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Relevant bibliographies by topics / Muscles agonistes

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Academic literature on the topic 'Muscles agonistes'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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Journal articles on the topic "Muscles agonistes"

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Girard, Marion, and Claire Leroux. "Gestion des muscles et des fonctions par le kinésithérapeute dans les traitements orthodontiques et ortho-chirurgicaux. Rééducation oro-myofonctionnelle." L'Orthodontie Française 86, no. 1 (March 2015): 95–111. http://dx.doi.org/10.1051/orthodfr/2015012.

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Peut-on espérer faire l’économie de la gestion des muscles et des fonctions dans les plans de traitement orthodontiques ou ortho-chirurgicaux ? En quoi le masseur-kinésithérapeute spécialisé peut-il aider, faciliter, stabiliser le travail de l’orthodontiste et du chirurgien maxillo-facial et éviter les récidives ? L’alignement dentaire et l’équilibre occlusal recherchés par les traitements sont en lien direct avec l’équilibre musculaire de la langue, des muscles peauciers, des muscles masticateurs, des muscles posturaux et les fonctions de la sphère oro-faciale. La réinstallation d’un équilibre entre muscles agonistes et antagonistes passe par un relâchement des muscles contracturés et par une tonification progressive des muscles déficients. La rééducation des dysfonctions oro-maxillo-faciales (linguales, labiales, jugales, masticatoires, ventilatoires) et de la posture globale, ainsi que la gestion des para-fonctions, nécessitent obligatoirement la participation active du patient pour un traitement efficace et pérenne. Cette rééducation est indispensable à l’orthopédie dento-faciale des enfants comme des adultes. L’illustration au travers de cas pratiques montrera ce que la rééducation myo-fonctionnelle peut apporter. Les résultats sont extrêmement satisfaisants pour rétablir les fonctions naturelles sous la condition d’exercices musculaires quotidiens et l’entraînement, tout au long de la journée, des bonnes postures et praxies enseignées, et cela pendant un à plusieurs trimestres sous la supervision du rééducateur.

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Colson, Serge S. "Quantification des niveaux d'activité électromyographique des muscles agonistes et antagonistes lors de contractions musculaires isométriques, concentriques et excentriques." Movement & Sport Sciences 85, no. 3 (2014): 93. http://dx.doi.org/10.3917/sm.085.0093.

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Colson, Serge S. "Quantification des niveaux d’activité électromyographique des muscles agonistes et antagonistes lors de contractions musculaires isométriques, concentriques et excentriques." Movement & Sport Sciences - Science & Motricité, no. 85 (December 11, 2013): 93–102. http://dx.doi.org/10.1051/sm/2013086.

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Elias, John J., Alfred F. Faust, Yung-Hua Chu, Edmund Y. Chao, and Andrew J. Cosgarea. "The Soleus Muscle Acts as an Agonist for the Anterior Cruciate Ligament: An in Vitro Experimental Study." American Journal of Sports Medicine 31, no. 2 (March 2003): 241–46. http://dx.doi.org/10.1177/03635465030310021401.

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Background: Although the quadriceps muscles are known antagonists for the anterior cruciate ligament and the hamstring muscles are known agonists, the influence of the calf muscles on knee stability is not well understood. Hypothesis: The soleus muscle acts as an anterior cruciate ligament agonist and the gastrocnemius muscle acts as an anterior cruciate ligament antagonist. Study Design: Controlled laboratory study. Methods: Six cadaveric knees were tested with individual and combined activation of the gastrocnemius and soleus muscles to determine the influence of simulated muscle contraction on tibiofemoral motion. Results: At all flexion angles, applying the soleus muscle force tended to translate the tibia posteriorly, whereas applying the gastrocnemius muscle force tended to translate the tibia anteriorly. Applying the soleus and gastrocnemius muscle forces together also tended to translate the tibia anteriorly. The average anterior and posterior tibial translations were greatest at 50° of flexion. Conclusions: The soleus muscle is capable of acting as an agonist for the anterior cruciate ligament and the gastrocnemius muscle can act as an antagonist. Clinical Relevance: A better understanding of the agonistic behavior of the soleus muscle on the anterior cruciate ligament may lead to the development of training and rehabilitation strategies that could reduce the incidence of injury and improve function in both patients with anterior cruciate ligament deficiency and patients who have undergone anterior cruciate ligament reconstruction.

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Sung, Tae Sik, Hongli Lu, Juno Sung, Jong Hoon Yeom, Brian A. Perrino, and Sang Don Koh. "The functional role of protease-activated receptors on contractile responses by activation of Ca2+ sensitization pathways in simian colonic muscles." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 6 (December 1, 2018): G921—G931. http://dx.doi.org/10.1152/ajpgi.00255.2018.

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It has been known that activation of protease-activated receptors (PARs) affects gastrointestinal motility. In this study, we tested the effects of PAR agonists on electrical and contractile responses and Ca2+ sensitization pathways in simian colonic muscles. The Simian colonic muscle was initially hyperpolarized by PAR agonists. After the transient hyperpolarization, simian colonic muscle repolarized to the control resting membrane potential (RMP) without a delayed depolarization. Apamin significantly reduced the initial hyperpolarization, suggesting that activation of small conductance Ca2+-activated K+ (SK) channels is involved in the initial hyperpolarization. In contractile experiments, PAR agonists caused an initial relaxation followed by an increase in contractions. These delayed contractile responses were not matched with the electrical responses that showed no after depolarization of the RMP. To investigate the possible involvement of Rho-associated protein kinase 2 (ROCK) pathways in the PAR effects, muscle strips were treated with ROCK inhibitors, which significantly reduced the PAR agonist-induced contractions. Furthermore, PAR agonists increased MYPT1 phosphorylation, and ROCK inhibitors completely blocked MYPT1 phosphorylation. PAR agonists alone had no effect on CPI-17 phosphorylation. In the presence of apamin, PAR agonists significantly increased CPI-17 phosphorylation, which was blocked by protein kinase C (PKC) inhibitors suggesting that Ca2+ influx is increased by apamin and is activating PKC. In conclusion, these studies show that PAR activators induce biphasic responses in simian colonic muscles. The initial inhibitory responses by PAR agonists are mainly mediated by activation of SK channels and delayed contractile responses are mainly mediated by the CPI-17 and ROCK Ca2+ sensitization pathways in simian colonic muscles. NEW & NOTEWORTHY In the present study, we found that the contractile responses of simian colonic muscles to protease-activated receptor (PAR) agonists are different from the previously reported contractile responses of murine colonic muscles. Ca2+ sensitization pathways mediate the contractile responses of simian colonic muscles to PAR agonists without affecting the membrane potential. These findings emphasize novel mechanisms of PAR agonist-induced contractions possibly related to colonic dysmotility in inflammatory bowel disease.

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CASSAR-MALEK, I., A. LISTRAT, and B. PICARD. "Contrôle hormonal des caractéristiques des fibres musculaires après la naissance." INRAE Productions Animales 11, no. 5 (December 6, 1998): 365–77. http://dx.doi.org/10.20870/productions-animales.1998.11.5.3965.

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Après la naissance, la croissance et les propriétés contractiles et métaboliques des fibres musculaires sont soumises à une régulation endocrinienne complexe. A l’exception des glucocorticoïdes, la plupart des hormones présente une action anabolique sur le tissu musculaire. Leur influence sur les caractéristiques des fibres est cependant très différente. Ainsi, les hormones somatotropes affectent peu la composition en fibres des muscles. La GH, comme l’IGF-1, régulerait cependant l’expression des isoformes de myosine. Les hormones thyroïdiennes augmentent la proportion des fibres rapides au détriment des lentes. Elles régulent l’expression des chaînes lourdes de myosine, en augmentant celles des isoformes rapides. L’insuline joue également un rôle important, le diabète s’accompagnant d’une diminution du pourcentage relatif des fibres rapides glycolytiques et de la quantité des myosines natives rapides. Les agonistes béta-adrénergiques des catécholamines augmentent la proportion des fibres rapides IIB au détriment des lentes. Leur influence sur l’expression des myosines reste toutefois peu connue. L’action des stéroïdes sexuels est par contre bien documentée : les androgènes diminuent la proportion des fibres rapides IIB, et l’accumulation des chaînes lourdes de myosine IIb. Les oestrogènes ont peu d’effets reconnus sur ces caractéristiques. Enfin, si les fibres IIB constituent la principale cible des glucocorticoïdes, leur effet sur les caractéristiques des fibres est encore mal connu. L’ensemble de ces données suggère que l’on peut modifier la croissance du muscle et sa composition en fibres en modifiant l’équilibre endocrinien des animaux par les techniques d’élevage.

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Chadwick, Jessica A., J. Spencer Hauck, Celso E. Gomez-Sanchez, Elise P. Gomez-Sanchez, and Jill A. Rafael-Fortney. "Gene expression effects of glucocorticoid and mineralocorticoid receptor agonists and antagonists on normal human skeletal muscle." Physiological Genomics 49, no. 6 (June 1, 2017): 277–86. http://dx.doi.org/10.1152/physiolgenomics.00128.2016.

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Mineralocorticoid and glucocorticoid receptors are closely related steroid hormone receptors that regulate gene expression through many of the same hormone response elements. However, their transcriptional activities and effects in skeletal muscles are largely unknown. We recently identified mineralocorticoid receptors (MR) in skeletal muscles after finding that combined treatment with the angiotensin-converting enzyme inhibitor lisinopril and MR antagonist spironolactone was therapeutic in Duchenne muscular dystrophy mouse models. The glucocorticoid receptor (GR) agonist prednisolone is the current standard-of-care treatment for Duchenne muscular dystrophy because it prolongs ambulation, likely due to its anti-inflammatory effects. However, data on whether glucocorticoids have a beneficial or detrimental direct effect on skeletal muscle are controversial. Here, we begin to define the gene expression profiles in normal differentiated human skeletal muscle myotubes treated with MR and GR agonists and antagonists. The MR agonist aldosterone and GR agonist prednisolone had highly overlapping gene expression profiles, supporting the notion that prednisolone acts as both a GR and MR agonist that may have detrimental effects on skeletal muscles. Co-incubations with aldosterone plus either nonspecific or selective MR antagonists, spironolactone or eplerenone, resulted in similar numbers of gene expression changes, suggesting that both drugs can block MR activation to a similar extent. Eplerenone treatment alone decreased a number of important muscle-specific genes. This information may be used to develop biomarkers to monitor clinical efficacy of MR antagonists or GR agonists in muscular dystrophy, develop a temporally coordinated treatment with both drugs, or identify novel therapeutics with more specific downstream targets.

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Cresser, Justin, Arend Bonen, Adrian Chabowski, Leslie E. Stefanyk, Roberto Gulli, Ian Ritchie, and David J. Dyck. "Oral administration of a PPAR-δ agonist to rodents worsens, not improves, maximal insulin-stimulated glucose transport in skeletal muscle of different fibers." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, no. 2 (August 2010): R470—R479. http://dx.doi.org/10.1152/ajpregu.00431.2009.

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Agonists targeting the nuclear receptor peroxisome proliferator-activated receptors (PPAR)-δ may be potential therapeutic agents for insulin-resistant related conditions, as they may be able to stimulate fatty acid (FA) oxidation and attenuate the accumulation of harmful lipid species in skeletal muscle. Several reports have demonstrated that PPAR-δ agonists improve whole body insulin sensitivity. However, whether these agonists exert their direct effects on glucose and FA metabolism in skeletal muscle, and specifically with different fiber types, is unknown. This study was undertaken to determine the effects of oral treatment with the PPAR-δ agonist, GW 501516, in conjunction with the administration of a high-saturated-fat diet on insulin-stimulated glucose transport in isolated oxidative (soleus) and glycolytic (epitrochlearis) rodent skeletal muscle in vitro. High-fat feeding significantly decreased maximal insulin-stimulated glucose transport in soleus, but not epitrochlearis muscle, and was associated with increased skeletal muscle diacylglycerol and ceramide content. Unexpectedly, treatment with the PPAR-δ agonist significantly reduced insulin-stimulated glucose transport in both soleus and epitrochlearis muscles, regardless of dietary fat content. The reduction in insulin-stimulated glucose transport induced by the agonist was associated with large increases in total muscle fatty acid translocase (FAT)/CD36protein content, but not diacylglycerol or ceramide contents. Agonist treatment did not alter the protein content of PPAR-δ, GLUT4, or insulin-signaling proteins (IRS-1, p85 PI3-K, Akt). Agonist treatment led to a small, but significant increase, in the oxidative capacity of glycolytic but not oxidative muscle. We propose that chronic treatment with the PPAR-δ agonist GW 501516 may induce or worsen insulin resistance in rodent skeletal muscle by increasing the capacity for FA transport across the sarcolemma without a sufficient compensatory increase in FA oxidation. However, an accumulation of diacylglycerol and ceramide, while associated with diet-induced insulin resistance, does not appear to be responsible for the agonist-induced reduction in insulin-stimulated glucose transport.

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Hinkle, Richard T., Elizabeth Donnelly, David B. Cody, Russell J. Sheldon, and Robert J. Isfort. "Activation of the vasoactive intestinal peptide 2 receptor modulates normal and atrophying skeletal muscle mass and force." Journal of Applied Physiology 98, no. 2 (February 2005): 655–62. http://dx.doi.org/10.1152/japplphysiol.00736.2004.

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Of the two known vasoactive intestinal peptide receptors (VPAC1R and VPAC2R), the VPAC2R is expressed in skeletal muscle. To evaluate the function of the VPAC2R in the physiological control of skeletal muscle mass, we utilized the VPAC1R selective agonist [K15,R16,L27]VIP(1-7) GRF(8-27)-NH2 and the VPAC2R selective agonist Ro-25-1553 to treat mice and rats undergoing either nerve damage-, corticosteroid-, or disuse-induced skeletal muscle atrophy. These analyses demonstrated that activation of VPAC2R, but not VPAC1R, reduced the loss of skeletal muscle mass and force during conditions of skeletal muscle atrophy resulting from corticosteroid administration, denervation, casting-induced disuse, increased skeletal muscle mass, and force of nonatrophying muscles. These studies indicate that VPAC2R agonists may have utility for the treatment of skeletal muscle-wasting diseases.

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Raiteri, Brent J., Andrew G. Cresswell, and Glen A. Lichtwark. "Ultrasound reveals negligible cocontraction during isometric plantar flexion and dorsiflexion despite the presence of antagonist electromyographic activity." Journal of Applied Physiology 118, no. 10 (May 15, 2015): 1193–99. http://dx.doi.org/10.1152/japplphysiol.00825.2014.

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Because of the approximate linear relationship between muscle force and muscle activity, muscle forces are often estimated during maximal voluntary isometric contractions (MVICs) from torque and surface electromyography (sEMG) measurements. However, sEMG recordings from a target muscle may contain cross-talk originating from nearby muscles, which could lead to erroneous force estimates. Here we used ultrasound imaging to measure in vivo muscle fascicle length ( Lf) changes and sEMG to measure muscle activity of the tibialis anterior, medial gastrocnemius, lateral gastrocnemius, and soleus muscles during ramp MVICs in plantar and dorsiflexion directions ( n = 8). After correcting longitudinal Lfchanges for ankle rotation, the antagonist Lfat peak antagonist root-mean-square (RMS) amplitude were significantly longer than the agonist Lfat this sEMG-matched level. On average, Lfshortened from resting length by 1.29 to 2.90 mm when muscles acted as agonists and lengthened from resting length by 0.43 to 1.16 mm when muscles acted as antagonists (depending on the muscle of interest). The lack of fascicle shortening when muscles acted as antagonists indicates that cocontraction was likely to be negligible, despite cocontraction as determined by sEMG of between 7 and 23% MVIC across all muscles. Different interelectrode distances (IEDs) over the plantar flexors revealed significantly higher antagonist RMS amplitudes for the 4-cm IEDs compared with the 2-cm IEDs, which further indicates that cross-talk was present. Consequently, investigators should be wary about performing agonist torque corrections for isometric plantar flexion and dorsiflexion based on the antagonist sEMG trace and predicted antagonist moment.

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Dissertations / Theses on the topic "Muscles agonistes"

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Le, Bozec Serge. "aspects et bases de la synergie des muscles agonistes chez l'Homme." Grenoble 2 : ANRT, 1986. http://catalogue.bnf.fr/ark:/12148/cb37599038x.

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Zinoubi, Sana. "Exercices et entraînement en co-contractions isométriques volontaires des muscles agonistes- antagonistes : facteurs d'influence." Thesis, Paris 10, 2015. http://www.theses.fr/2015PA100187/document.

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L’objectif général de la présente thèse était d’étudier les effets et les facteurs d’influence des exercices et des programmes d’entraînement consistant en la co-contraction maximale isométrique volontaire (CCMIV) de l’articulation du coude : effet de l’entraînement en CCMIV sur la force explosive (Etude A), influence de l’heure habituelle d’entraînement (Etude B) et de charges additionnelles pendant les CCMIV (Etude C). Les résultats ont montré que 6 semaines d’entraînement en CCMIV peuvent améliorer simultanément la force maximale volontaire des muscles sans altération de la force explosive (Etude A et B) et indépendamment de l’heure habituelle d’entraînement (Etude B). Ces gains de force s’accompagnaient d’une augmentation de l’activité électromyographique des muscles agonistes (Etude A et B). Cependant, les résultats de l’étude B suggèrent que l’entraînement le matin s’accompagne d’un meilleur gain de la force musculaire, masquant ainsi les différences de force entre le matin et le soir. Par ailleurs, l’étude C a montré qu’une charge additionnelle (50% FMV) associée à une CCMIV modifie le pattern d’activation des muscles agonistes-antagonistes : augmentation du niveau d’activation des muscles agonistes et diminution de celui des antagonistes. Par conséquent, un programme d’entraînement en CCMIV avec charge additionnelle devrait comprendre des exercices avec charge pour les fléchisseurs et les extenseurs. De plus, les résultats de l’étude C suggèrent que le concept du fléchisseur équivalent pourrait être appliqué non seulement quand les fléchisseurs agissent comme agonistes mais aussi quand ils agissent comme antagonistes
The aim of the present thesis was to study the effects and the influencing factors during the elbow joint maximal isometric voluntary co-contractions (MIVCC) exercises and training program: effect of the MIVCC training on the explosive force (Study A), influence of the time-of-day at which training was scheduled (Study B) and additional load during MIVCC (Study C). The results showed that six weeks of MIVCC training can simultaneously improve the maximum voluntary force, without altering the explosive force (Study A and B) and independently of the time-of-day at which training was scheduled (Study B). These improvements were accompanied by an increase in electromyography activity of agonist muscles (Study A and B). However, the results of study B suggest that morning training is accompanied by a higher strength improvement, by masking the strength differences between the morning and evening. Furthermore, the study C showed that additional load (50% MVF) associated with MIVCC modifies the activation pattern of the agonist-antagonist muscles: by increasing the activation level of the agonist muscles and decreasing the co-activation level of the antagonist muscles. Therefore, MIVCC training program with additional load should include exercises with load for flexor and extensor muscles. In addition, the results of the study C suggest that the concept of “flexor equivalent” may be applied not only when the flexor muscles acting as agonist but also when they acting as antagonist muscles

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Bejaoui, Khémissa. "Les réflexes d'étirement des muscles fléchisseurs et extenseurs du coude : comparaison entre muscles agonistes : essai d'identification dans le transport manuel d'une charge." Paris 11, 1986. http://www.theses.fr/1986PA112349.

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Ce travail a eu pour but de comparer l’activité myoelectrique réflexe de différents muscles d’un même groupe agoniste, en réponse à leur étirement passif et d’essayer de déterminer l’intervention possible de ces mécanismes réflexes lors d’une activité naturelle comme le transport d’une charge. Une première partie est consacrée à l’étude des muscles extenseurs du coude, l’anconeus et le triceps brachii. Une seconde partie traite de l’activité des muscles fléchisseurs du coude : biceps brachii et brachioradialis en réponse à l’étirement passif et lors du transport de charges. L’étirement des groupes musculaires est provoqué sur un fond d’activité tonique afin de se rapprocher le plus possible des conditions naturelles. L’enregistrement porte sur les activités électromyographiques de surface et sur les variables mécaniques : déplacement, vitesse et accélération du mouvement passif. En réponse à la flexion passive du coude : l’amplitude de la réponse monosynaptique (M₁) et de la réponse réflexe tardive (M₂₋₃) des deux muscles extenseurs du coude est plus importante lorsque le coude est initialement plus fléchi ou/et lorsque le niveau d’activité tonique initial du triceps brachii est plus élevé. La latence des réponses, dans ces conditions, est aussi légèrement plus brève. L’amplitude des activités EMG réflexes des deux muscles fléchisseurs du coude augmente en fonction de l’accélération de l’étirement et se stabilise pour les accélérations les plus élevées. Il n’existe pas de différence significative entre les activités EMG réflexes des deux muscles extenseurs, ni entre celles des deux muscles fléchisseurs du coude. Le rapport de l’amplitude de la composante M₁ à celle de la composante M₂₋₃ ne va pas dans le sens d’une activité réflexe monosynaptique plus importante pour les muscles fléchisseurs que pour les muscles extenseurs. Lors du transport d’une charge : il existe, à la suite du contact du talon avec le sol, lors de la marche, une augmentation rapide de l’activité EMG du brachioradialis compatible avec un réflexe d’étirement.

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Bejaoui, Khémissa. "Les Réflexes d'étirement dans les muscles fléchisseurs et extenseurs du coude comparaison entre muscles agonistes, essai d'identification dans le transport manuel d'une charge." Grenoble 2 : ANRT, 1986. http://catalogue.bnf.fr/ark:/12148/cb37595791b.

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Charissou, Camille. "Etude de la contribution du couplage intermusculaire au contrôle de l’activité des muscles synergistes agonistes et antagonistes lors de contractions isométriques volontaires." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0122/document.

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Le corps humain possède une grande redondance musculo-squelettique, se traduisant par une infinité de coordinations musculaires possibles pour produire un effort résultant. Lors d'un mouvement, le système nerveux central est confronté à la gestion de cette redondance. A travers l’analyse de cohérence entre les signaux électromyographiques, ce travail de thèse étudie le rôle fonctionnel du couplage intermusculaire et explore la contribution des mécanismes nerveux impliqués dans la régulation de la redondance musculaire en termes de contrôle de l’activité des muscles agonistes, et antagonistes impliqués dans le phénomène de co-contraction. Nos résultats ont révélé que le couplage intermusculaire entre deux muscles agonistes est modulé en présence de fatigue et en fonction de l’expertise sportive. De plus, le couplage entre muscles agonistes et antagonistes dépend des contraintes mécaniques et du rôle fonctionnel des muscles, et semble directement lié au niveau de co-contraction. La cohérence intermusculaire est modulée dans plusieurs bandes de fréquence, témoignant de l’implication de différentes commandes centrales communes d’origines spinales et supra-spinales. Nos conclusions amènent à penser que la coordination musculaire est en partie contrôlée par des commandes nerveuses communes dont la contribution est modulée suivant les propriétés fonctionnelles des muscles concernées, pour s’adapter de manière optimale aux contraintes internes ou externes de la tâche. Les travaux déjà engagés proposent de contribuer à une meilleure compréhension des mécanismes sous-jacents l’altération de la fonction motrice chez des patients cérébro-lésés
The human motor system is characterized by high musculoskeletal redundancy, implying that a given resultant effort can result from infinity of feasible muscle coordinations. During a movement, the central nervous system has to manage such redundancy. Through coherence analysis between electromyographic signals, this thesis work aims at investigating the functional role of intermuscular coupling and at better understanding the contribution of central nervous mechanisms responsible for the regulation of muscle redundancy, in terms of agonist muscle activity and also antagonist muscles activity involved in co-contraction. Our results revealed that intermuscular coupling between agonist muscles is modulated according to both the fatigue level and the training status. We also showed that the coupling between agonist and antagonist muscles depends on the mechanical configuration and functional role of muscle pairs, and seems directly related to co-contraction. The modulation of intermuscular coherence occurs in several frequency bands, suggesting the involvement of different common central drives of spinal and supra-spinal origins according to task constraints. Taken together, our results lead us to conclude that common neural drives take part in the control of muscular coordination, with different relative contribution according to the functional properties of recruited muscles, in order to optimally adapt to both internal and external task contraints. Work already undertaken proposes to provide a better understanding of the mechanisms underlying impairment of motor function in brain-injured patients

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Gayral, Stéphanie. "Prolifération et différenciation des cellules musculaires lisses aortiques : implication des messagers phospholipidiques nucléaires." Paris 7, 2007. http://www.theses.fr/2007PA077071.

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La prolifération et la différenciation des cellules musculaires lisses vasculaires (CML) sont impliquées dans le développement de l'athérosclérose et de la resténose post-angioplastie. Des études récentes montrent un métabolisme lipidique intranucléaire autonome impliqué dans ces deux processus cellulaires. Toutefois, peu de travaux ont concerné le métabolisme nucléaire du phosphatidylinositol-3,4,5-/ràphosphate (PI(3,4,5)P3) et des phosphatidylcholines (PC). Nous nous intéressons donc plus particulièrement aux voies de signalisation impliquant ces deux métabolismes dans des noyaux purifiés de CML. Nous avons pu identifier pour la première fois la présence intranucléaire des 3- et 5-phosphatases actives, PTEN et SHIP-2, dans les CML. D'autre part, nous avons montré que seule la phospholipase Dl (PLDl) est exprimée dans le noyau des CML, alors que la PLDl et la PLD2 sont présentes dans les CML. Les agonistes des récepteurs couplés aux protéines G, comme l'acide lysophosphatidique (LPA) induisent une augmentation de l'activité PLDl, alors que les agonistes des récepteurs à activité tyrosine kinase n'ont pas d'effet significatif. Nous avons précisé que l'activation de la PLDl nucléaire par le LPA implique une voie PI3K/PKCζ, et la translocation de la PKCζ, ainsi que l'activation nucléaire de RhoA. Nos résultats indiquent aussi une régulation de la PLDl intranucléaire au cours de la modulation phénotypique des CML. Ainsi, la caractérisation des enzymes associées au métabolisme endogène du PI(3,4,5)P3 et des PC dans le noyau des CML pourrait aboutir à l'identification de nouvelles cibles thérapeutiques dans le traitement de pathologies fibroprolifératives de la paroi artérielle
Vascular smooth muscle cells (VSMC) proliferation and migration are hallmarks of atherosclerosis development and postangioplasty restenosis. Recent studies highlight the existence of an autonomous nuclear lipid metabolism related to cellular proliferation and differentiation. However, the importance of nuclear phosphatidylinositol-3,4,5-Jn'sphosphate (PI(3,4,5)P3) and phosphatidylcholine (PC) metabolism is poorly understood. Therefore, we are interested in nuclear phosphatase and phospholipase identification which hydrolyse PI(3,4,5)P3 and PC respectively, in second messengers implicated in proliferative and differentiative signal pathways. For the first time, we identified active intranuclear 3- and 5-phosphatases PTEN (Phosphatase and tensin homolog deleted on chromosome ten) and SHIP-2 (SH2 containing-inositol 5-phosphatase) in membrane-free nuclei isolated from pig aorta VSMC. On the other hand, we demonstrated that only PLDl is expressed in VSMC nuclei, while PLDl and PLD2 are present in VSMCs. Moreover, specific G-protein coupled receptor agonists, like lysophosphatidic acid (LPA) induced an increase of intranuclear PLD activity, whereas tyrosine kinase receptor agonists have no significant effect. We also showed that LPA-induced nuclear PLDl activation implied PI3K/PKCζ pathway activation and PKCζ. Nuclear translocation as well as nuclear RhoA activation. Interestingly, we also demonstrated that PLDl is regulated during phenotypic modulation of VSMC. Thus, the characterization of an endogenous PI(3,4,5)P3 and PC metabolism inside VSMC nucleus, and their associated enzymes, provides new perspectives in the control of vascular fibroproliferative disorders

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Joassard, Olivier. "Mécanismes moléculaires du contrôle de la masse musculaire sous l'action du β2-agoniste formotérol." Phd thesis, Université Jean Monnet - Saint-Etienne, 2013. http://tel.archives-ouvertes.fr/tel-01001862.

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Les β2-agonistes sont couramment utilisés pour prévenir et réduire les symptômes de l'asthme et de la bronchoconstriction induite par l'exercice. Mais, pris en quantités supérieures aux doses thérapeutiques, les β2-agonistes ont un effet anabolisant qui a été clairement démontré in vivo. Un certain nombre d'acteurs sont mis en jeu dans la réponse biologique du tissu musculaire aux β2-agonistes. L'un de ces acteurs est la voie de signalisation PI3K/Akt/mTOR, voie d'initiation de la traduction, ayant un rôle majeur dans la synthèse protéique. Dans ce contexte, notre première étude avait pour objectif de déterminer la cinétique des événements moléculaires responsables de l'hypertrophie du muscle squelettique de rat après administration de formotérol pendant 1 jour (J1), 3 jours (J3) et 10 jours (J10). Nous avons montré que l'administration de formotérol induisait une hypertrophie musculaire à J3 et J10 associée à l'activation transitoire de la voie de signalisation PI3K/Akt/mTOR (J1 et J3), et à une diminution de l'expression de l'E3 ubiquitine ligase MAFbx/Atrogin-1 (J3). La voie autophagie lysosome ne semblait pas être affectée. Ainsi, l'ensemble de ces résultats suggère que l'activation de la voie PI3K/Akt/mTOR est associée à la voie ubiquitine-protéasome mais pas à la voie autophagie-lysosome. La régulation transitoire de la voie PI3K/Akt/mTOR suggère que d'autres voies de signalisation sont impliquées dans l'hypertrophie musculaire induite par le formotérol. Le 007-AM, analogue de l'AMPc, a été décrit comme pouvant stimuler la voie de signalisation PI3K/Akt/mTOR via l'activation de la protéine Epac, suggérant que le 007-AM puisse constituer une molécule de substitution à l'utilisation des β2-agonistes. Notre seconde étude avait pour but de déterminer si le 007-AM avait une action anabolisante sur le tissu musculaire, mais également de déterminer si la 007-AM était une molécule stable permettant d'envisager son usage dans un cadre pharmacologique. L'administration de 007-AM pendant 7 jours chez des souris n'engendrait pas d'hypertrophie musculaire. En revanche, in vitro sur cellules C2C12, le 007-AM activait la voie de signalisation PI3K/Akt/mTOR comme en témoignait l'augmentation de la phosphorylation des protéines rpS6 et 4E-BP1. Nos résultats montraient également que le 007-AM était instable dans le plasma alors que son produit de dégradation, le 007 était plus stable. Pris ensembles, ces résultats suggèrent qu'un traitement de 7 jours au 007-AM n'est pas suffisant pour induire une hypertrophie musculaire et que l'absence d'hypertrophie musculaire pourrait provenir de l'instabilité du 007-AM dans le plasma. Toutefois, des études supplémentaires seront nécessaires pour confirmer ces résultats

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Sweet, Andrew. "#beta#-adrenergic agonists and lean deposition in animals." Thesis, University of Nottingham, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292616.

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Salazar, Degracia Anna 1991. "Mechanisms of muscle wasting in cachexia models : therapeutic implications." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/666924.

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La caquexia afecta negativamente a los pacientes con enfermedades crónicas y sobre todo en el cáncer. Las estrategias terapéuticas son aún limitadas. Los beta2-agonistas (formoterol) y el soporte nutricional (L-carnitina) pueden atenuar los efectos deletéreos en el músculo. En la presente tesis, el tratamiento con formoterol y L-carnitina indujo efectos beneficiosos (peso corporal y muscular, estructura, apoptosis, proteólisis y vías de señalización) en el diafragma y músculos de las extremidades en un modelo experimental de caquexia cancerosa (hepatoma ascitico Yoshida AH-130, en ratas). En ratones con caquexia cancerosa (células de adenocarcinoma del pulmón LP07), el tratamiento del tumor con anticuerpos monoclonales (anti-PD1, anti-CTLA4, anti-CD137, y anti-CD19) indujo efectos beneficiosos de la misma índole como consecuencia de la disminución del tamaño y la carga tumoral. En esta tesis se ha demostrado que diversas vías de señalización y mecanismos implicados en la degradación proteica y muscular se ven atenuadas, mejorando las características fenotípicas y funcionales de los músculos diafragma y periféricos en respuesta a diversas estrategias terapéuticas. (165 palabras)
Cachexia negatively affects patients with chronic diseases and especially in cancer. Therapeutic strategies are still limited. The beta2-agonists (formoterol) and the nutritional support (L-carnitine) can attenuate the deleterious effects in the muscle. In this thesis, treatment with formoterol and L-carnitine induced beneficial effects (total body and muscle weights, structure, apoptosis, proteolysis and signaling pathways) in the diaphragm and limb muscles in an experimental model of cancer cachexia (AH-130 Yoshida hepatoma ascites cells, in rats). In mice with cancer cachexia (LP07 lung adenocarcinoma cells), treatment of the tumor with monoclonal antibodies (anti-PD1, anti-CTLA4, anti-CD137, and anti-CD19) induced beneficial effects of the same kind as a consequence of the decrease in size and tumor burden. This thesis has shown that various signaling pathways and mechanisms involved in protein and muscle degradation are attenuated, improving the phenotypic and functional characteristics of the diaphragm and peripheral muscles in response to various therapeutic strategies. (149 words)

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Gibson, Michael. "Characterisation of cannabinoid receptors and their ligands in isolated smooth muscle preparations." Thesis, University of Aberdeen, 2000. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU602011.

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In recent years it has been shown conclusively that at least two cannabinoid receptors, termed CB1 and CB2, exist in mammalian tissues. Previous studies using the mouse isolated vas deferens have yielded results which suggest that this tissue contains cannabinoid CB1 receptors which, when activated, can mediate inhibition of electrically-evoked contractions. However, there is evidence which indicates that several of the cannabinoid receptor agonists investigated in this study may exert their effects via non-CB, or even non- cannabinoid mechanisms. In the present study, this evidence was further investigated using the cannabinoid-mediated inhibition of electrically-evoked contractions in the mouse isolated vas deferens as a model of study. The results obtained from studies using the cannabinoid receptor antagonists O-1184 and the CB1-selective SR141716A highlighted the existence of a level of agonist-dependent antagonism in mouse isolated vas deferens. This was indicated by discrepancies obtained in the pKB values of these antagonists against the compounds under investigation. In this series of investigations it was observed that the endogenous cannabinoid receptor agonist, anandamide and the capsaicin-anandamide hybrid compound, arvanil were less potently antagonised by the CB1selective antagonist/inverse agonist, SR141716A than the highly CB1-selective agonist methanandamide. Such discrepancies in pKB values indicate that anandamide and arvanil may be acting on a receptor type distinct from the cannabinoid CB1 receptor. Additionally this series of studies indicated that anandamide and WIN55212-2 were more potently antagonised when non-cumulative responses to these compounds were constructed, indicating the possibility of tolerance developing to these compounds during the construction of cumulative concentration response curves. Several, more recent studies have indicated that anandamide and its metabolically more stable analogue methanandamide may exert their actions in part through vanilloid VR1 receptors. Upon further investigation using the vanilloid VR1 receptor antagonist capsazepine in addition to SR141716A, it was observed that the effects of anandamide, methanandamide, and the capsaicin-anandamide hybrid arvanil could be attenuated by both antagonists. These results indicate that these three agonists can act through both receptor types to mediate their effects in the mouse isolated vas deferens. In this study the putative water-soluble cannabinoid receptor agonist, O-1057 was shown to inhibit the of electrically-evoked contractions in the mouse isolated vas deferens when only water was used as a vehicle. This effect was inhibited by the cannabinoid receptor antagonists O-1184 and SR141716A, providing evidence that this novel water-soluble compound was acting through the CB1 receptor. In a further study the ability of the endogenous compound palmitoylethanolamide and a range of cannabinoids which can act on the CB2 in addition to the CB1 receptor, to downregulate mast cell degranulation was investigated. It was observed that PEA, CP55940 and WIN55212-2 but not the highly CB2 receptor-selective L759656 could exert this effect. It was not possible to investigate the effects of the CB2 receptor antagonist/inverse agonist SR144528 at this time.

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Books on the topic "Muscles agonistes"

1

Cook, Stephen John. Studies of agonists at b-adrenoreceptors acting on airway smooth muscle. Manchester: University of Manchester, 1993.

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Morton, Richard Hedley. Age-related effects of growth promoting [Beta]2-Adrenergic agonists on mammalian skeletal muscle. Manchester: University of Manchester, 1994.

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Johnson, Malcolm, and Roger Small. Beta-Adrenoceptor Agonists and the Airways. Royal Society of Medicine Press Ltd, 1995.

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Liu, Cheng-chung. Interaction between glucocorticoid status and B-adrenergic agonists in control of muscle growth and protein degradation. 1989.

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Dr, Johnson Malcolm, Small Roger, British Pharmacological Society Meeting, and Glaxo Group Research Limited, eds. [Beta]-adrenoceptor agonists and the airways: Held as satellite meeting to the British Pharmacological Society Meeting, School of Biological Sciences, University of Manchester, 12-15 April 1994. London: Royal Society of Medicine Press, 1995.

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Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.

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Frise, Matthew C., and Jonathan B. Salmon. Disorders of potassium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0251.

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Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.

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Esen, Figen. Disorders of magnesium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0252.

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Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.

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Otis, James A. D. Non-Opioid Pharmacotherapies for Chronic Pain (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190265366.003.0015.

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The objective of chapter 15 is to describe analgesic approaches to chronic pain, excluding opioids. As such, it emphasizes, first, the available pharmacotherapies; and then procedures. The pharmacotherapies divide into analgesics, such as non-steroidal anti-inflammatory drugs (NSAIDs); adjuvant analgesics, such as tricyclic antidepressants and anticonvulsants; oral anesthetic agents (cardiotropics); adrenergic agonists; topical agents such as capsaicin and local anesthetic solutions and ointments; and muscle relaxants such as cyclobenzaprine, tizanidine, and baclofen. Interventions include many best administered by anesthesiologists such as infusions of anesthetic agents; trigger point injections; local and regional blockade, spinal injections including corticosteroids; and electrical spinal cord stimulation. A text box is provided with additional resources.

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Shorter, Edward, and Max Fink. The Neuroleptic Malignant Syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190881191.003.0009.

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Reports of fatal febrile, hypertensive, tachycardic neurotoxic cases followed quickly on the introduction of potent new neuroleptic drugs in the 1970s. Patients became mute, rigid, posturing, and staring, showing the signs of catatonia. Labeled the neuroleptic malignant syndrome (NMS), attention was first given to neuroleptic blockade of dopamine receptors as the cause, but treatments with dopamine agonists (bromocriptine) and muscle relaxants (dantrolene) offered little benefit. When catatonia was recognized, treatments with benzodiazepines (lorazepam, diazepam) and induced seizures (electroshock, ECT) led to clinical relief and the saving of lives. The recognition of NMS as catatonia stimulated a revision of the century-long view of catatonia as a form of schizophrenia, with calls for catatonia to be considered independent of schizophrenia.

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Book chapters on the topic "Muscles agonistes"

1

Kitazawa, Toshio, and Andrew P. Somlyo. "Modulation of Ca2+ Sensitivity by Agonists in Smooth Muscle." In Advances in Experimental Medicine and Biology, 97–109. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-6003-2_10.

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Miller, T. A., and A. E. Chalmers. "Actions of GABA Agonists and Antagonists on Invertebrate Nerves and Muscles." In ACS Symposium Series, 2–13. Washington, DC: American Chemical Society, 1987. http://dx.doi.org/10.1021/bk-1987-0356.ch001.

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Declerck, Ingrid, Guy Droogmans, and Rik Casteels. "Excitatory Agonists and Ca-Permeable Channels in Arterial Smooth Muscle Cells." In Essential Hypertension 2, 45–56. Tokyo: Springer Japan, 1989. http://dx.doi.org/10.1007/978-4-431-68090-1_4.

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Raeymaekers, Luc, Bernd Nilius, Thomas Voets, Ludwig Missiaen, Kurt Van Baelen, Jo Vanoevelen, and Frank Wuytack. "Additional Fluxes of Activator Ca2+ Accompanying Ca2+ Release from the Sarcoplasmic Reticulum Triggered by InsP3 -Mobilizing Agonists." In Role Of The Sarcoplasmic Reticulum In Smooth Muscle, 71–80. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470853050.ch6.

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Owens, Gary K. "Role of Contractile Agonists in Growth Regulation of Vascular Smooth Muscle Cells." In Advances in Experimental Medicine and Biology, 71–79. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-6015-5_6.

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McDonald, Terence F., Siegried Pelzer, and Dieter J. Pelzer. "Interactions of calcium antagonists and agonists with calcium channels in muscle cells." In Developments in Cardiovascular Medicine, 291–304. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-011-3990-8_24.

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Oshita, Kazushige. "Tactile Cue by Touching the Agonist Muscle Increases the Muscle Activity During Arm Curl Exercise." In IFMBE Proceedings, 295–300. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-66169-4_36.

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Takuwa, Yoh. "Regulation of the RHO Signaling Pathway by Excitatory Agonists in Vascular Smooth Muscle." In Advances in Experimental Medicine and Biology, 67–75. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9029-7_6.

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Masuda, Hiroaki, Shuhei Ikemoto, and Koh Hosoda. "Common Dimensional Autoencoder for Identifying Agonist-Antagonist Muscle Pairs in Musculoskeletal Robots." In Intelligent Autonomous Systems 15, 325–33. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-01370-7_26.

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Miller, R. C., V. Schini, and P. Schoeffter. "Modulation by the Endothelium of Agonist-Induced Contractions of Vascular Smooth Muscle." In Relaxing and Contracting Factors, 241–65. Totowa, NJ: Humana Press, 1988. http://dx.doi.org/10.1007/978-1-4612-4588-9_12.

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Conference papers on the topic "Muscles agonistes"

1

Kindel, G., and J. Fareed. "MODULATORY EFFECT OF SERINE PROTEASES AND RELATED ENZYMES ON ISOLATED SMOOTH MUSCLE PREPARATIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644602.

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Thrombin and related proteases produce varying pharmacologic responses in animal models. To more specifically study the in vivo actions of thrombin and related proteases, we have used isolated tissue preparations of the rabbit aortic strip (RAS), isolated guinea pig ileum (GPI) and isolated rat uterus (RU). Standard tissue-agonist regimens include epinephrine, thromboxane B2 with RAS; bradykinin, acetylcholine, histamine and serotonin with GPI; and acetylcholine, bradykinin and angiotensin with RU. The smooth muscle modulant action of numerous proteinases were screened in these regimens by bracketing the median dose response of the individual agonists. Protease complexes such as serum (rabbit, human and guinea pig), activated and nonactivated prothrombin complex concentrates and pancreatin were shown to produce varying but similar contractile responses as obtained by the standard agonists. Sera produced a dose-dependent contraction of the RAS, GPI and RU preparations. Various forms of thrombin produced different degrees of contraction of RAS accompanied by a desensitization process. On a molar basis the order of contractile activity ranged α > β>γ > nitro > DIP. All thrombins were found to augment the epinephrine and thromboxane B2 induced contraction of the RAS. Bovine and human factor Xa produced marked dilatation of the RAS but did not have any effect on the GPI and RU preparations. These results suggest that proteases exert direct musculotropic actions on smooth muscles. This should be taken into consideration in the pathophysiology of vascular spasms.

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2

Vilimek, Miloslav. "The Comparison of Muscle Forces Derived From Different Muscle Models." In ASME 2005 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2005. http://dx.doi.org/10.1115/detc2005-84776.

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This study, investigated the accuracy, practicality, and sensitivity of several different methods of calculating muscle forces during functional activities in humans. The upper extremity dynamic system was chosen, where the movement flexion / extension elbow joint was studied. The redundant mechanisms were solved using optimization criteria with and without models of individual muscles according to their active and passive properties. Exploration of the control problem for the redundant elbow system was performed using muscle models with and without tendon and activation dynamics. Comparisons with known movements solved by inverse dynamics approach and optimization techniques, provided similar results across to all optimization criteria. Moreover, if muscle models with active and passive properties are included in these analyses, it is relatively easy to calculate muscle forces of both agonists and antagonists. These approaches may be used to provide input data for dynamic FEM stress analysis of bones and bone-implant systems.

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3

Koo, Bonsung, and Alexander Leonessa. "An Adaptive Block Backstepping Control Design for Functional Electrical Stimulation of Agonist-Antagonist Muscles." In ASME 2011 Dynamic Systems and Control Conference and Bath/ASME Symposium on Fluid Power and Motion Control. ASMEDC, 2011. http://dx.doi.org/10.1115/dscc2011-6143.

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In this paper, an adaptive block backstepping controller is developed for stimulation of agonist-antagonist muscles by using Functional Electrical Stimulation (FES). FES is an alternative method that stimulates a paralyzed muscle in lieu of inactive motor neurons, which was first implemented in the 1960s ([1]). However, many challenges need to be addressed before clinical trials with Spinal Cord Injury (SCI) patients can be performed, which include designing a controller, modeling muscles, developing interface equipment, just to mention a few. To contribute to the FES control field, a nonlinear controller and its evaluation through a computer simulation are presented.

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Al-Jumaily, A. M., M. Mathur, and M. J. Jo-Avila. "Enhancement of Bronchodilation Using Length Oscillations." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80080.

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In asthma treatment β-agonists such as isoproterenol are used for their ability to relax airway smooth muscle (ASM) through stimulation of cAMP production. In vitro experiments conducted on ASM tissues suggest that length oscillations applied to contracted muscle result in a reduction in the contractile ability of the tissue. Conducting experiments on tissues from two different species leads to a fact that length oscillation enhances ASM relaxation induced by β-agonists agent independent of the species.

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5

Nguyen, Thang, Holly Warner, Hanieh Mohammadi, Dan Simon, and Hanz Richter. "On the State Estimation of an Agonistic-Antagonistic Muscle System." In ASME 2017 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dscc2017-5304.

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In this paper, an agonistic-antagonistic muscle system is presented. This dual muscle system is based on the Hill muscle model. The problem of estimating the state variables and activation signals of the dual muscle system is addressed. A proposed estimation scheme which combines a super-twisting observer and an input estimator is given to provide a solution to the problem. A backstepping control method is used to track a reference trajectory. Numerical results are conducted to show that the relative error for state estimation is about 1% and that for the unknown inputs is about 3% when the measurements of the length of a muscle and its nonlinear spring force are affected by noise profiles whose normalized amplitude is 0.005.

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Wang, Lejun, Yong Huang, Mingxin Gong, Jiangbo Wu, Zhanqiang Li, and Zengke Zengke Yue. "Fatigue related electromyographic coherence analysis between agonistic elbow flexion muscles." In 2011 4th International Congress on Image and Signal Processing (CISP 2011). IEEE, 2011. http://dx.doi.org/10.1109/cisp.2011.6100785.

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Artz, Edward J., Amy A. Blank, and Marcia K. O’Malley. "Proportional sEMG Based Robotic Assistance in an Isolated Wrist Movement." In ASME 2015 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/dscc2015-9979.

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Numerous studies have demonstrated the efficacy of robots for motor therapy. Surface electromyography (sEMG) is appealing for user intent detection as the signal relates the individual’s desired muscle contractile force. A drawback to sEMG interfaces is subject- and session-dependent calibration. We sought to investigate the effect of a simple sEMG assistive controller on user performance in the MAHI Exo-II, therapeutic exoskeleton. Agonist-antagonist muscles were related after normalization based on sub-maximal isometric contraction. Six subjects performed a target tracking task with four levels of assistance in wrist flexion-extension. Performance metrics were mean absolute position error and estimated muscular activity. In low levels of assistance, subject performance was not significantly affected, while increasing the assistance resulted in higher position errors. In characterizing the performance assistance trade-off, we better understand the capabilities of this simple controller. This investigation validates the feasibility of using a proportional control scheme for a therapeutic wrist exoskeleton system and motivates further testing with impaired subjects to optimize the system for use in a clinical setting.

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Li, Maoheng, Jinbao Li, and Minglei Shu. "Detection of Muscle Fatigue by Fusion of Agonist and Synergistic Muscle sEMG Signals." In 2020 IEEE 33rd International Symposium on Computer-Based Medical Systems (CBMS). IEEE, 2020. http://dx.doi.org/10.1109/cbms49503.2020.00025.

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Yamashita, Yuto, Kazuya Maegaki, Kazuhiro Matsui, Takanori Oku, Kanna Uno, Keitaro Koba, Pipatthana Phatiwuttipat, et al. "Functional Electrical Stimulation for Equilibrium-Point Control of Human Ankle Movement: Frequency Domain System Identification of Human Ankle Dynamics." In ASME 2014 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/dscc2014-6200.

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This paper presents a novel method for creating an electrical stimulation pattern to control the equilibrium-point (EP) of human ankle movement. Focusing on the synergetic activation of agonist–antagonist (AA) muscles, the proposed method employs the ES-AA ratio (the ratio of the electrical stimulation levels for AA muscles) and the ES-AA sum (the sum of the electrical stimulation levels for AA muscles), which are based on the AA ratio (the ratio of the electromyography (EMG) voltage levels for AA muscles) and the AA sum (the sum of the EMG voltage levels for AA muscles) used in human movement analysis [1, 2]. The ES-AA ratio is related to the EP of the joint whereas the ES-AA sum is associated with mechanical stiffness of the joint. Using the AA concepts, we estimated the transfer function between the input ES-AA ratio (for the tibialis anterior (TA ) and gastrocnemius (GC)) and the force output of the endpoint in the ankle joint in an isometric environment by investigating the frequency characteristics, and finally found that the ankle-joint system was a second-order system with dead time in terms of the ES-AA ratio and foot force.

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10

Schultz, Joshua A., and Jun Ueda. "Analysis of Antagonist Stiffness for Nested Compliant Mechanisms in Agonist-Antagonist Arrangements." In ASME 2011 Dynamic Systems and Control Conference and Bath/ASME Symposium on Fluid Power and Motion Control. ASMEDC, 2011. http://dx.doi.org/10.1115/dscc2011-5953.

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Members of the animal kingdom produce motion by muscle contraction. Biological muscle can be viewed as a unidirectional actuator. To achieve bidirectional motion, each muscle has a corresponding antagonist muscle whose contraction produces motion in the opposite direction. This gives biological systems the unique ability to modulate the stiffness of a joint, which is important when interacting with the environment. Certain bio-inspired robotic systems incorporate antagonistic pairs in an attempt to produce similar desirable properties. The cellular actuator employs nested compliant mechanisms to produce human-scale motion from piezoelectric stack actuators, which on their own have a small displacement. The expression for the stiffness of the actuator composed of these mechanisms takes the form of a continued fraction, which results from the nested structure. In this way, the stiffness can be easily approximated to a desired degree of accuracy by considering only the outermost mechanisms.

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