Добірка наукової літератури з теми "Muscles striés – Physiologie"
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Ознайомтеся зі списками актуальних статей, книг, дисертацій, тез та інших наукових джерел на тему "Muscles striés – Physiologie".
Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.
Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.
Статті в журналах з теми "Muscles striés – Physiologie":
1
Vainshtein, Anna, Lawrence Kazak, and David A. Hood. "Effects of endurance training on apoptotic susceptibility in striated muscle." Journal of Applied Physiology 110, no. 6 (June 2011): 1638–45. http://dx.doi.org/10.1152/japplphysiol.00020.2011.
Анотація:
An increase in the production of reactive oxygen species occurs with muscle disuse, ischemic cardiomyopathy, and conditions that arise with senescence. The resulting oxidative stress is associated with apoptosis-related myopathies. Recent research has suggested that chronic exercise is protective against mitochondrially mediated programmed cell death. To further investigate this, we compared soleus (Sol) and cardiac muscles of voluntary wheel-trained (T; 10 wk) and untrained (C) animals. Training produced a 52% increase in muscle cytochrome c oxidase (COX) activity. Sol and left ventricle (LV) strips were isolated and incubated in vitro with H2O2 for 4 h. Strips were then fractionated into cytosolic and mitochondrial fractions. Whole muscle apoptosis-inducing factor (AIF) and Bax/Bcl-2 levels were reduced in both the Sol and LV from T animals. H2O2 treatment induced increases in JNK phosphorylation, cofilin-2 localization to the mitochondria, as well as cytosolic AIF in both Sol and LV of T and C animals, respectively. Mitochondrial Bax and cytosolic cytochrome c were augmented under oxidative stress in the LV only. The H2O2-induced increases in P-JNK, mitochondrial Bax, and cytosolic AIF were ablated in the LV of T animals. These data suggest that short-term oxidative stress can induce apoptotic signaling in striated muscles in vitro. In addition, training can attenuate oxidative stress-induced apoptotic signaling in a tissue-specific manner, with an effect that is most prominent in cardiac muscle.
2
Church, Jarrod E., Stefan M. Gehrig, Annabel Chee, Timur Naim, Jennifer Trieu, Glenn K. McConell, and Gordon S. Lynch. "Early functional muscle regeneration after myotoxic injury in mice is unaffected by nNOS absence." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 5 (November 2011): R1358—R1366. http://dx.doi.org/10.1152/ajpregu.00096.2011.
Анотація:
Nitric oxide (NO) is an important signaling molecule produced in skeletal muscle primarily via the neuronal subtype of NO synthase (NOS1, or nNOS). While many studies have reported NO production to be important in muscle regeneration, none have examined the contribution of nNOS-derived NO to functional muscle regeneration (i.e., restoration of the muscle's ability to produce force) after acute myotoxic injury. In the present study, we tested the hypothesis that genetic deletion of nNOS would impair functional muscle regeneration after myotoxic injury in nNOS−/− mice. We found that nNOS−/− mice had lower body mass, lower muscle mass, and smaller myofiber cross-sectional area and that their tibialis anterior (TA) muscles produced lower absolute tetanic forces than those of wild-type littermate controls but that normalized or specific force was identical between the strains. In addition, muscles from nNOS−/− mice were more resistant to fatigue than those of wild-type littermates ( P < 0.05). To determine whether deletion of nNOS affected muscle regeneration, TA muscles from nNOS−/− mice and wild-type littermates were injected with the myotoxin notexin to cause complete fiber degeneration, and muscle structure and function were assessed at 7 and 10 days postinjury. Myofiber cross-sectional area was lower in regenerating nNOS−/− mice than wild-type controls at 7 and 10 days postinjury; however, contrary to our original hypothesis, no difference in force-producing capacity of the TA muscle was evident between the two groups at either time point. Our findings reveal that nNOS is not essential for functional muscle regeneration after acute myotoxic damage.
3
Ayada, Kentaro, Makoto Watanabe, and Yasuo Endo. "Elevation of histidine decarboxylase activity in skeletal muscles and stomach in mice by stress and exercise." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 6 (December 1, 2000): R2042—R2047. http://dx.doi.org/10.1152/ajpregu.2000.279.6.r2042.
Анотація:
The effects of different types of stress (water bathing, cold, restraint, and prolonged walking) on histidine decarboxylase (HDC) activity in masseter, quadriceps femoris, and pectoralis superficial muscles, and in the stomach were examined in mice. All of these stresses elevated gastric HDC activity. Although water bathing, in which muscle activity was slight, was sufficiently stressful to produce gastric hemorrhage and to increase gastric HDC activity, it produced no detectable elevation of HDC activity in any of the muscles examined. The other stresses all elevated HDC activity in all three muscles. We devised two methods of restraint, one accompanied by mastication and the other not. The former elevated HDC activity in the masseter muscle, but the latter did not. These results suggest that 1) HDC activity in the stomach is an index of responses to stress, 2) the elevation of HDC activity in skeletal muscles during stress is induced partly or wholly by muscle activity and/or muscle tension, and 3) stress itself does not always induce an elevation of HDC activity in skeletal muscles.
4
Csapo, R., V. Malis, J. Hodgson, and S. Sinha. "Age-related greater Achilles tendon compliance is not associated with larger plantar flexor muscle fascicle strains in senior women." Journal of Applied Physiology 116, no. 8 (April 15, 2014): 961–69. http://dx.doi.org/10.1152/japplphysiol.01337.2013.
Анотація:
The aim of the present study was to test the hypothesis that the age-associated decrease of tendon stiffness would necessitate greater muscle fascicle strains to produce similar levels of force during isometric contraction. Greater fascicle strains could force sarcomeres to operate in less advantageous regions of their force-length and force-velocity relationships, thus impairing the capacity to generate strong and explosive contractions. To test this hypothesis, sagittal-plane dynamic velocity-encoded phase-contrast magnetic resonance images of the gastrocnemius medialis (GM) muscle and Achilles tendon (AT) were acquired in six young (YW; 26.1 ± 2.3 yr) and six senior (SW; 76.7 ± 8.3 yr) women during submaximal isometric contraction (35% maximum voluntary isometric contraction) of the plantar flexor muscles. Multiple GM fascicle lengths were continuously determined by automatically tracking regions of interest coinciding with the end points of muscle fascicles evenly distributed along the muscle's proximo-distal length. AT stiffness and Young's modulus were measured as the slopes of the tendon's force-elongation and stress-strain curves, respectively. Despite significantly lower AT stiffness at older age (YW: 120.2 ± 52.3 N/mm vs. SW: 53.9 ± 44.4 N/mm, P = 0.040), contraction-induced changes in GM fascicle lengths were similar in both age groups at equal levels of absolute muscular force (4–5% fascicle shortening in both groups), and even significantly larger in YW (YW: 11–12% vs. SW: 6–8% fascicle shortening) at equal percentage of maximum voluntary contraction. These results suggest that factors other than AT stiffness, such as age-associated changes in muscle composition or fascicle slack, might serve as compensatory adaptations, limiting the degree of fascicle strains upon contraction.
5
Siu, Parco M., Emidio E. Pistilli, and Stephen E. Alway. "Age-dependent increase in oxidative stress in gastrocnemius muscle with unloading." Journal of Applied Physiology 105, no. 6 (December 2008): 1695–705. http://dx.doi.org/10.1152/japplphysiol.90800.2008.
Анотація:
Oxidative stress increases during unloading in muscle from young adult rats. The present study examined the markers of oxidative stress and antioxidant enzyme gene and protein expressions in medial gastrocnemius muscles of aged and young adult (30 and 6 mo of age) Fischer 344 × Brown Norway rats after 14 days of hindlimb suspension. Medial gastrocnemius muscle weight was decreased by ∼30% in young adult and aged rats following suspension. When muscle weight was normalized to animal body weight, it was reduced by 12% and 22% in young adult and aged rats, respectively, after suspension. Comparisons between young adult and aged control animals demonstrated a 25% and 51% decline in muscle mass when expressed as absolute muscle weight and muscle weight normalized to the animal body weight, respectively. H2O2 content was elevated by 43% while Mn superoxide dismutase (MnSOD) protein content was reduced by 28% in suspended muscles compared with control muscles exclusively in the aged animals. Suspended muscles had greater content of malondialdehyde (MDA)/4-hydroxyalkenals (4-HAE) (29% and 58% increase in young adult and aged rats, respectively), nitrotyrosine (76% and 65% increase in young adult and aged rats, respectively), and catalase activity (69% and 43% increase in young adult and aged rats, respectively) relative to control muscles. Changes in oxidative stress markers MDA/4-HAE, H2O2, and MnSOD protein contents in response to hindlimb unloading occurred in an age-dependent manner. These findings are consistent with the hypotheses that oxidative stress has a role in mediating disuse-induced and sarcopenia-associated muscle losses. Our data suggest that aging may predispose skeletal muscle to increased levels of oxidative stress both at rest and during unloading.
6
Clarkson, Priscilla M., and Stephen P. Sayers. "Etiology of Exercise-Induced Muscle Damage." Canadian Journal of Applied Physiology 24, no. 3 (June 1, 1999): 234–48. http://dx.doi.org/10.1139/h99-020.
Анотація:
Muscle damage is caused by strenuous and unaccustomed exercise, especially exercise involving eccentric muscle contractions, where muscles lengthen as they exert force. Damage can be observed both directly at the cellular level and indirectly from changes in various indices of muscle function. Several mechanisms have been offered to explain the etiology of the damage/repair process, including mechanical factors such as tension and strain, disturbances in calcium homeostasis. the inflammatory response, and the synthesis of stress proteins (heat shock proteins). Changes in muscle function following eccentric exercise have been observed at the cellular level as an impairment in the amount and action of transport proteins for glucose and lactate/H+, and at the systems level as an increase in muscle stiffness and a prolonged loss in the muscle's ability to generate force. This paper will briefly review factors involved in the damage/repair process and alterations in muscle function following eccentric exercise. Key words: eccentric exercise, inflammation, stress proteins, muscle function
7
Stauber, W. T., G. R. Miller, J. G. Grimmett, and K. K. Knack. "Adaptation of rat soleus muscles to 4 wk of intermittent strain." Journal of Applied Physiology 77, no. 1 (July 1, 1994): 58–62. http://dx.doi.org/10.1152/jappl.1994.77.1.58.
Анотація:
The effect of repeated strains on rat soleus muscles was investigated by stretching active muscles 3 times/wk for 4 wk with two different methods of stretching. The adaptation of myofibers and noncontractile tissue was followed by histochemical techniques and computer-assisted image analysis. Muscle hypertrophy was seen in the slow-stretched muscles, which increased in mass by 13% and increased in myofiber cross-sectional area by 30%. In the fast-stretched muscle, mass increased by 10% but myofiber cross-sectional area actually decreased. This decrease in mean fiber area was the result of a population of very small fibers (population A) that coexisted with slightly smaller normal-sized fibers (population B). Fibers in population A did not have the distribution expected from atrophy compared with atrophic fibers from unloaded muscles; they were much smaller. In addition, there was a 44% increase in noncontractile tissue in the fast-stretched muscles. Thus, soleus muscles subjected to repeated strains respond differently to slow and fast stretching. Slow stretching results in typical muscle hypertrophy, whereas fast stretching produces somewhat larger muscles but with a mixture of small and normal-sized myofibers accompanied by a marked proliferation of noncontractile tissue.
8
van Lunteren, E., and P. Manubay. "Contractile properties of feline genioglossus, sternohyoid, and sternothyroid muscles." Journal of Applied Physiology 72, no. 3 (March 1, 1992): 1010–15. http://dx.doi.org/10.1152/jappl.1992.72.3.1010.
Анотація:
Despite a wealth of information about the respiratory behavior of pharyngeal dilator muscles such as the genioglossus, sternohyoid, and sternothyroid muscles, little is known about their contractile and endurance properties. Strips of these muscles (as well as of the diaphragm) were surgically removed from anesthetized cats and studied in vitro at 37 degrees C. The isometric contraction times of the muscles were 38 +/- 1, 31 +/- 1, 28 +/- 2, and 35 +/- 1 ms for genioglossus, sternothyroid, sternohyoid, and diaphragm, respectively. Contraction times were significantly longer for the genioglossus than for the sternohyoid and sternothyroid muscles and significantly longer for the diaphragm than for the sternohyoid muscle. Twitch-to-tetanic ratios were largest for the diaphragm and lowest for the sternohyoid muscle, and the force-frequency relationship of the sternohyoid was most rightward positioned and that of the diaphragm was most leftward positioned. During repetitive stimulation, the decrement in force was greatest for the diaphragm and least for the genioglossus muscle, with the force loss of the two hyoid muscles being intermediate in magnitude. The Burke fatigue index was significantly greater for the genioglossus than for the diaphragm, despite similar tension-time indexes during repetitive stimulation. These data indicate heterogeneity among pharyngeal dilator muscles in their contractile and endurance properties, that certain pharyngeal dilator muscle properties differ from diaphragmatic properties, and that pharyngeal muscles have relatively fast contractile kinetics yet reasonable endurance characteristics.
9
Kim, Minkyung, Grant W. Hennig, Terence K. Smith, and Brian A. Perrino. "Phospholamban knockout increases CaM kinase II activity and intracellular Ca2+ wave activity and alters contractile responses of murine gastric antrum." American Journal of Physiology-Cell Physiology 294, no. 2 (February 2008): C432—C441. http://dx.doi.org/10.1152/ajpcell.00418.2007.
Анотація:
Phospholamban (PLB) inhibits the sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA), and this inhibition is relieved by Ca2+ calmodulin-dependent protein kinase II (CaM kinase II) phosphorylation. We previously reported significant differences in contractility, SR Ca2+ release, and CaM kinase II activity in gastric fundus smooth muscles as a result of PLB phosphorylation by CaM kinase II. In this study, we used PLB-knockout (PLB-KO) mice to directly examine the effect of PLB absence on contractility, CaM kinase II activity, and intracellular Ca2+ waves in gastric antrum smooth muscles. The frequencies and amplitudes of spontaneous phasic contractions were elevated in antrum smooth muscle strips from PLB-KO mice. Bethanecol increased the amplitudes of phasic contractions in antrum smooth muscles from both control and PLB-KO mice. Caffeine decreased and cyclopiazonic acid (CPA) increased the basal tone of antrum smooth muscle strips from PLB-KO mice, but the effects were less pronounced compared with control strips. The CaM kinase II inhibitor KN-93 was less effective at inhibiting caffeine-induced relaxation in antrum smooth muscle strips from PLB-KO mice. CaM kinase II autonomous activity was elevated, and not further increased by caffeine, in antrum smooth muscles from PLB-KO mice. Similarly, the intracellular Ca2+ wave frequency was elevated, and not further increased by caffeine, in antrum smooth muscles from PLB-KO mice. These findings suggest that PLB is an important modulator of gastric antrum smooth muscle contractility by modulation of SR Ca2+ release and CaM kinase II activity.
10
Wang, Z., F. M. Pavalko, and S. J. Gunst. "Tyrosine phosphorylation of the dense plaque protein paxillin is regulated during smooth muscle contraction." American Journal of Physiology-Cell Physiology 271, no. 5 (November 1, 1996): C1594—C1602. http://dx.doi.org/10.1152/ajpcell.1996.271.5.c1594.
Анотація:
Regulation of the attachment of actin filaments to the cell membrane at membrane-associated dense plaque (MADP) sites could allow smooth muscle cells to modulate their cytostructure in response to changes in external stress. In this study, changes in the tyrosine phosphorylation of the MADP protein paxillin were measured by Western blot during the contraction and relaxation of tracheal smooth muscle strips. Tyrosine phosphorylation of paxillin increased by three- to fourfold with a time course similar to force development during contractile stimulation with acetylcholine (ACh), 5-hydroxytryptamine, and KCl and decreased during washout of contractile stimuli and during relaxation induced by forskolin. Immunoprecipitation of muscle extracts with multiple rounds of anti-phosphotyrosine antibody removed approximately 20% of the total paxillin in resting muscles and approximately 60% of paxillin in muscles maximally stimulated with ACh. These results provide the first evidence associating the tyrosine phosphorylation of paxillin with the active contraction of smooth muscle or with any functional response of a fully differentiated tissue in vivo. The results are consistent with a role for MADP proteins in the regulation of force development in smooth muscle.
Дисертації з теми "Muscles striés – Physiologie":
1
Cieniewski-Bernard, Caroline. "Etude de la O-N-acétylglucosaminylation dans le muscle squelettique et son implication dans la physiologie musculaire." Lille 1, 2005. https://ori-nuxeo.univ-lille1.fr/nuxeo/site/esupversions/6c6c2181-20d5-4300-a42e-9935d6c2e7b6.
Анотація:
Le travail de thèse a porté sur l'étude de la 0- N-acétylglucosaminylation (0-GlcNAc) dans le muscle squelettique et son implication dans la physiologie musculaire. Nous avons identifié par approche protéomique des protéines musculaires modifiées par la O-GlcNAc, jouant un rôle clé dans tous les moyens de régénération d'énergie du muscle squelettique ainsi que dans le processus contractile. Nous mettons également en évidence la possible implication de la O-GlcNAc dans l'atrophie fonctionnelle induite par le modèle d'hypodynamie-hypokinésie, les taux de O-GlcNAc étant corrélés au degré d'atrophie du muscle après hypodynamie-hypokinésie. Enfin, l'analyse du rôle de la O-GlcNAc sur l'activité contractile, et sur la sensibilité calcique des fibres musculaires, démontre que cette glycosylation pourrait jouer un rôle clé dans le processus contractile. Nos résultats suggèrent que la O-GlcNAc pourrait intervenir dans les interactions protéine-protéine qui régissent la contraction musculaire.
2
Bidon, Caroline Annie. "Approche thérapeutique de la sarcopénie : Effet d'un extrait de Ginkgo biloba sur l'expression génique et la physiologie du muscle strié." Paris 5, 2007. http://www.theses.fr/2007PA05D023.
Анотація:
La sarcopénie constitue une des pathologies les plus fréquentes, mais aussi les plus mal connues. Pour cette raison, nous avons analysé les modifications de l'expression des gènes musculaires au cours du vieillissement puis, après traitement par un extrait de Ginkgo biloba : l'EGb 761. Cette étude a été réalisée chez le rat Wistar han. L'expression des gènes a été comparée chez des animaux jeunes et des rats âgés témoins et traités. Dans ces trois groupes, les muscles soleus, EDL et gastocnemius ont été prélevés puis analysés. Nous avons mis en évidence l'expression différentielle de gènes spécifiques dans les trois muscles au cours du vieillissement et après traitement. Dans la seconde partie de notre travail, nous avons montré que les modifications morphologiques et moléculaires observées dans les muscles vieillissants se traduisent par une régulation corrélée de la force musculaire et de la transmission synaptique et que l'EGb 761 exerce un effet thérapeutique sur ces paramètresSarcopenia constitutes one of the most frequent pathologies, but also most badly known. For this reason, gene expression changes, during ageing and after treatment with a Ginkgo biloba extract, were investigated in rat soleus, EDL and gastrocnemius muscles. Gene expression was compared in young animals, old controls and treated rats and our data highlighted a profound modification of gene expression in aged and treated rat skeletal muscles. We then showed that these transcriptional changes were associated with age-related strength and neurotransmitter release modifications and that EGb 761 coud improve these physiological responses
3
Lemoine, Sophie. "Détection du récepteur musculaire des oestrogènes : influence du sexe, de l'entraînement et de la typologie." Rennes 2, 2001. http://www.theses.fr/2001REN20047.
Анотація:
Les adaptations physiologiques à l'exercice aigu et à l'entraînement sont différentes chez l'homme et chez la femme et sont probablement liées au climat hormonal de la femme. Ces hormones agissent par l'intermédiaire de récepteurs spécifiques. Notre objectif a été de rechercher la présence des récepteurs des oestrogènes (RE) au niveau du muscle strié squelettique humain et de préciser les facteurs de variation de leur expression : sexe, entraînement et type de muscle. Les transcrits codant pour l'isoforme α du RE (ARNm REα) ont été détectés et estimés par la technique de Nested Reverse Transcriptase-Polymerase Chain Reaction (Nested RT-PCR) au niveau du muscle deltoi͏̈de d'homme et de femme ainsi qu'au niveau du muscle pectoral de femme. Le taux d'ARNm REα était identique dans les deux sexes. Afin d'observer les effets d'un entraînement en endurance sur l'expression du REα au niveau du muscle strié squelettique, des rats mâles et des rats femelles ont été entraînés pendant 7 semaines. L'entraînement en endurance a augmenté le taux d'ARNm REα au niveau du gastrocnémien de rats femelles mais ne l'a pas modifié au niveau du gastrocnémien de rats mâles. Cette adaptation observée à l'entraînement et au niveau d'un muscle mixte, a été recherchée au sein de muscles squelettiques à typologie différente. Le taux d'ARNm REα a été estimé et comparé dans des muscles intermédiaire (gastrocnémien), lent (soléaire) et rapide (Extensor Digitorum Longus (EDL)). Chez les animaux contrôles, le taux d'ARNm REα était supérieur au niveau du soléaire comparé au gastrocnémien età l'EDL. Après entraînement, le taux d'ARNm REα était supérieur au niveau du soléaire et du gastrocnémien comparé à EDL. En effet, l'entraînement en endurance a augmenté le taux d'ARNm REα au niveau du gastrocnémien, l'a diminué au niveau de l'EDL et ne l'a pas modifié au niveau du soléaireEstrogens exert, in women, significant muscle effects during exercise. Their actions via specific receptors suppose the presence of estrogen receptors in skeletal muscle. The presence of estrogen receptor alpha mRNA (ERα mRNA) was investigated in human skeletal muscle by Nested Reverse Transcriptase-Polymerase Chain Reaction technique (Nested RT-PCR). ERα mRNA was detected in male and female deltoid muscles as well as in female pectoral muscle. There is no gender difference in ERα mRNA levels in skeletal muscle. In order to observe endurance training effect on ERα expression in skeletal muscle, male and female rats were trained during 7 weeks. ERα mRNA levels were determinated by RT-PCR. These levels increased in the female trained group but not in the male trained group. This adaptation, observed on intermediate muscle, was determined in muscles with different typology. ERα mRNA levels were estimated in intermediate muscle (gastrocnemius), slow twitch muscle (soleus) and fast twitch muscle (Extensor Digitorum Longus (EDL). In the control group, ERα mRNA level was significantly higher in soleus muscle compared to gastrocnemius and eXtensor digitorum longus muscles. After training, ERα mRNA level was significantly higher in soleus and gastrocnemius muscles compared to extensor digitorum longus muscle. Indeed, ERα mRNA level significantly increased in gastrocnemius muscle, significantly decreased in EDL and was not significantly modified in soleus
4
Bozzo, Cyrille. "Variations de phosphorylation de la chaîne légère de myosine en relation avec la plasticité du muscle squelettique." Lille 1, 2004. https://ori-nuxeo.univ-lille1.fr/nuxeo/site/esupversions/ff009903-132c-4613-ac8c-ba43288d7d05.
Анотація:
La chaîne légère de myosine (MLC2) est connue pour son rôle dans la régulation de la contraction musculaire. Au niveau du muscle squelettique, les deux isoformes lente et rapide de MLC2 sont phosphorylables. Cette modification post-traductionnelle permet la potentialisation de la contraction du muscle après contraction tétanique, essentiellement pour le muscle de type rapide. La phosphorylation de la MLC2 est ainsi supposée être un mécanisme rapide et transitoire, utilisé par le muscle rapide pour lutter contre le phénomène de fatigue engendré par la contraction. Aucune donnée ne décrit les variations de phosphorylation de la MLC2 suite â des transformations phénotypiques relevant de la plasticité du muscle squelettique, et qui permettent son adaptation à des contraintes de longue durée (~15 jours). Nous avons analysé les variations de phosphorylation de la MLC2 dans des cas de transformations phénotypiques de type lent~rapide, induites par des altérations de la commande nerveuse dans l'EDL (muscle typiquement rapide), et le solens (muscle typiquement lent). Nous nous sommes également attachés à décrire les mécanismes de régulations de cette phosphorylation (voie de régulation, enzymes de phosphorylation-MLCK/déphosphorylation-MP)Nous avons démontré que la phosphorylation de la MLC2 après des transformations phénotypiques du muscle à long terme est corrélée aux changements phénotypiques, avec une augmentation de phosphorylation lors de transformations lent -> rapide (hypodynamie-hypokinésie, dénervation du soleus, clenbuterol), et une diminution lors de transformations rapide -> lent (hypergravité du soleus, dénervation de l'EDL, électrosimulation chronique à basse fréquence de l'EDL). La corrélation entre la phosphorylation de la MLC2 et les changements phénotypiques induits par altération de la commande nerveuse ne semble pas exclusivement dépendante de la voie calcineurine-NFAT. Enfin, la régulation de la phosphorylation s'établit par une modulation de l'expression du rapport MLCK/MP. Nous avons donc proposé l'hypothèse que l'augmentation de phosphorylation observée lors de l'expression du phénotype musculaire rapide, permettrait l'établissement d'un niveau de phosphorylation basal dans le muscle rapide, lui permettant de répondre aux contraintes liées à la fatigue après effort de façon transitoire mais performante, comme révélé lors des analyses de la phosphorylation à court terme
5
Hédou, Julie. "Analyses fonctionnelle et protéomique du rôle de la O-N-acétylglucosaminylation dans la physiologie du muscle squelettique." Thesis, Lille 1, 2008. http://www.theses.fr/2008LIL10102/document.
Анотація:
La O-N-acétylglucosaminylation ou O-GlcNAc, est une glycosylation cytosolique et nucléaire correspondant à l'addition d'un motif O-GlcNAc sur des résidus sérine et thréonine des protéines. Cette glycosylation dynamique et réversible est impliquée dans de nombreux processus cellulaires comme la transcription, le cycle cellulaire, la signalisation intracellulaire ... mais également dans des pathologies comme le cancer, les maladies neurodégénératives et le diabète. Peu de travaux se sont intéressés au rôle que la O-GlcNAc pourrait jouer dans le muscle strié. Pourtant, le muscle squelettique est un modèle intéressant pour l'étude de la O-GlcNAc, puisque son métabolisme dépend fortement du glucose, que de nombreux processus musculaires, tels que la contraction, dépendent de la phosphorylation et qu'il peut adapter son métabolisme énergétique aux conditions physiologiques. Or, la O-GlcNAc est à la fois dépendante du taux de glucose mais peut également interférer avec la phosphorylation par l'intermédiaire d'une balance phosphorylation/ O-N-acétylglucosaminylation. Nous avons identifié un grand nombre de protéines modifiées par la O-GlcNAc, en particulier les chaînes lourdes et légères de myosine, l'actine et la tropomyosine. L'analyse du rôle de la O-GlcNAc sur l'activité contractile, et en particulier sur la sensibilité calcique des fibres musculaires, démontre que cette glycosylation pourrait jouer un rôle modulateur dans l'activité contractile des fibres musculaires via des interactions protéine-protéine mais également des motifs qui ne sont pas engagés dans des interactions. Nous avons identifié plusieurs sites O-GlcNAc sur deux protéines clés de la machinerie contractile du muscle squelettique, l'actine et la myosine. Un site a été localisé sur la séquence 198-207 de l'actine et quatre autres ont été identifiés dans la partie hélicoïdale de la région carboxy-terminale de la myosine et correspondent aux séquences 1094-1106; 1295-1303; 1701-1712; 1913-1922. Ces sites pourraient être impliqués dans des interactions protéine-protéine, dans polymérisation des protéines et également jouer un rôle dans la modulation des propriétés contractiles du muscle squelettique. Enfin, nous mettons en évidence la possible implication de la O-GlcNAc dans un modèle d'atrophie fonctionnelle (Bed-rest) chez l'humain. En premier lieu, nous avons démontré l'existence d'une balance phosphorylation/O-GlcNAc de la MLC2 au cours de l'atrophie musculaire. Cette balance pourrait moduler l'activité ou les propriétés de cette protéine au rôle important dans la modulation de la force de contraction. En outre, l'analyse du taux global de O-GlcNAc suggère que le taux de O-GlcNAc est lié au développement de l'atrophie musculaire. L'ensemble de ces résultats démontre que la O-GlcNAc joue un rôle qui pourrait être tout autant important dans la physiologie musculaire que la phosphorylationThe O-linked N-acetylglucosaminylation termed O-GlcNAc is a dynamic cytosolic and nuclear glycosylation on serine and threonine residus. This dynamic and reversible glycosylation is involved in many physiological as weIl as pathological processes such as diabetes, neurodegenerative diseases, cancer or cardiac ischemia. Only few studies have been performed about the role of O-GlcNAc in skeletal muscle. However, the skeletal muscle is an interesting model to study the O-GlcNAc since i) its metabolism depends on glucose, ii) many muscular processes such as contraction are dependent on phosphorylation, and iii) there is a plasticity of the muscle metabolism depending on the physiological conditions. O-GlcNAc is dependent also on the level of glucose and can interfere with phosphorylation through a phosphorylation/glycosylation balance. We clearly demonstrated that a number of key contractile proteins i.e myosin heavy and light chains and actin are O-GlcNAc modified. The role of this post-translational modification in the contractile properties was investigated by establishing T/pCa curves on skinned fibers. This study demonstrated that O-GlcNAc moieties involved in protein-protein interactions or not could modulate calcium activation properties and therefore that O-GlcNAc motifs could be involved in the modulation of contractile force. Using a mass spectrometry-based method, we determined the localization of one O-GlcNAc site in the suddomain 4 of actin (séquence 198-207) and four O-GleNAc sites in the light meromyosin region of myosin heavy chains (séquences 1094-1106; 1295-1303; 1701-1712; 1913-1922). These sites might be involved in protein-protein interactions or in the polymerization of MHC or could modulate the contractile properties of skeletal muscle. Finally, we studied the implication of O-GlcNAc in a human model of muscle atrophy (Bed-Rest). We demonstrated the existence of a phosphorylation/O-GleNAc balance for MLC2 that could modulate the activity and properties of this protein which bas a key role in the modulation of force. Moreover, our data suggested that O-GlcNAc level might be involved in the control of protein homeostasis and muscular atrophy in human as in rat. AlI these data demonstrate that O-GlcNAc is an important post-translational modification in the muscle physiology
6
Chakir, Abderrazzak. "Etude des effets de l'exposition intermittente à l'hypoxie hypobare sur la performance du rat à l'endurance." Lyon 1, 1998. http://www.theses.fr/1998LYO10164.
Анотація:
Le present travail a ete realise suite a l'observation faite au laboratoire que l'exposition de rats a l'hypoxie intermittente (altitude equivalente a 4500 m, 2 3 h / j, pendant 5 jours) provoque une reduction de gluconeogenese et de l'ureogenese (experiences in vitro d'hepatocytes isoles). Comme ces deux voies metaboliques sont impliquees lors de l'exercice musculaire prolonge, l'objectif du travail a consiste a etudier, en condition normoxiques, l'endurance a l'exercice et les modifications metaboliques associees chez des rats exposes prealablement a l'hypoxie intermittente par rapport a des rats temoins en ayant fait l'hypothese que l'endurance devait etre diminuee chez les rats exposes. Les resultats obtenus font apparaitre une augmentation du temps de nage (lest 5%, augmentation de 100%) et de course sur tapis roulant en echelon rectangulaire (30 m. Min1, pente = 0%, 70% de vo2max, augmentation de 40 a 60%) et en epreuve triangulaire (augmentation de 14%) chez les animaux prealablement exposes a l'hypoxie. Les echanges gazeux (vo 2, vco 2) lors des epreuves sur tapis roulant a puissance constante ne sont pas differentes entre les deux groupes d'animaux. Cependant, les animaux exposes realisent un palier de puissance de plus que les animaux de controles dans l'epreuve triangulaire. L'etat metabolique des animaux n'est pas modifie a l'issue de l'exposition a l'hypoxie. Cependant, une legere augmentation d'hematocrite et du taux d'hemoglobine est observee. A l'issue des exercices epuisants, les quantites de glycogene et de glucose consommees sont identiques chez les animaux exposes par rapport aux temoins, malgre les durees d'exercice largement superieures chez les animaux exposes. Le lactate musculaire, la lactatemie et l'alaninemie a la fin des epreuves epuisantes sont inferieures chez les animaux exposes. L'augmentation de l'endurance des rats exposes prealablement a l'hypoxie intermittente peut etre la consequence d'une eventuelle amelioration de la livraison d'oxygene aux tissus. Par ailleurs, contrairement a l'hypothese de depart formulee a partir de donnees obtenues in vitro, une augmentation de la gluconeogenese in vivo peut etre envisagee, ou une efficacite differente de cette voie metabolique en fonction de la duree de l'exercice musculaire en relation avec une modification des reponses hormonales, nerveuses et cardio-respiratoires survenant lors de l'exercice suite au protocole d'hypoxie.
7
Deval, Emmanuel. "Activité et expression de l'échangeur Na+/Ca2+ dans les cellules musculaires squelettiques de mammifère en culture primaire." Poitiers, 2001. http://www.theses.fr/2001POIT2259.
Анотація:
Chez les mammiferes, trois isoformes differentes de l'echangeur na +/ca 2 + ont ete clonees : ncx1, ncx2 et ncx3, ncx1 est quasi ubiquitaire, et c'est la seule isoforme exprimee dans le cur. En revanche, ncx2 et ncx3 semblent plus specifiques du cerveau et du muscle squelettique. Dans le muscle squelettique, le role de l'echange n'est toujours pas elucide, et les mecanismes relatifs aux efflux de calcium sont mal connus. Au regard de ces considerations, il nous a semble interessant d'etudier l'echangeur na +/ca 2 + dans les cellules musculaires squelettiques. Les experiences ont ete realisees a partir de cellules squelettiques humaines et de rat en culture. Premierement, ce travail a consiste en une caracterisation moleculaire et fonctionnelle de l'echangeur au sein des cellules de rat en culture primaire. Puis, l'expression, la localisation cellulaire, et l'activite de l'echangeur ont ete comparees au niveau des myotubes humains sains et dmd cocultives. Dans les cellules de rat, les resultats montrent une expression croissante de ncx1 au cours de la myogenese in vitro. De plus, des images confocales de myotubes, marques avec un anticorps specifique de ncx1, revelent une localisation sarcolemmiene de cette premiere isoforme. Enfin, des courants membranaires, dependant des na + e x t et ca 2 + e x t, ont pu etre enregistres. Ces courants sont correles avec des variations de ca 2 + i n t, et leur densite augmente au cours du developpement des cellules. Les cellules humaines saines et dmd presentent une localisation membranaire de ncx1 et ncx3. Toutefois, contrairement aux cellules saines, la stimulation de l'echange na +/ca 2 + dans les cellules dmd provoque une liberation de ca 2 + a partir du reticulum sarcoplasmique. Il semble desormais important d'etudier plus precisement l'expression de l'echangeur dans ces deux types de myotubes (sains et dmd) afin de verifier si ce mecanisme ne serait pas implique dans les perturbations de l'homeostasie calcique observees dans les myotubes dmd.
8
Siracusa, Julien. "Étude des microARNs circulants comme biomarqueurs de lésions musculaires." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS330.
Анотація:
Les lésions musculaires sont des événements fréquents. Le diagnostic repose sur la mesure de biomarqueurs sanguins. Les outils actuels présentent des limites qui justifient la recherche de nouveaux candidats biomarqueurs. Récemment, des petits ARNs non codants, les microARNs (miARNs), ont été identifiés. Détectables dans le plasma, certains sont spécifiques d’un tissu et ont été proposés comme de potentiels biomarqueurs de lésions tissulaires. Toutefois, leur intérêt dans le diagnostic des lésions musculaires chez l’individu sain n’est pas connu. Le but de ce travail était d’identifier et de caractériser la réponse des miARNs circulants à des lésions musculaires chez le rat.Nous avons premièrement étudié les profils plasmatiques des miARNs en réponse à des lésions musculaires myotoxiques chez le rat sain pour identifier des candidats biomarqueurs et leurs cinétiques de détection. Un criblage par RT-qPCR nous a conduits à identifier l’augmentation importante des niveaux plasmatiques de miARNs spécifiques du tissu musculaire, miR-1-3p, -133a-3p, -133b-3p, -206-3p, -208b-3p et -499-5p avec un pic de détection à 12 h. De plus, deux miARNs non spécifiques du muscle, miR-378a-3p et miR-434-3p, avaient des profils comparables. L’évaluation des performances diagnostiques a montré que les miARNs sélectionnés pouvaient discriminer les rats lésés des rats non lésés avec peu d’erreurs et une approche combinatoire nous permettait d’améliorer encore ces performances. Ces résultats ont été confirmés chez des rates femelles et des rats mâles âgés. Par ailleurs, nous avons évalué la robustesse des miARNs que nous avons sélectionnés. Malgré des profils d’expression différents des miARNs dans les fibres lentes ou rapides, le phénotype du muscle lésé avait une influence limitée sur la réponse des miARNs. Nous avons ensuite observé que la lésion d’une masse musculaire croissante ne s’accompagnait pas d’une réponse proportionnelle des miARNs circulants. Les miARNs sélectionnés n’augmentaient pas en réponse à des lésions musculaires traumatiques. Néanmoins, nous avons observé que miR-133a-3p et -133b-3p pourraient être des marqueurs intéressant pour détecter un remodelage musculaire précoce après des lésions neurologiques. Enfin, l’hémolyse et la contamination plaquettaire, deux paramètres préanalytiques connus pour induire des modifications des profils circulants, n’avaient pas d’effet sur les miARNs que nous avions identifiés.Pris dans leur ensemble, nos résultats montrent que les miARNs circulants spécifiques du muscle ainsi que miR-378a-3p et miR-434-3p, sont des biomarqueurs robuste et prometteur de lésions musculaires aigues chez le ratSkeletal muscle damage is an often-occuring event. Diagnosis is based on blood biomarkers assessment. Yet, the markers currently available suffer limitations and new biomarker candidates are needed. Recently, small non-coding RNA, microRNAs (miRNAs), were identified. Detectable in plasma, some miRNAs are tissue-specific and have been proposed as biomarkers of tissue damage. However, their relevance as biomarkers of skeletal muscle damage in healthy individuals is unknown. The aim of this work was to identify and characterize the circulating miRNAs response to muscle damage in rats.First, we studied circulating miRNAs response to myotoxic muscle damage in healthy rats in order to identify biomarker candidates and their detection kinetics. RT-qPCR profiling led to the identification of muscle-specific miRNAs that subtantially increased in plasma in response to muscle damage, namely miR-1-3p, -133a-3p, -133b-3p, -206-3p, -208b-3p, and -499-5p with a peak value at 12 h. Two non-muscle-specific miRNAs, miR-378a-3p and miR-434-3p, had similar profiles. The evaluation of the diagnostic accuracy has shown that selected miRNAs were able to discriminate damaged from non-damaged rats with almost no error and a combinatory approach was able to further increase this accuracy. Similar results were found in female and aged rats. Moreover, we sought to evaluate the robustness of selected miRNAs. Despite diferente expression of selected miRNAs in slow and fast fibers, the phenotype of injured muscle had a very limited influence on the plasma miRNA response. Then, we induced muscle damage in an increasing muscle mass and we observed that damage responsive miRNA response was not proportional to the extent of muscle damage. Selected miRNAs did not increased in response to traumatic muscle damage. However, we observed that miR-133a-3p et -133b-3p could be useful markers to detect an early muscle remodeling following neurologic damage. Finally, hemolysis and platelet contamination, two pre-analytical factors known to affect circulating miRNA profiles, had no effect on the miRNAs we selected.Taken together, our results show that circulating muscle-specific miRNAs as well as miR-378a-3p and miR-434-3p, are robust and promising biomarkers of acute muscle damage in rats
9
Thorel, Quentin. "Rôle de l'horloge circadienne dans le maintien de l'homéostasie du muscle squelettique : Implications physiologiques et pathologiques." Thesis, Université de Lille (2018-2021), 2021. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2021/2021LILUS052.pdf.
Анотація:
L’homéostasie du muscle squelettique est assurée par sa remarquable aptitude à réguler différents paramètres physiologiques tels que ses fonctions métaboliques ou sa masse. La régulation de la masse musculaire représente un enjeu important pour l’organisme car une dérégulation de cette dernière impacte le métabolisme énergétique global ainsi que d’autres paramètres tels que la locomotion. Ce tissu présente également une capacité importante de régénération suite à des blessures causées par des exercices intensifs ou des myopathies. La régénération du muscle squelettique nécessite une interaction spatio-temporelle précise entre les cellules satellites (SC) et les cellules immunitaires, qui fournissent le microenvironnement optimal pour la prolifération et la différenciation des SCs.Les rythmes circadiens, générés par notre horloge biologique, contrôlent diverses fonctions physiologiques telles que le métabolisme et l’immunité. Ce système permet aux organismes d'anticiper des changements environnementaux prévisibles tels que l’alternance jour/nuit. Au niveau métabolique, il coordonne la mise en place des voies nécessaires au stockage des nutriments ou au contraire à la dépense énergétique. Concernant l’immunité, le rôle majeur de l’horloge est de réguler la circulation et la fonction des différentes cellules immunitaires afin de préparer ce système durant les phases de la journée où le risque d’infection est le plus élevé. Dans ce contexte, nous nous sommes intéressés au rôle de l’horloge circadienne dans le contrôle de la masse du muscle squelettique mais également dans sa capacité régénérative. Le laboratoire a préalablement démontré un rôle majeur de Rev-erbα, un composant moléculaire de l’horloge circadienne, dans la fonction du muscle squelettique. En effet, ce récepteur nucléaire régule la capacité oxydative musculaire en contrôlant les processus de biogenèse mitochondriale et d’autophagie. Les résultats obtenus durant ma thèse mettent en évidence un rôle essentiel de Rev-erbα dans le contrôle de la masse musculaire. Précisément, une délétion globale de Rev-erbα chez la souris entraine une diminution de la masse musculaire associée à une augmentation de l’expression des gènes relatifs à l’atrophie musculaire. De façon intéressante, l’activation pharmacologique de ce récepteur permet de contrer l’atrophie musculaire induite par un traitement aux glucocorticoïdes.En parallèle, j’ai également mis en évidence le rôle de l’horloge biologique dans le processus de régénération musculaire. Nous avons montré que des perturbations environnementale et génétique de l'horloge ont un impact sur la régénération du muscle squelettique associé à une altération du recrutement des cellules immunitaires et principalement des cellules myéloïdes. En outre, l’utilisation de modèles génétiques d’altération de l’horloge dans les cellules myéloïdes a mis en évidence des défauts de régénération démontrant l’importance d’une horloge fonctionnelle au sein de cette population pour contrôler la réparation du muscle squelettique. Des analyses transcriptomiques nous ont permis de relier ce défaut de régénération à une expression perturbée de chimiokines, essentielles dans la communication entre les cellules immunitaires et les cellules satellites, pouvant être à l’origine du défaut de myogenèse observé dans nos modèles.Par ailleurs, nous nous sommes intéressés dans ce contexte de régénération musculaire à l’étude d’une population immunitaire nouvellement identifiée : les cellules lymphoïdes innées (ILCs). Ces cellules de l’immunité innée sont présentes essentiellement dans les tissus muqueux comme les poumons ou les intestins où elles assurent un rôle de sentinelle. Dans ce contexte, nous avons montré que les ILCs, et principalement les ILC2, étaient présentes dans le muscle squelettique après une blessure. De surcroît, nous avons mis en évidence que la délétion en ILC2 conduisait à un processus de régénération altéréSkeletal muscle homeostasis is ensured by its remarkable ability to control many of its physiological parameters such as its metabolic function or its mass according to the needs of the organism. Muscle mass regulation is essential for global health since its deregulation not only impacts overall energy metabolism but also other parameters such as locomotion. This tissue has an important capacity to regenerate following injuries caused by intensive exercises or myopathies. Skeletal muscle regeneration requires a well-orchestrated spatio-temporal interaction between satellite cells (SCs) and immune cells, which provides the optimal microenvironment for SC proliferation and differentiation.Circadian rhythms, generated by our biological clock, control various physiological functions such as metabolism and immunity. This ancestral system is present in all organisms allowing them to anticipate and optimize physiological functions to predictable daily changes. The clock integrates signals related to energy state and, in turn, regulates many metabolic pathways gating them to the most relevant time of the day. Concerning immunity, the major role of the clock is to coordinate leucocyte circulation and function allowing the body to anticipate phases of the day with higher risk of infections. In this context, we are interested in the role of the circadian clock in the control of skeletal muscle mass but also in its regenerative capacity. The role of Rev-erbα, a key component of the biological clock, has already been demonstrated in this tissue by our laboratory. Indeed, this nuclear receptor regulates muscle oxidative capacity by controlling mitochondrial biogenesis and autophagy. My thesis results highlight that Rev-erbα is also essential in the regulation of muscle mass. Specifically, global deletion of Rev-erbα leads to muscle mass decrease associated with increased expression of genes related to muscle atrophy. Interestingly, pharmacological activation of this receptor prevents muscle atrophy induced by glucocorticoid treatment.During my thesis, I also highlighted the role of the circadian clock in the control of muscle regeneration process. We have shown that environmental and genetic clock disruption lead to defective skeletal muscle regeneration associated with an alteration of immune cells recruitment, mainly myeloid cells. Furthermore, regenerative process defects observed in our myeloid cells-specific genetic clock disruption models bring out the importance of a functional clock in these cells to control skeletal muscle repair. Transcriptomic analyses allowed us to associate this regeneration defect to disturbed expression of chemokines essential in the communication between immune cells and satellite cells, which could elicit myogenesis alteration.In the context of muscle regeneration, we also investigated the role of a newly identified immune population: innate lymphoid cells (ILCs). This innate immune cells are located essentially in mucosal tissues such as lung or intestine where they ensure a sentinel function. We have shown that ILCs, and mainly ILC2, are present in skeletal muscle after injury. Interestingly, we have demonstrated that ILC2 depletion results in impaired regenerative process
10
Lemieux, Kathleen. "Mécanismes d'action de la contraction musculaire sur le transport du glucose dans le muscle squelettique de rat." Thesis, Université Laval, 2003. http://www.theses.ulaval.ca/2003/20639/20639.pdf.
Анотація:
Chez les mammifères, le muscle squelettique constitue un tissu d'importance majeure dans la régulation du transport et du métabolisme du glucose durant l'exercice physique ou en période postprandiale. La captation musculaire de glucose induite par l'insuline et la contraction musculaire s'effectue grâce à la translocation des transporteurs de glucose GLUT4 à la membrane plasmique et aux tubules transversaux à partir d'un réservoir interne. La première partie des travaux constituant cette thèse a été effectuée dans le but de clarifier si l'insuline et la contraction musculaire activent la translocation de GLUT4 à partir de réservoirs internes distincts. Par fractionnement et immunoadsorption membranaire, nous avons démontré que la contraction musculaire recrutait GLUT4 à partir de deux compartiments distincts : un compartiment associé au récepteur de la transferrine sélectivement mobilisé à la membrane plasmique et insensible à l'insuline, et un second compartiment non associé à cette protéine recruté au niveau des tubules transversaux. Cette étude a permis de déterminer que l'insuline et la contraction musculaire recrutaient GLUT4 à partir de réservoirs distincts et que la contraction musculaire induisait la translocation de GLUT4 à la surface cellulaire à partir d'au moins deux différentes populations de vésicules GLUT4.
Les deux dernières parties des travaux faisant l'objet de cette thèse ont permis de déterminer l'implication de certains médiateurs intracellulaires dans la stimulation du transport du glucose induite par la contraction musculaire ou par le AICAR, un agent mimétique de la contraction. Tout d'abord, nos travaux ont révélé que l'infusion de AICAR induit sélectivement la translocation de GLUT4 à la membrane plasmique à partir d'un compartiment enrichi en récepteur de la transferrine. De plus, nous avons démontré que la stimulation du transport du glucose par le AICAR était dépendante de l'activation de la p38 MAPK, une kinase proposée comme agent régulateur de l'activité intrinsèque de GLUT4. D'autre part, une dernière étude nous a permis de déterminer que le AICAR active spécifiquement le transport du glucose au niveau des muscles glycolytiques isolés et que le monoxyde d'azote n'est pas impliqué dans l'effet stimulateur du AICAR sur la captation du glucose au niveau de ce type de muscle. Toutefois, l'infusion de AICAR in vivo stimule le transport de glucose dans tous les types de fibres musculaires ainsi que la production de monoxyde d'azote. De plus, l'injection de AICAR stimule la phosphorylation et l'activation de eNOS, suggérant que l'activation du transport du glucose induite par le AICAR in vivo est dépendante de l'augmentation du flot sanguin via la production de monoxyde d'azote. Globalement, ces études nous ont permis de mieux comprendre les mécanismes intracellulaires par lesquels la contraction musculaire active le transport du glucose in vitro et in vivo dans le muscle squelettique.
Книги з теми "Muscles striés – Physiologie":
1
Perry, S. V. Molecular mechanisms in striated muscle. Cambridge: Cambridge University Press, 1996.
2
Mitchell, Laura. Simple relaxation: The Mitchell method of physiological relaxation for easing tension. London: J. Murray, 1988.
3
Kindenberg, Ulla. Vad händer med våra muskler vid stress: Om sambandet mellan fysisk och psykisk belastning. Solna: Arbetsmiljöverket, 2002.
4
Morozov, Vladimir I. Exercise and cellular mechanisms of muscle injury. Hauppauge, N.Y: Nova Science, 2009.
5
Epstein, M. Theoretical models of skeletal muscle. Chichester: Wiley, 1998.
6
Biewener, Andrew A., and Shelia N. Patek, eds. Muscles and Skeletons. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198743156.003.0002.
Анотація:
Animal locomotion depends on the organization, physiology and biomechanical properties of muscles and skeletons. Musculoskeletal systems encompass the mechanical interactions of muscles and skeletal elements that ultimately transmit force for movement and support. Muscles not only perform work by contracting and shortening to generate force, they can also operate as brakes to slow the whole body or a single appendage. Muscles can also function as struts (rod-like) to maintain the position of a joint and facilitate elastic energy storage and recovery. Skeletal muscles share a basic organization and all rely on the same protein machinery for generating force and movement. Variation in muscle function, therefore, depends on the underlying mechanical and energetic components, enzymatic properties, and activation by the nervous system. Muscles require either an internal, external or hydrostatic skeletal system to transmit force for movement and support.
7
(Editor), David B. Burr, and Chuck Milgrom (Editor), eds. Musculoskeletal Fatigue and Stress Fractures. CRC Press, 2001.
8
Inactivity: Physiological effects. Orlando: Academic Press, 1986.
Частини книг з теми "Muscles striés – Physiologie":
1
Palstra, A. P., M. Schaaf, and J. V. Planas. "Exercise Physiology of Zebrafish: Swimming Effects on Skeletal and Cardiac Muscle Growth, on the Immune System, and the Involvement of the Stress Axis." In Swimming Physiology of Fish, 323–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-31049-2_14.
2
Stubbs, Brianna J., and Peter Hespel. "Intermittent Exogenous Ketosis for Athletic Performance, Recovery, and Adaptation." In Ketogenic Diet and Metabolic Therapies, edited by Susan A. Masino, Detlev Boison, Dominic P. D’Agostino, Eric H. Kossoff, and Jong M. Rho, 518–40. Oxford University Press, 2022. http://dx.doi.org/10.1093/med/9780197501207.003.0040.
Анотація:
Sports nutrition science seeks to determine optimal dietary protocols for athletes pushing the limits of human physiology in power, endurance, and skill. Traditionally, dietary interventions aimed to stimulate performance have focused on strategic intake of carbohydrates, protein, and fat. However, recent development of oral ketone supplements has increased the popularity of intermitted exogenous ketosis (IEK) as a potential nutritional strategy to stimulate training adaptation and performance in athletes. Several physiologic mechanisms are implicated in acute modulation of exercise performance by IEK. These include use of ketone bodies as an alternative substrate for oxidative ATP production in contracting muscles and ketone-mediated inhibition of glycolytic flux. The latter could lead to glycogen sparing, which may increase endurance; on the other hand, glycolytic inhibition in conjunction with ketoacidosis could be ergolytic in short maximal exercise bouts. Furthermore, preliminary evidence suggests that acute and chronic post-exercise ketosis may stimulate recovery from training. Acute IEK could stimulate muscle protein synthesis and glycogen repletion, and chronic ketone ester intake blunted overreaching symptoms during short-term endurance training overload. This protection could be attributed to improved autonomic neural balance, appetite and stress hormone regulation, and possibly attenuation of exercise-induced inflammation and oxidative stress. Such effects could conceivably either down- or upregulate training adaptation. However, research to date describing both acute and chronic exogenous ketosis in exercise and training is limited and inconclusive. Further studies are required to elucidate the specific contexts and mechanisms whereby IEK could maximally benefit athletes.
3
Rodnick, Kenneth J., and Josep V. Planas. "The Stress and Stress Mitigation Effects of Exercise: Cardiovascular, Metabolic, and Skeletal Muscle Adjustments." In Fish Physiology, 251–94. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-802728-8.00007-2.
4
Auchus, Richard J., and Keith L. Parker. "The Adrenal Glands." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0016.
Анотація:
The basic function of the adrenal glands is to protect the organism against acute and chronic stress, a concept popularized as the fight-or-flight response for the medulla and as the alarm reaction for the cortex. The steroid hormones of the cortex and the catecholamines of the medulla probably developed as protection against immediate stress or injury and more prolonged deprivation of food and water. In acute stress, catecholamines mobilize glucose and fatty acids for energy and prepare the heart, lungs, and muscles for action, while glucocorticoids protect against overreactions from the body’s responses to stress. In the more chronic stress of food and fluid deprivation, adrenocortical steroid hormones stimulate gluconeogenesis to maintain the supply of glucose and increase sodium reabsorption to maintain body fluid volume. Based on the widespread effects of its secreted products in multiple tissues, adrenal dysfunction is associated with protean manifestations. Diseases associated with adrenocortical hypofunction are relatively rare, while those associated with adrenocortical hyperfunction are slightly more common. However, both of these conditions are life threatening if untreated, and a high index of suspicion must therefore be maintained. Subtle increases in cortisol secretion or tissue sensitivity to glucocorticoids may be involved in many of the devastating effects of chronic stress, including visceral obesity, hypertension, diabetes mellitus, dyslipidemia, infertility, and depression. Moreover, exogenous glucocorticoids are widely used to treat numerous diseases and, when used in supraphysiological doses, can induce all of the manifestations of glucocorticoid excess. Perhaps because the adrenal medulla accounts for only 10 % of total sympathetic nervous activation, we can live quite well without it, and syndromes due to hypofunction are not clinically significant. However, conditions of excess catecholamine output due to tumors called pheochromocytomas are a rare but potentially life-threatening cause of secondary hypertension.
5
Maalouf, Naim M. "Calcium Homeostasis." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0017.
Анотація:
Ionized calcium plays a pivotal role in many physiological and biochemical processes, including the contraction of muscles, the clotting of blood, and impulse conduction in the heart and nervous system. Moreover, it acts as a secondary messenger within the cell to initiate other cascades important for cell signaling and both exocrine and endocrine secretion. The major storage sites for calcium in the body are the teeth and skeleton. These hard tissues, which contain 99 % of the body’s calcium (approximately 1 kg), provide the structure necessary for mastication, locomotion, and protection of internal organs. In the blood, calcium is found in three forms — ionized (50%), protein-bound (40 %), and soluble complexes (10 %). Unlike the other two forms of calcium, the protein-bound fraction, which is primarily bound to albumin, is not filtered by the kidney. In normal individuals, the range of serum total calcium is 8.5 to 10.3 mg/dl. In a given individual, however, the diurnal variation of serum calcium is limited to 0.3 mg/dl. This chapter reviews calcium homeostasis in the extracellular fluid, the integrated response to calcium stressors, and disorders of calcium metabolism. The bone, kidneys, and intestines are the most important calcium-transporting tissues and play an important role in calcium homeostasis. These three corners of the calcium homeostasis triangle are discussed individuallyin the sections that follow. The bone is a dynamic tissue that is constantly changing. From birth until the completion of puberty, bone lengthens and changes shape by a process called modeling. In the adult skeleton, remodeling is the process used to repair damaged areas, to strengthen sites of stress or injury, and to remove unnecessary bone from sparsely used skeletal sites. The entire skeleton is demolished and refabricated by this process within 10 years. There are two main types of bone that remodel at different rates. Cortical bone, which makes up 80 % of the bone mass, is highly calcified, dense tissue found mainly in the appendicular skeleton such as the arms and legs.
6
Wallace, Daniel J., and Janice Brock Wallace. "Work and Disability." In All About Fibromyalgia. Oxford University Press, 2002. http://dx.doi.org/10.1093/oso/9780195147537.003.0035.
Анотація:
Most of us have to work for a living. There are bills to pay and families to provide for. Since fibromyalgia patients do not usually look ill and on superficial examination appear strong, complaints of difficulty performing the job can be hard to believe. This chapter will review definitions as they apply to disability, impairments reported in fibromyalgia patients, and constructive approaches that allow individuals with the syndrome to work most effectively. The World Health Organization defines disability as a limitation of function that compromises the ability to perform an activity within a range considered normal. Efforts to manage work disabilities considers issues such as age, sex, level of education, psychological profile, past attainments, motivation, retraining prospects, and social support systems. Additionally, work disability issues take into account work-related self-esteem, motivation, stress, fatigue, personal value systems, and availability of financial compensation. An impairment is an anatomic, physiologic, or psychological loss that leads to disability. Impairments include pain from work activities (e.g., heavy lifting), emotional stress (e.g., working in a complaint department), or muscle dysfunction (e.g., cerebral palsy). A handicap is a job limitation or something that cannot be done (e.g., deafness). Patients with a disability can be permanently, totally disabled and thus potentially eligible for Social Security Disability and Medicare health benefits. Other classifications include being permanently, partially disabled, whereby vocational rehabilitation, occupational therapy, and psychological or ergonomic evaluations can address impairments or handicaps to optimize employment retraining possibilities. Temporary, partial disability allows one to work with restrictions (e.g., no lifting more than ten pounds) while treatment is in progress. Temporary, total disability involves a leave of absence from employment while undergoing treatment so that one can return to work. Subjective factors of disability include symptoms such as pain or fatigue, while objective factors of disability are physical signs such as a heart murmur or a swollen joint. One can be disabled from a work category and granted disability even if employment is ongoing in a different work category. Work categories are rated as sedentary, light work, light medium work, medium work, heavy work, or very heavy work, each defined by how much exertion is used over a time interval.
7
Schenck, Carlos H., and Mark W. Mahowald. "Parasomnias." In New Oxford Textbook of Psychiatry, 943–50. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199696758.003.0120.
Анотація:
Parasomnias are defined as undesirable physical and/or experiential phenomena accompanying sleep that involve skeletal muscle activity (movements, behaviours), autonomic nervous system changes, and/or emotional-perceptual events. Parasomnias can emerge during entry into sleep, within sleep, or during arousals from any stage of sleep; therefore, all of sleep carries a vulnerability for parasomnias. Parasomnias can be objectively diagnosed by means of polysomnography (i.e. the physiologic monitoring of sleep—figures 4.14.4.1, 4.14.4.2), and can be successfully treated in the majority of cases. Understanding of the parasomnias, based on polysomnographic documentation, has expanded greatly over the past two decades, as new disorders have been identified, and as known disorders have been recognized to occur more frequently, across a broader age group, and with more serious consequences than previously understood. Parasomnias demonstrate how our instinctual behaviours, such as locomotion, feeding, sex, and aggression, can be released during sleep, itself a basic instinct. There are at least eight reasons why parasomnias should be of interest and importance to psychiatrists: 1 Parasomnias can be misdiagnosed and inappropriately treated as a psychiatric disorder. 2 Parasomnias can be a direct manifestation of a psychiatric disorder, e.g. dissociative disorder, nocturnal bulimia nervosa. 3 The emergence and/or recurrence of a parasomnia can be triggered by stress. 4 Psychotropic medications can induce the initial emergence of a parasomnia, or aggravate a preexisting parasomnia. 5 Parasomnias can cause psychological distress or can induce or reactivate a psychiatric disorder in the patient or bed partner on account of repeated loss of self-control during sleep and sleep-related injuries. 6 Familiarity with the parasomnias will allow psychiatrists to be more fully aware of the various medical and neuro-logical disorders, and their therapies, that can be associated with disturbed (sleep-related) behaviour and disturbed dreaming. 7 Parasomnias present a special opportunity for interlinking animal basic science research (including parasomnia animal models) with human (sleep) behavioural disorders. 8 Parasomnias carry forensic implications, as exemplified by the newly-recognized entity of ‘Parasomnia Pseudo-suicide.’ Also, psychiatrists are often asked to render an expert opinion in medicolegal cases pertaining to sleep-related violence.
Тези доповідей конференцій з теми "Muscles striés – Physiologie":
1
Milićević, Bogdan, Miloš Ivanović, Boban Stojanović, and Nenad Filipović. "HUXLEY SURROGATE MODEL FOR TWITCH MUSCLE CONTRACTION." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac,, 2021. http://dx.doi.org/10.46793/iccbi21.239m.
Анотація:
Biophysical muscle models, often called Huxley-type models, are based on the underlying physiology of muscles, making them suitable for modeling non-uniform and unsteady contractions. This kind of model can be computationally intensive, which makes the usage of large-scale simulations difficult. To enable more efficient usage of the Huxley muscle model, we created a data-driven surrogate model, which behaves similarly to the original Huxley muscle model, but it requires significantly less computational power. From several numerical simulations, we acquired a lot of data and trained deep neural networks so that the behavior of the neural network resembles the behavior of the Huxley model. Since muscle models are history-dependent we used time series as an input and we trained a recurrent neural network to produce stress and instantaneous stiffness. The real challenge was to get the neural network to predict these values precisely enough for the numerical simulation to work properly and produce accurate results. In our work, we showed results obtained with the original Huxley model and surrogate Huxley model for several muscle twitch contractions. Based on similarities between the surrogate model and the original model we can conclude that the surrogate has the potential to replace the original model within numerical simulations.