was significantly reduced in fish fed diet A relative to controls from weeks 3,5. In contrast, maximal pyloric sphincter (PS) circular smooth muscle contraction in response to KCl was significantly elevated in fish fed diet A in weeks 4 and 5. Serum osmolality was elevated in GDAS-affected fish from week 2 of the SW trial. Fluid transport from the mucosal to serosal surface of isolated pyloric caeca was significantly reduced in weeks 3, 4 and 5 in SW fish fed diet A. Gastric evacuation from the stomach of healthy fish was shown to be significantly different when diets of low- and high-cohesion were fed. The results are consistent with the intestinal brake playing a role in the development of the disease. [source] Influence of gum-chewing on the haemodynamics in female masseter muscleJOURNAL OF ORAL REHABILITATION, Issue 4 2009N. ABE Summary, Blood flow in active skeletal muscles provides energy substrate, oxygen and reduction of excessive heat and metabolic by-products. Although cyclic jaw motions such as those during mastication and speech articulation are the primitive oro-facial functions, possible effects of the cyclic muscle contractions on the intramuscular haemodynamics of the jaw muscles remains scarcely known. We investigated the masseteric haemodynamics during and after gum-chewing. Ten healthy female adults participated in the study. Electromyography, kinetics of masseter muscle oxygenation, electrocardiogram and blood pressure were recorded simultaneously. The subjects were asked to perform gum-chewing and cyclic jaw motion without gum bolus (empty-chewing task). The haemodynamics parameters were compared between the two experimental conditions. During gum-chewing task, deoxygenated haemoglobin and sympathetic nerve activity increased, while tissue blood oxygen saturation decreased. Blood pressure and parasympathetic nerve activity did not change. The overall behaviour of haemodynamic parameters during empty-chewing task was similar to that observed during gum-chewing task. However, the latency periods from the end of chewing until significant changes in the haemodynamic parameters were notably shorter (P < 0·05) in gum-chewing task as compared with those associated with empty-chewing task. The duration of the changes was shorter with empty-chewing than with gum-chewing. Fluctuations in masseter muscle haemodynamics associated with chewing jaw movement differed depending on the level of muscle contraction during movement. The differences became statistically significant immediately after the commencement of chewing and after the cessation movement. During the chewing movement, automatic nerve activities increased in response to the level of muscle contraction during movement. [source] | ||||||||||||||||||||||||||||||||||