Статті в журналах з теми "Muscles striés – Physiologie"
Щоб переглянути інші типи публікацій з цієї теми, перейдіть за посиланням: Muscles striés – Physiologie.
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Ознайомтеся з топ-50 статей у журналах для дослідження 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.
Переглядайте статті в журналах для різних дисциплін та оформлюйте правильно вашу бібліографію.
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.
11
Lynch, G. S., J. A. Rafael, R. T. Hinkle, N. M. Cole, J. S. Chamberlain, and J. A. Faulkner. "Contractile properties of diaphragm muscle segments from old mdx and old transgenic mdx mice." American Journal of Physiology-Cell Physiology 272, no. 6 (June 1, 1997): C2063—C2068. http://dx.doi.org/10.1152/ajpcell.1997.272.6.c2063.
Анотація:
Diaphragm muscles of young (4- to 6-mo-old) mdx mice show severe fiber necrosis and have normalized forces and powers 60 and 46% of the values for control C57BL/10 mice. In contrast, microinjection of mdx mouse embryos with a truncated dystrophin minigene has produced young transgenic mdx (tg-mdx) mice with a level of dystrophin expression and structural and functional properties of diaphragm muscle strips measured in vitro not different from those of control mice. Whether dystrophin expression and functional corrections persist for the life span of these animals is not know. We tested the null hypothesis that, in old (24 mo) tg-mdx mice, dystrophin expression is adequate and diaphragm muscle strips have forces and powers not different from values for diaphragm muscle strips from young tg-mdx mice or control mice. Compared with control values, diaphragm muscle strips from old mdx mice had normalized forces and powers of 48 and 31%, respectively. Expression of dystrophin persisted in diaphragm muscles of old tg-mdx mice, and functional properties were not different from diaphragm muscles of young tg-mdx or young or old control mice. These results suggest that, with a transgenic animal approach, dystrophin expression and functional corrections persist for the life span of the animals.
12
Fredsted, Anne, Hanne Gissel, Klavs Madsen, and Torben Clausen. "Causes of excitation-induced muscle cell damage in isometric contractions: mechanical stress or calcium overload?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 6 (June 2007): R2249—R2258. http://dx.doi.org/10.1152/ajpregu.00415.2006.
Анотація:
Prolonged or unaccustomed exercise leads to muscle cell membrane damage, detectable as release of the intracellular enzyme lactic acid dehydrogenase (LDH). This is correlated to excitation-induced influx of Ca2+, but it cannot be excluded that mechanical stress contributes to the damage. We here explore this question using N-benzyl- p-toluene sulfonamide (BTS), which specifically blocks muscle contraction. Extensor digitorum longus muscles were prepared from 4-wk-old rats and mounted on holders for isometric contractions. Muscles were stimulated intermittently at 40 Hz for 15–60 min or exposed to the Ca2+ ionophore A23187. Electrical stimulation increased 45Ca influx 3–5 fold. This was followed by a progressive release of LDH, which was correlated to the influx of Ca2+. BTS (50 μM) caused a 90% inhibition of contractile force but had no effect on the excitation-induced 45Ca influx. After stimulation, ATP and creatine phosphate levels were higher in BTS-treated muscles, most likely due to the cessation of ATP-utilization for cross-bridge cycling, indicating a better energy status of these muscles. No release of LDH was observed in BTS-treated muscles. However, when exposed to anoxia, electrical stimulation caused a marked increase in LDH release that was not suppressed by BTS but associated with a decrease in the content of ATP. Dynamic passive stretching caused no increase in muscle Ca2+ content and only a minor release of LDH, whereas treatment with A23187 markedly increased LDH release both in control and BTS-treated muscles. In conclusion, after isometric contractions, muscle cell membrane damage depends on Ca2+ influx and energy status and not on mechanical stress.
13
Holroyd, S. M., C. L. Gibbs, and A. R. Luff. "Shortening heat in slow- and fast-twitch muscles of the rat." American Journal of Physiology-Cell Physiology 270, no. 1 (January 1, 1996): C293—C297. http://dx.doi.org/10.1152/ajpcell.1996.270.1.c293.
Анотація:
Shortening heat has been reported in several amphibian skeletal muscles. In this investigation, shortening heat has been investigated in both soleus and extensor digitorum longus (EDL) muscles of young rats. The procedure involved shortening the muscles through two different distances, at near maximum velocity and at the onset of a summated twitch from different initial lengths. At the end of the shortening period, the muscle contracted isometrically, and the stress and associated heat production were recorded. These heat-stress data were compared with heat-stress data of isometric twitches at different initial lengths. There was a parallel upward shift in energy output when shortening occurred, indicating the presence of a shortening heat. Shortening heat increased with the distance shortened in soleus, but this was not the case for EDL. The values for the shortening heat coefficient for both muscle types are slightly higher than those reported for amphibian skeletal muscle and suggest that shortening heat is a significant component of the energy output of mammalian skeletal muscle.
14
Chen, Ting, Timothy M. Moore, Mark T. W. Ebbert, Natalie L. McVey, Steven R. Madsen, David M. Hallowell, Alexander M. Harris, et al. "Liver kinase B1 inhibits the expression of inflammation-related genes postcontraction in skeletal muscle." Journal of Applied Physiology 120, no. 8 (April 15, 2016): 876–88. http://dx.doi.org/10.1152/japplphysiol.00727.2015.
Анотація:
Skeletal muscle-specific liver kinase B1 (LKB1) knockout mice (skmLKB1-KO) exhibit elevated mitogen-activated protein kinase (MAPK) signaling after treadmill running. MAPK activation is also associated with inflammation-related signaling in skeletal muscle. Since exercise can induce muscle damage, and inflammation is a response triggered by damaged tissue, we therefore hypothesized that LKB1 plays an important role in dampening the inflammatory response to muscle contraction, and that this may be due in part to increased susceptibility to muscle damage with contractions in LKB1-deficient muscle. Here we studied the inflammatory response and muscle damage with in situ muscle contraction or downhill running. After in situ muscle contractions, the phosphorylation of both NF-κB and STAT3 was increased more in skmLKB1-KO vs. wild-type (WT) muscles. Analysis of gene expression via microarray and RT-PCR shows that expression of many inflammation-related genes increased after contraction only in skmLKB1-KO muscles. This was associated with mild skeletal muscle fiber membrane damage in skmLKB1-KO muscles. Gene markers of oxidative stress were also elevated in skmLKB1-KO muscles after contraction. Using the downhill running model, we observed significantly more muscle damage after running in skmLKB1-KO mice, and this was associated with greater phosphorylation of both Jnk and STAT3 and increased expression of SOCS3 and Fos. In conclusion, we have shown that the lack of LKB1 in skeletal muscle leads to an increased inflammatory state in skeletal muscle that is exacerbated by muscle contraction. Increased susceptibility of the muscle to damage may underlie part of this response.
15
Yang, Jun, Brian Balog, Kangli Deng, Brett Hanzlicek, Anna Rietsch, Mei Kuang, Shinji Hatakeyama, Estelle Lach-Trifilieff, Hui Zhu, and Margot S. Damaser. "Therapeutic potential of muscle growth promoters in a stress urinary incontinence model." American Journal of Physiology-Renal Physiology 319, no. 3 (September 1, 2020): F436—F446. http://dx.doi.org/10.1152/ajprenal.00122.2020.
Анотація:
Weakness of urinary sphincter and pelvic floor muscles can cause insufficient urethral closure and lead to stress urinary incontinence. Bimagrumab is a novel myostatin inhibitor that blocks activin type II receptors, inducing skeletal muscle hypertrophy and attenuating muscle weakness. β2-Adrenergic agonists, such as 5-hydroxybenzothiazolone derivative (5-HOB) and clenbuterol, can enhance muscle growth. We hypothesized that promoting muscle growth would increase leak point pressure (LPP) by facilitating muscle recovery in a dual-injury (DI) stress urinary incontinence model. Rats underwent pudendal nerve crush (PNC) followed by vaginal distension (VD). One week after injury, each rat began subcutaneous (0.3 mL/rat) treatment daily in a blinded fashion with either bimagrumab (DI + Bim), clenbuterol (DI + Clen), 5-HOB (DI + 5-HOB), or PBS (DI + PBS). Sham-injured rats underwent sham PNC + VD and received PBS (sham + PBS). After 2 wk of treatment, rats were anesthetized for LPP and external urethral sphincter electromyography recordings. Hindlimb skeletal muscles and pelvic floor muscles were dissected and stained. At the end of 2 wk of treatment, all three treatment groups had a significant increase in body weight and individual muscle weight compared with both sham-treated and sham-injured rats. LPP in DI + Bim rats was significantly higher than LPP of DI + PBS and DI + Clen rats. There were more consistent urethral striated muscle fibers, elastin fibers in the urethra, and pelvic muscle recovery in DI + Bim rats compared with DI + PBS rats. In conclusion, bimagrumab was the most effective for increasing urethral pressure and continence by promoting injured external urethral sphincter and pelvic floor muscle recovery.
16
Lopez, Michael A., Sherina Bontiff, Mary Adeyeye, Aziz I. Shaibani, Matthew S. Alexander, Shari Wynd, and Aladin M. Boriek. "Mechanics of dystrophin deficient skeletal muscles in very young mice and effects of age." American Journal of Physiology-Cell Physiology 321, no. 2 (August 1, 2021): C230—C246. http://dx.doi.org/10.1152/ajpcell.00155.2019.
Анотація:
The MDX mouse is an animal model of Duchenne muscular dystrophy, a human disease marked by an absence of the cytoskeletal protein, dystrophin. We hypothesized that 1) dystrophin serves a complex mechanical role in skeletal muscles by contributing to passive compliance, viscoelastic properties, and contractile force production and 2) age is a modulator of passive mechanics of skeletal muscles of the MDX mouse. Using an in vitro biaxial mechanical testing apparatus, we measured passive length-tension relationships in the muscle fiber direction as well as transverse to the fibers, viscoelastic stress-relaxation curves, and isometric contractile properties. To avoid confounding secondary effects of muscle necrosis, inflammation, and fibrosis, we used very young 3-wk-old mice whose muscles reflected the prefibrotic and prenecrotic state. Compared with controls, 1) muscle extensibility and compliance were greater in both along fiber direction and transverse to fiber direction in MDX mice and 2) the relaxed elastic modulus was greater in dystrophin-deficient diaphragms. Furthermore, isometric contractile muscle stress was reduced in the presence and absence of transverse fiber passive stress. We also examined the effect of age on the diaphragm length-tension relationships and found that diaphragm muscles from 9-mo-old MDX mice were significantly less compliant and less extensible than those of muscles from very young MDX mice. Our data suggest that the age of the MDX mouse is a determinant of the passive mechanics of the diaphragm; in the prefibrotic/prenecrotic stage, muscle extensibility and compliance, as well as viscoelasticity, and muscle contractility are altered by loss of dystrophin.
17
Prado, Lucas G., Irina Makarenko, Christian Andresen, Martina Krüger, Christiane A. Opitz, and Wolfgang A. Linke. "Isoform Diversity of Giant Proteins in Relation to Passive and Active Contractile Properties of Rabbit Skeletal Muscles." Journal of General Physiology 126, no. 5 (October 17, 2005): 461–80. http://dx.doi.org/10.1085/jgp.200509364.
Анотація:
The active and passive contractile performance of skeletal muscle fibers largely depends on the myosin heavy chain (MHC) isoform and the stiffness of the titin spring, respectively. Open questions concern the relationship between titin-based stiffness and active contractile parameters, and titin's importance for total passive muscle stiffness. Here, a large set of adult rabbit muscles (n = 37) was studied for titin size diversity, passive mechanical properties, and possible correlations with the fiber/MHC composition. Titin isoform analyses showed sizes between ∼3300 and 3700 kD; 31 muscles contained a single isoform, six muscles coexpressed two isoforms, including the psoas, where individual fibers expressed similar isoform ratios of 30:70 (3.4:3.3 MD). Gel electrophoresis and Western blotting of two other giant muscle proteins, nebulin and obscurin, demonstrated muscle type–dependent size differences of ≤70 kD. Single fiber and single myofibril mechanics performed on a subset of muscles showed inverse relationships between titin size and titin-borne tension. Force measurements on muscle strips suggested that titin-based stiffness is not correlated with total passive stiffness, which is largely determined also by extramyofibrillar structures, particularly collagen. Some muscles have low titin-based stiffness but high total passive stiffness, whereas the opposite is true for other muscles. Plots of titin size versus percentage of fiber type or MHC isoform (I-IIB-IIA-IID) determined by myofibrillar ATPase staining and gel electrophoresis revealed modest correlations with the type I fiber and MHC-I proportions. No relationships were found with the proportions of the different type II fiber/MHC-II subtypes. Titin-based stiffness decreased with the slow fiber/MHC percentage, whereas neither extramyofibrillar nor total passive stiffness depended on the fiber/MHC composition. In conclusion, a low correlation exists between the active and passive mechanical properties of skeletal muscle fibers. Slow muscles usually express long titin(s), predominantly fast muscles can express either short or long titin(s), giving rise to low titin-based stiffness in slow muscles and highly variable stiffness in fast muscles. Titin contributes substantially to total passive stiffness, but this contribution varies greatly among muscles.
18
Muinuddin, Ahmad, Leila Neshatian, Herbert Y. Gaisano, and Nicholas E. Diamant. "Calcium source diversity in feline lower esophageal sphincter circular and sling muscle." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 2 (February 2004): G271—G277. http://dx.doi.org/10.1152/ajpgi.00291.2003.
Анотація:
Within muscular equivalents of cat lower esophageal sphincter (LES), the circular muscle develops greater spontaneous tone, whereas the sling muscle is more responsive to cholinergic stimulation. Smooth muscle contraction involves a combination of calcium release from stores and of calcium entry via several pathways. We hypothesized that there are differences in the sources of Ca2+used for contraction in sling and circular muscles and that these differences could contribute to functional asymmetry observed within LES. Contraction of muscle strips from circular and sling regions of LES was assessed in the presence of TTX. In Ca2+-free Krebs, tone was inhibited to a greater degree in circular than sling muscle. L-type Ca2+channel blockade with nifedipine or verapamil inhibited tone in LES circular but not sling muscle. Sarcoplasmic reticulum (SR) Ca2+-ATPase inhibitor cyclopiazonic acid (CPA) caused greater increase in tone in sling than in circular muscle. The phospholipase C inhibitor U-73122 and the SR inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] receptor blocker 2-aminoethoxydiphenyl borate (2-APB) inhibited tone in circular and sling muscles, demonstrating that continuous release of Ca2+from Ins(1,4,5)P3-sensitive stores is important in tone generation in both muscles. In Ca2+-free Krebs, ACh-induced contractions (AChC) were inhibited to a greater degree in sling than circular muscles. However, nifedipine and verapamil greatly inhibited AChC in the circular but not sling muscle. Depletion of SR Ca2+stores with CPA or inhibition of Ins(1,4,5)P3-mediated store release with either U-73122 or 2-APB inhibited AChC in both muscles. We demonstrate that LES circular and sling muscles 1) use intracellular and extracellular Ca2+sources to different degrees in the generation of spontaneous tone and AChC and 2) use different Ca2+entry pathways. These differences hold the potential for selective modulation of LES tone in health and disease.
19
Hirunsai, Muthita, and Ratchakrit Srikuea. "Heat stress ameliorates tenotomy-induced inflammation in muscle-specific response via regulation of macrophage subtypes." Journal of Applied Physiology 128, no. 3 (March 1, 2020): 612–26. http://dx.doi.org/10.1152/japplphysiol.00594.2019.
Анотація:
During disuse-induced muscle atrophy, macrophages play a significant role in inflammatory responses that occur with muscle degeneration and repair. Heat treatment has been shown to alleviate muscle atrophy; however, the effect of heat on inflammatory responses following tenotomy has not been evaluated. This study examined the effects of heat stress on proinflammatory (M1-like) and anti-inflammatory (M2-like) macrophage populations. Also, cytokine protein expression in oxidative soleus and glycolytic plantaris muscles following Achilles tendon transection (tenotomy) was analyzed. Male Wistar rats were assigned into control, control plus heat stress, tenotomy, and tenotomy plus heat stress groups. Tenotomy was performed for 8 (TEN8) and 14 (TEN14) days to induce muscle inflammation. Heat treatments, 30 min at 40.5–41.5°C, were given 24 h before and 1–6 consecutive days after tenotomy (TEN8 group) or every other day (TEN14 group). Tenotomy induced muscle necrosis, extensive infiltration of M1- (CD68+), and M2- (CD163+) like macrophages and increased tumor necrosis factor-α (TNFα) but not interleukin-10 (IL-10) protein expression. Heat stress caused a reduction in necrotic fibers, M1-like macrophage invasion, and TNFα protein expression in tenotomized soleus muscle. Additionally, heat stress enhanced M2-like macrophage accumulation during the 14 days following tenotomy in soleus muscle but did not affect IL-10 protein level. Our results indicate that heat stress can limit tenotomy-induced inflammatory responses through modulation of macrophage subtypes and TNFα protein expression, preferentially in oxidative muscle. These findings shed light on the ability of heat stress as a therapeutic strategy to manipulate macrophages for optimal inflammation during muscle atrophy. NEW & NOTEWORTHY We investigated differential effects of heat stress on modulating inflammation following 8 and 14 days of tenotomy in soleus and plantaris muscles. Heat exposure could reduce necrosis, suppress pro-inflammatory macrophage infiltration, and diminish TNFα protein expression in tenotomized muscle, which preferentially occurred in soleus muscle. Additionally, heat stress enhanced anti-inflammatory macrophages in soleus muscle in the 14-day study period. Neither tenotomy nor heat stress had an impact on IL-10 protein expression in either muscle examined.
20
Gayan-Ramirez, Ghislaine, and Marc Decramer. "Mechanisms of striated muscle dysfunction during acute exacerbations of COPD." Journal of Applied Physiology 114, no. 9 (May 1, 2013): 1291–99. http://dx.doi.org/10.1152/japplphysiol.00847.2012.
Анотація:
During acute exacerbations of chronic obstructive pulmonary disease (COPD), limb and respiratory muscle dysfunction develops rapidly and functional recovery is partial and slow. The mechanisms leading to this muscle dysfunction are not yet fully established. However, recent evidence has shown that several pathways involved in muscle catabolism, apoptosis, and oxidative stress are activated in the vastus lateralis muscle of patients during acute exacerbations of COPD, while those implicated in mitochondrial function are downregulated. These pathways may be targeted in different ways by factors related to exacerbations. These factors include enhanced systemic inflammation, oxidative stress, impaired energy balance, hypoxia, hypercapnia and acidosis, corticosteroid treatment, and physical inactivity. Data on the respiratory muscles are limited, but these muscles are undoubtedly overloaded during exacerbations. While they are also subjected to the same systemic elements as the limb muscles (except for inactivity), they also face a specific mechanical disadvantage caused by changes in lung volume during exacerbation. The latter will affect the ability to generate force by the foreshortening of the muscle (especially for the diaphragm), but also by altering rib orientation and motion (especially for the parasternal intercostals and the external intercostals). Because acute exacerbations of COPD are associated with an increase in both prevalence and severity of generalized muscle dysfunction, and both remain present even during recovery, early interventions to minimize muscle dysfunction during exacerbation are warranted. Although rehabilitation may be promising, other therapeutic strategies such as counterbalancing the adverse effects of exacerbations on skeletal muscle pathways may also be used.
21
Kelly, D. A., P. M. Tiidus, M. E. Houston, and E. G. Noble. "Effect of vitamin E deprivation and exercise training on induction of HSP70." Journal of Applied Physiology 81, no. 6 (December 1, 1996): 2379–85. http://dx.doi.org/10.1152/jappl.1996.81.6.2379.
Анотація:
Kelly, D. A., P. M. Tiidus, M. E. Houston, and E. G. Noble.Effect of vitamin E deprivation and exercise training on induction of HSP70. J. Appl. Physiol. 81(6): 2379–2385, 1996.—To investigate the effects of dietary vitamin E deprivation and chronic exercise on the relative content of selected isoforms of the heat-shock protein 70 (HSP70) family in rat hindlimb muscle, vitamin E was withheld for 16 wk from female rats that underwent treadmill run training during the final 8 wk. As indicated by increased ( P < 0.05) content of the stress-inducible isoform (HSP72), training did stress the exercising muscles. However, vitamin E deficiency did not alter HSP72 content in nontrained rats and was associated with a lesser induction ( P < 0.01) in some muscles of trained animals. The constitutive isoform, which exhibited similar levels in muscles of varying fiber types, was demonstrated to be largely refractory to exercise, with an equivocal response to vitamin E deprivation. HSP72 content was correlated to type I myosin heavy chain (MHC-I) content but only in muscles of sedentary normal-diet rats. After training, HSP72 content in a muscle essentially devoid of MHC-I (superficial vastus lateralis) reached levels comparable to those in a muscle high in MHC-I (soleus).
22
NOSEK, THOMAS M., MARCO A. P. BROTTO, DAVID A. ESSIG, RUBEN MESTRIL, RICHARD C. CONOVER, WOLFGANG H. DILLMANN, and RALPH C. KOLBECK. "Functional properties of skeletal muscle from transgenic animals with upregulated heat shock protein 70." Physiological Genomics 4, no. 1 (November 9, 2000): 25–33. http://dx.doi.org/10.1152/physiolgenomics.2000.4.1.25.
Анотація:
The influence of inducible heat stress proteins on protecting contracting skeletal muscle against fatigue-induced injury was investigated. A line of transgenic mice overexpressing the inducible form of the 72-kDa heat shock protein (HSP72) in skeletal muscles was used. We examined the relationship between muscle contractility and levels of the constitutive (HSC73) and inducible (HSP72) forms of the 72-kDa heat shock protein in intact, mouse extensor digitorum longus (EDL), soleus (SOL), and the diaphragm (DPH). In all transgenic muscles, HSP72 was expressed at higher levels compared with transgene-negative controls, where HSP72 was below the level of detection. At the same time, HSC73 levels were downregulated in all transgenic muscle types. Shipment-related stress caused an elevation in the levels of HSP72 in all muscles for 1 wk after arrival of the animals. We also found that, although no statistical differences in response to intermittent fatiguing stimulation in the contractile properties of intact transgene-positive muscles compared with their transgene-negative counterparts were observed, the response of intact transgene-positive EDL muscles to caffeine was enhanced. These findings demonstrate that elevated HSP72 does not protect EDL, SOL, or DPH muscles from the effects of intermittent fatiguing stimulation. However, HSP72 may influence the excitation-contraction coupling (ECC) process, either directly or indirectly, in EDL muscle. If the effects on ECC were indirect, then these results would suggest that manipulation of a specific gene might cause functional effects that seem independent of the manipulated gene/protein.
23
Wilson, T. A., and A. De Troyer. "Respiratory effect of the intercostal muscles in the dog." Journal of Applied Physiology 75, no. 6 (December 1, 1993): 2636–45. http://dx.doi.org/10.1152/jappl.1993.75.6.2636.
Анотація:
In a previous paper (J. Appl. Physiol. 73: 2283–2288, 1992), respiratory effect was defined as the change in airway pressure produced by active tension in a muscle with the airway closed, mechanical advantage was defined as the respiratory effect per unit mass per unit active stress, and it was shown that mechanical advantage is proportional to muscle shortening during the relaxation maneuver. Here, we report values of mechanical advantage and maximum respiratory effect of the intercostal muscles of the dog. Orientations of the intercostal muscles in the third and sixth interspaces were measured. Mechanical advantages of the muscles in these interspaces were computed by computing their shortening from these data and data in the literature on rib displacement. We found that parasternal internal intercostals and dorsal external intercostals of the upper interspace have large inspiratory mechanical advantages and that dorsal internal intercostals of the lower interspace and triangularis sterni have large expiratory mechanical advantages. Mass distributions in the two interspaces were also measured, and maximum respiratory effects of the muscles were calculated from their mass, mechanical advantage, and the value for maximum stress in skeletal muscle. Estimated maximum respiratory effects of the inspiratory and expiratory muscle groups of the entire rib cage were tested by measuring the maximum inspiratory pressures that were generated by the parasternal and external intercostals acting alone. Measured pressures, -13 cmH2O for the parasternals and -11 cmH2O for the external intercostals, agreed well with the computed values.
24
Knoepp, Louis F., Colleen M. Brophy, and Arthur Beall. "Physiologic Effects of Stress on Vascular Smooth Muscle." Journal of Vascular and Interventional Radiology 10, no. 7 (July 1999): 989. http://dx.doi.org/10.1016/s1051-0443(99)70175-2.
25
Gunst, S. J., and S. Bandyopadhyay. "Contractile force and intracellular Ca2+ during relaxation of canine tracheal smooth muscle." American Journal of Physiology-Cell Physiology 257, no. 2 (August 1, 1989): C355—C364. http://dx.doi.org/10.1152/ajpcell.1989.257.2.c355.
Анотація:
Muscle strips loaded with the Ca2+ indicator aequorin were studied in vitro to determine the effects of inhibitory stimuli on force and cytosolic free Ca2+. In muscles contracted isometrically with acetylcholine (ACh), 5-hydroxytryptamine (5-HT), carbachol, decreases in muscle force caused by isoproterenol (10(-5) M) or forskolin (10(-5) M) were accompanied by proportional decreases in aequorin luminescence. A similar relationship between decreases in muscle force and aequorin luminescence was observed when muscles were relaxed by stimulating Na+-K+-ATPase activity. These results suggest that the Ca2+ sensitivity of contractile proteins was not decreased during adenosine 3',5'-cyclic monophosphate (cAMP)-dependent relaxation. However, aequorin luminescence did not decrease when muscles contracted by K+ depolarization were relaxed with isoproterenol. Incubation of muscles in forskolin depressed increases in both force and aequorin luminescence in response to 5-HT or ACh. Incubation of muscles in isoproterenol had a similar effect on responses to 5-HT but depressed increases in force without depressing increases in luminescence in response to ACh. Results indicate that under most conditions the reduction of cytosolic Ca2+ plays an important role in the cAMP-dependent relaxation of canine tracheal smooth muscle.
26
Gea, Joaquim, Alvar Agustí, and Josep Roca. "Pathophysiology of muscle dysfunction in COPD." Journal of Applied Physiology 114, no. 9 (May 1, 2013): 1222–34. http://dx.doi.org/10.1152/japplphysiol.00981.2012.
Анотація:
Muscle dysfunction often occurs in patients with chronic obstructive pulmonary disease (COPD) and may involve both respiratory and locomotor (peripheral) muscles. The loss of strength and/or endurance in the former can lead to ventilatory insufficiency, whereas in the latter it limits exercise capacity and activities of daily life. Muscle dysfunction is the consequence of complex interactions between local and systemic factors, frequently coexisting in COPD patients. Pulmonary hyperinflation along with the increase in work of breathing that occur in COPD appear as the main contributing factors to respiratory muscle dysfunction. By contrast, deconditioning seems to play a key role in peripheral muscle dysfunction. However, additional systemic factors, including tobacco smoking, systemic inflammation, exercise, exacerbations, nutritional and gas exchange abnormalities, anabolic insufficiency, comorbidities and drugs, can also influence the function of both respiratory and peripheral muscles, by inducing modifications in their local microenvironment. Under all these circumstances, protein metabolism imbalance, oxidative stress, inflammatory events, as well as muscle injury may occur, determining the final structure and modulating the function of different muscle groups. Respiratory muscles show signs of injury as well as an increase in several elements involved in aerobic metabolism (proportion of type I fibers, capillary density, and aerobic enzyme activity) whereas limb muscles exhibit a loss of the same elements, injury, and a reduction in fiber size. In the present review we examine the current state of the art of the pathophysiology of muscle dysfunction in COPD.
27
Arbogast, Sandrine, Jacqueline Smith, Yves Matuszczak, Brian J. Hardin, Jennifer S. Moylan, Jeffrey D. Smith, Jeffrey Ware, Ann R. Kennedy, and Michael B. Reid. "Bowman-Birk inhibitor concentrate prevents atrophy, weakness, and oxidative stress in soleus muscle of hindlimb-unloaded mice." Journal of Applied Physiology 102, no. 3 (March 2007): 956–64. http://dx.doi.org/10.1152/japplphysiol.00538.2006.
Анотація:
Antigravity muscles atrophy and weaken during prolonged mechanical unloading caused by bed rest or spaceflight. Unloading also induces oxidative stress in muscle, a putative cause of weakness. We tested the hypothesis that dietary supplementation with Bowman-Birk inhibitor concentrate (BBIC), a soy protein extract, would oppose these changes. Adult mice were fed a diet supplemented with 1% BBIC during hindlimb unloading for up to 12 days. Soleus muscles of mice fed the BBIC-supplemented diet weighed less, developed less force per cross-sectional area, and developed less total force after unloading than controls. BBIC supplementation was protective, blunting decrements in soleus muscle weight and force. Cytosolic oxidant activity was assessed using 2′,7′-dichlorofluorescin diacetate. Oxidant activity increased in unloaded muscle, peaking at 3 days and remaining elevated through 12 days of unloading. Increases in oxidant activity correlated directly with loss of muscle mass and were abolished by BBIC supplementation. In vitro assays established that BBIC directly buffers reactive oxygen species and also inhibits serine protease activity. We conclude that dietary supplementation with BBIC protects skeletal muscle during prolonged unloading, promoting redox homeostasis in muscle fibers and blunting atrophy-induced weakness.
28
Brass, E. P., A. M. Scarrow, L. J. Ruff, K. A. Masterson, and E. Van Lunteren. "Carnitine delays rat skeletal muscle fatigue in vitro." Journal of Applied Physiology 75, no. 4 (October 1, 1993): 1595–600. http://dx.doi.org/10.1152/jappl.1993.75.4.1595.
Анотація:
Carnitine has been used to enhance human exercise performance. To test the hypothesis that carnitine can directly modify skeletal muscle function, fatigue of isolated rat skeletal muscle strips was studied in vitro. Carnitine (10 mM) did not modify the initial force of soleus contraction. The time over which force declined by 50% during repetitive electrical stimulation of the soleus muscle (fiber type I) was prolonged 25% in the presence of 10 mM carnitine. In contrast, carnitine had no effect on the fatigue of extensor digitorum longus muscle strips (fiber type II). The beneficial effect of carnitine on soleus muscle strips was not observed if the routine 30-min preincubation in the presence of carnitine was decreased to 5 min; it was associated with a five- to sixfold increase in muscle total carnitine content and a 50#x2013;150% increase in muscle long-chain acylcarnitine content. Carnitine did not consistently modify lactate accumulation or glycogen depletion during the fatigue protocol. Incubation with propionyl-L-carnitine resulted in a decreased initial force of contraction and a delay in reaching maximal contractile force. Thus, carnitine can directly improve the fatigue characteristics of muscles enriched in type I fibers.
29
Tang, Dachun, Dolly Mehta, and Susan J. Gunst. "Mechanosensitive tyrosine phosphorylation of paxillin and focal adhesion kinase in tracheal smooth muscle." American Journal of Physiology-Cell Physiology 276, no. 1 (January 1, 1999): C250—C258. http://dx.doi.org/10.1152/ajpcell.1999.276.1.c250.
Анотація:
We investigated the role of the integrin-associated proteins focal adhesion kinase (FAK) and paxillin as mediators of mechanosensitive signal transduction in tracheal smooth muscle. In muscle strips contracted isometrically with ACh, we observed higher levels of tyrosine phosphorylation of FAK and paxillin at the optimal muscle length ( L o) than at shorter muscle lengths of 0.5 or 0.75 L o. Paxillin phosphorylation was also length sensitive in muscles activated by K+ depolarization and adjusted rapidly to changes in muscle length imposed after contractile activation by either ACh or K+depolarization. Ca2+ depletion did not affect the length sensitivity of paxillin and FAK phosphorylation in muscles activated with ACh, indicating that the mechanotransduction process can be mediated by a Ca2+-independent pathway. Since Ca2+-depleted muscles do not generate significant active tension, this suggests that the mechanotransduction mechanism is sensitive to muscle length rather than tension. We conclude that FAK and paxillin participate in an integrin-mediated mechanotransduction process in tracheal smooth muscle. We propose that this pathway may initiate alterations in smooth muscle cell structure and contractility via the remodeling of actin filaments and/or via the mechanosensitive regulation of signaling molecules involved in contractile protein activation.
30
Locke, M., E. G. Noble, and B. G. Atkinson. "Inducible isoform of HSP70 is constitutively expressed in a muscle fiber type specific pattern." American Journal of Physiology-Cell Physiology 261, no. 5 (November 1, 1991): C774—C779. http://dx.doi.org/10.1152/ajpcell.1991.261.5.c774.
Анотація:
The most prominent group of stress or heat-shock proteins (HSPs) has an Mr of approximately 70,000 and is collectively referred to as the HSP70 family. The extent of stress inducibility and subcellular location of the various HSP70 isoforms differ, but all appear to be involved with ATP-dependent stabilization or solubilization of proteins. One isoform, termed the inducible isoform of HSP70 (HSP72i), is normally absent in unstressed cells. In a previous study, we detected a protein corresponding in Mr and pI to HSP72i in unstressed rat muscle. Therefore, it was of interest to determine if this expression in unstressed muscle cells is general or confined to specific muscle fiber types. To answer this question we have employed various rat hindlimb muscles that differ in fiber type proportion from predominantly type I (soleus) to predominantly type IIB (white gastrocnemius). Proteins from muscle homogenates were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, blotted to a nylon membrane, probed with a monoclonal antibody for HSP72i, and visualized using an alkaline phosphatase-conjugated secondary antibody. Immunoblot analyses demonstrate the constitutive expression of HSP72i in rat muscles comprised primarily of type I muscle fibers (soleus), but not in muscles comprised primarily of type IIB fibers (white gastrocnemius). In muscles of mixed fiber type, HSP72i content is roughly proportional to the percentage of type I fibers. These results substantiate that unstressed rat muscles express the inducible HSP72 isoform and demonstrate that its constitutive expression is proportional to the type I muscle fiber composition.
31
Gefen, A., N. Gefen, E. Linder-Ganz, and S. S. Margulies. "In Vivo Muscle Stiffening Under Bone Compression Promotes Deep Pressure Sores." Journal of Biomechanical Engineering 127, no. 3 (January 31, 2005): 512–24. http://dx.doi.org/10.1115/1.1894386.
Анотація:
Pressure sores (PS) in deep muscles are potentially fatal and are considered one of the most costly complications in spinal cord injury patients. We hypothesize that continuous compression of the longissimus and gluteus muscles by the sacral and ischial bones during wheelchair sitting increases muscle stiffness around the bone-muscle interface over time, thereby causing muscles to bear intensified stresses in relentlessly widening regions, in a positive-feedback injury spiral. In this study, we measured long-term shear moduli of muscle tissue in vivo in rats after applying compression (35 KPa or 70 KPa for 1∕4–2 h, N=32), and evaluated tissue viability in matched groups (using phosphotungstic acid hematoxylin histology, N=10). We found significant (1.8-fold to 3.3-fold, p<0.05) stiffening of muscle tissue in vivo in muscles subjected to 35 KPa for 30 min or over, and in muscles subjected to 70 KPa for 15 min or over. By incorporating this effect into a finite element (FE) model of the buttocks of a wheelchair user we identified a mechanical stress wave which spreads from the bone-muscle interface outward through longissimus muscle tissue. After 4 h of FE simulated motionlessness, 50%–60% of the cross section of the longissimus was exposed to compressive stresses of 35 KPa or over (shown to induce cell death in rat muscle within 15 min). During these 4 h, the mean compressive stress across the transverse cross section of the longissimus increased by 30%–40%. The identification of the stiffening-stress-cell-death injury spiral developing during the initial 30 min of motionless sitting provides new mechanistic insight into deep PS formation and calls for reevaluation of the 1 h repositioning cycle recommended by the U.S. Department of Health.
32
Locke, Marius, and Stephanie A. Salerno. "Ovariectomy alters lengthening contraction induced heat shock protein expression." Applied Physiology, Nutrition, and Metabolism 45, no. 5 (May 2020): 530–38. http://dx.doi.org/10.1139/apnm-2019-0212.
Анотація:
Estrogen appears to play a role in minimizing skeletal muscle damage as well as regulating the expression of the protective heat shock proteins (HSPs). To clarify the relationship between estrogen, muscle HSP content, and muscle damage, tibialis anterior (TA) muscles from ovary-intact (OVI; n = 12) and ovariectomized (OVX; 3 weeks, n = 12) female Sprague–Dawley rats were subjected to either 20 or 40 lengthening contractions (LCs). Twenty-four hours after stimulation, TA muscles were removed, processed, and assessed for HSP25 and HSP72 content as well as muscle (damage) morphology. No differences in muscle contractile properties were observed in TA muscles between OVI and OVX animals for peak torque during the LCs. In unstressed TA muscles, the basal expression of HSP72 expression was decreased in OVX animals (P < 0.05) while HSP25 content remained unchanged. Following 20 LCs, HSP25 content was elevated (P < 0.05) in TA muscles from OVX animals but unchanged in muscles from OVI animals. Following 40 LCs, HSP25 content was elevated (P < 0.01) in TA muscles from both OVI and OVX animals while HSP72 content was elevated only in TA muscles from OVI animals (P < 0.05). Taken together, these data suggest the loss of ovarian hormones, such as estrogen, may impair the skeletal muscle cellular stress response thereby rendering muscles more susceptible to certain types of contraction induced damage. Novelty Ovariectomy alters muscle HSP72 content. Muscle contractile measures are maintained following ovariectomy.
33
Wakabayashi, Yuka, Yuki Tamura, Karina Kouzaki, Naoki Kikuchi, Kenji Hiranuma, Kunitaka Menuki, Takafumi Tajima, et al. "Acetaldehyde dehydrogenase 2 deficiency increases mitochondrial reactive oxygen species emission and induces mitochondrial protease Omi/HtrA2 in skeletal muscle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 318, no. 4 (April 1, 2020): R677—R690. http://dx.doi.org/10.1152/ajpregu.00089.2019.
Анотація:
Acetaldehyde dehydrogenase 2 (ALDH2) is an enzyme involved in redox homeostasis as well as the detoxification process in alcohol metabolism. Nearly 8% of the world’s population have an inactivating mutation in the ALDH2 gene. However, the expression patterns and specific functions of ALDH2 in skeletal muscles are still unclear. Herein, we report that ALDH2 is expressed in skeletal muscle and is localized to the mitochondrial fraction. Oxidative muscles had a higher amount of ALDH2 protein than glycolytic muscles. We next comprehensively investigated whether ALDH2 knockout in mice induces mitochondrial adaptations in gastrocnemius muscle (for example, content, enzymatic activity, respiratory function, supercomplex formation, and functional networking). We found that ALDH2 deficiency resulted in partial mitochondrial dysfunction in gastrocnemius muscle because it increased mitochondrial reactive oxygen species (ROS) emission (2′,7′-dichlorofluorescein and MitoSOX oxidation rate during respiration) and the frequency of regional mitochondrial depolarization. Moreover, we determined whether ALDH2 deficiency and the related mitochondrial dysfunction trigger mitochondrial stress and quality control responses in gastrocnemius muscle (for example, mitophagy markers, dynamics, and the unfolded protein response). We found that ALDH2 deficiency upregulated the mitochondrial serine protease Omi/HtrA2 (a marker of the activation of a branch of the mitochondrial unfolded protein response). In summary, ALDH2 deficiency leads to greater mitochondrial ROS production, but homeostasis can be maintained via an appropriate stress response.
34
Full, R. J., D. R. Stokes, A. N. Ahn, and R. K. Josephson. "Energy absorption during running by leg muscles in a cockroach." Journal of Experimental Biology 201, no. 7 (April 1, 1998): 997–1012. http://dx.doi.org/10.1242/jeb.201.7.997.
Анотація:
Biologists have traditionally focused on a muscle's ability to generate power. By determining muscle length, strain and activation pattern in the cockroach Blaberus discoidalis, we discovered leg extensor muscles that operate as active dampers that only absorb energy during running. Data from running animals were compared with measurements of force and power production of isolated muscles studied over a range of stimulus conditions and muscle length changes.We studied the trochanter-femoral extensor muscles 137 and 179, homologous leg muscles of the mesothoracic and metathoracic legs, respectively. Because each of these muscles is innervated by a single excitatory motor axon, the activation pattern of the muscle could be defined precisely. Work loop studies using sinusoidal strains at 8 Hz showed these trochanter-femoral extensor muscles to be quite capable actuators, able to generate a maximum of 19-25 W kg-1 (at 25 degreesC). The optimal conditions for power output were four stimuli per cycle (interstimulus interval 11 ms), a strain of approximately 4 %, and a stimulation phase such that the onset of the stimulus burst came approximately half-way through the lengthening phase of the cycle. High-speed video analysis indicated that the actual muscle strain during running was 12 % in the mesothoracic muscles and 16 % in the metathoracic ones. Myographic recordings during running showed on average 3-4 muscle action potentials per cycle, with the timing of the action potentials such that the burst usually began shortly after the onset of shortening. Imposing upon the muscle in vitro the strain, stimulus number and stimulus phase characteristic of running generated work loops in which energy was absorbed (-25 W kg-1) rather than produced. Simulations exploring a wide parameter space revealed that the dominant parameter that determines function during running is the magnitude of strain. Strains required for the maximum power output by the trochanter-femoral extensor muscles simply do not occur during constant, average-speed running. Joint angle ranges of the coxa-trochanter-femur joint during running were 3-4 times greater than the changes necessary to produce maximum power output. None of the simulated patterns of stimulation or phase resulted in power production when strain magnitude was greater than 5 %. The trochanter-femoral extensor muscles 137/179 of a cockroach running at its preferred speed of 20 cm s-1 do not operate under conditions which maximize either power output or efficiency. In vitro measurements, however, demonstrate that these muscles absorb energy, probably to provide control of leg flexion and to aid in its reversal.
35
Atomi, Yoriko, Kyoko Toro, Tsuyoshi Masuda та Hideo Hatta. "Fiber-type-specific αB-crystallin distribution and its shifts with T3 and PTU treatments in rat hindlimb muscles". Journal of Applied Physiology 88, № 4 (1 квітня 2000): 1355–64. http://dx.doi.org/10.1152/jappl.2000.88.4.1355.
Анотація:
Changes in αB-crystallin content in adult rat soleus and extensor digitorum longus (EDL) were examined after 8 wk of 3,5,3′-triiodothyronine (T3) and propylthiouracil (PTU) treatments. Cellular distributions of αB-crystallin expression related to fiber type, and distribution shifts with these treatments were also examined in detail from the gray level of reactivity to specific anti-αB-crystallin antibody. αB-crystallin content in both soleus and EDL muscles was significantly decreased after T3, and that in EDL was significantly increased over twofold after PTU treatment. In both control soleus and EDL muscles, the gray level of type I fibers was higher than that of type II fibers. αB-crystallin expression among type II subtypes was muscle specific; the order was type I > IIa > IIx > IIb in control EDL muscle and type IIx ≥ IIa in soleus muscle. The relation was basically unchanged in both muscles after T3 treatment and was, in particular, well maintained in EDL muscle. Under hypothyroidism conditions with PTU, the mean αB-crystallin levels of type IIa and IIx fibers were significantly lower than levels under control conditions. Thus the relation between fiber type and the expression manner of stress protein αB-crystallin is muscle specific and also is well regulated under thyroid hormone, especially in fast EDL muscle.
36
Banas, Krystyna, Charlene Clow, Bernard J. Jasmin, and Jean-Marc Renaud. "The KATP channel Kir6.2 subunit content is higher in glycolytic than oxidative skeletal muscle fibers." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 4 (October 2011): R916—R925. http://dx.doi.org/10.1152/ajpregu.00663.2010.
Анотація:
It has long been suggested that in skeletal muscle, the ATP-sensitive K+ channel (KATP) channel is important in protecting energy levels and that abolishing its activity causes fiber damage and severely impairs function. The responses to a lack of KATP channel activity vary between muscles and fibers, with the severity of the impairment being the highest in the most glycolytic muscle fibers. Furthermore, glycolytic muscle fibers are also expected to face metabolic stress more often than oxidative ones. The objective of this study was to determine whether the t-tubular KATP channel content differs between muscles and fiber types. KATP channel content was estimated using a semiquantitative immunofluorescence approach by staining cross sections from soleus, extensor digitorum longus (EDL), and flexor digitorum brevis (FDB) muscles with anti-Kir6.2 antibody. Fiber types were determined using serial cross sections stained with specific antimyosin I, IIA, IIB, and IIX antibodies. Changes in Kir6.2 content were compared with changes in CaV1.1 content, as this Ca2+ channel is responsible for triggering Ca2+ release from sarcoplasmic reticulum. The Kir6.2 content was the lowest in the oxidative soleus and the highest in the glycolytic EDL and FDB. At the individual fiber level, the Kir6.2 content within a muscle was in the order of type IIB > IIX > IIA ≥ I. Interestingly, the Kir6.2 content for a given fiber type was significantly different between soleus, EDL, and FDB, and highest in FDB. Correlations of relative fluorescence intensities from the Kir6.2 and CaV1.1 antibodies were significant for all three muscles. However, the variability in content between the three muscles or individual fibers was much greater for Kir6.2 than for CaV1.1. It is suggested that the t-tubular KATP channel content increases as the glycolytic capacity increases and as the oxidative capacity decreases and that the expression of KATP channels may be linked to how often muscles/fibers face metabolic stress.
37
Reid, W. Darlene, Tyler James Clarke, and Alison M. Wallace. "Respiratory Muscle Injury: Evidence to Date and Potential Mechanisms." Canadian Journal of Applied Physiology 26, no. 4 (August 1, 2001): 356–87. http://dx.doi.org/10.1139/h01-023.
Анотація:
Respiratory muscle dysfunction associated with ventilatory loading may be partially attributed to respiratory muscle injury. Exertion-induced muscle injury can be defined as structural alterations of the muscle, however, a better understanding of the biochemical, morphologic, and functional correlates of injured respiratory muscles will facilitate discrimination of how injury, fatigue, and weakness contribute to respiratory muscle dysfunction. In addition to the increased loads associated with lung disease, many factors such as poor arterial blood gases, immobilization, sepsis, decreased nutrition, and corticosteroids may increase susceptibility to exertion-induced respiratory muscle injury. Respiratory muscle injury in humans is not well-described, however, more extensive evidence has been shown in animal models of increased ventilatory loading. Potential mechanisms of respiratory muscle injury are mechanical stress, metabolic stress, and inflammation. In order to optimize therapeutic interventions, a better understanding of these mechanisms and the patients that are most susceptible to respiratory muscle injury needs to be determined. Key words: resistive loading, respiratory muscles, exertion, muscle adaptation, muscle injury
38
Linder-Ganz, E., and A. Gefen. "Mechanical compression-induced pressure sores in rat hindlimb: muscle stiffness, histology, and computational models." Journal of Applied Physiology 96, no. 6 (June 2004): 2034–49. http://dx.doi.org/10.1152/japplphysiol.00888.2003.
Анотація:
Pressure sores affecting muscles are severe injuries associated with ischemia, impaired metabolic activity, excessive tissue deformation, and insufficient lymph drainage caused by prolonged and intensive mechanical loads. We hypothesize that mechanical properties of muscle tissue change as a result of exposure to prolonged and intensive loads. Such changes may affect the distribution of stresses in soft tissues under bony prominences and potentially expose additional uninjured regions of muscle tissue to intensified stresses. In this study, we characterized changes in tangent elastic moduli and strain energy densities of rat gracilis muscles exposed to pressure in vivo (11.5, 35, or 70 kPa for 2, 4, or 6 h) and incorporated the abnormal properties that were measured in finite element models of the head, shoulders, pelvis, and heels of a recumbent patient. Using in vitro uniaxial tension testing, we found that tangent elastic moduli of muscles exposed to 35 and 70 kPa were 1.6-fold those of controls ( P < 0.05, for strains ≤5%) and strain energy densities were 1.4-fold those of controls ( P < 0.05, for strains ≥5%). Histological (phosphotungstic acid hematoxylin) evaluation showed that this stiffening accompanied extensive necrotic damage. Incorporating these effects into the finite element models, we were able to show that the increased muscle stiffness in widening regions results in elevated tissue stresses that exacerbate the potential for tissue necrosis. Interfacial pressures could not predict deep muscle (e.g., longissimus or gluteus) stresses and injuring conditions. We conclude that information on internal muscle stresses is required to establish new criteria for pressure sore prevention.
39
Weisbrodt, N. W., and R. A. Murphy. "Myosin phosphorylation and contraction of feline esophageal smooth muscle." American Journal of Physiology-Cell Physiology 249, no. 1 (July 1, 1985): C9—C14. http://dx.doi.org/10.1152/ajpcell.1985.249.1.c9.
Анотація:
We tested the hypothesis that phosphorylation of the 20,000-Da light chain of myosin (LC 20) is related to mechanical activation of esophageal smooth muscle. Circular muscle layer strips of cat esophagus were taken from the lower esophageal sphincter (LES) and the distal esophageal body (EB). The LES strips developed tone spontaneously, and the EB strips were tonically contracted with carbachol. Both tissues relaxed in response to electrical-field stimulation. Phosphorylation of the LC 20 was determined in tissues quick-frozen during relaxation and during stress redevelopment after cessation of field stimulation. Stress and phosphorylation levels were low after 30 s of field stimulation, and a rapid contraction followed field stimulation. Phosphorylation in the LES increased from 0.043 +/- 0.029 to 0.328 +/- 0.043 mol Pi/mol LC 20 within 10 s after stimulation of the inhibitory nerves was terminated, while stress was still rising rapidly. Phosphorylation in the LES then declined to a steady-state value of 0.162 +/- 0.034 mol Pi/mol LC 20 after 10 min. Isotonic shortening velocities at a constant afterload following a quick release showed changes with time that were proportional to the level of phosphorylation. This was also true for values of maximal shortening velocity estimated for zero external load and for the rate of stress redevelopment after a step shortening. Comparable measurements were made in the carbachol-contracted EB. These results indicate that visceral smooth muscles, which normally function tonically (LES) or phasically (EB), exhibit an initial rapid mechanical activation associated with myosin phosphorylation.(ABSTRACT TRUNCATED AT 250 WORDS)
40
Yoshihara, Toshinori, Toshiharu Natsume, Takamasa Tsuzuki, Shuo-Wen Chang, Ryo Kakigi, Shuichi Machida, Takao Sugiura, and Hisashi Naito. "Long-term physical inactivity exacerbates hindlimb unloading-induced muscle atrophy in young rat soleus muscle." Journal of Applied Physiology 130, no. 4 (April 1, 2021): 1214–25. http://dx.doi.org/10.1152/japplphysiol.00494.2020.
Анотація:
NEW & NOTEWORTHY: Long-term physical inactivity exacerbates hindlimb unloading-induced disuse muscle atrophy in young rat soleus muscles, possibly mediated by oxidative stress-induced protein ubiquitination via HDAC4- and NF-κB p65-induced MuRF1 mRNA upregulation.
41
Blazevich, Anthony J. "Adaptations in the passive mechanical properties of skeletal muscle to altered patterns of use." Journal of Applied Physiology 126, no. 5 (May 1, 2019): 1483–91. http://dx.doi.org/10.1152/japplphysiol.00700.2018.
Анотація:
The aim of this mini-review is to describe the present state of knowledge regarding the effects of chronic changes in the patterns of muscle use (defined as changes lasting >1 wk), including muscle stretching, strengthening, and others, on the passive mechanical properties of healthy human skeletal muscles. Various forms of muscle stretch training and some forms of strength training (especially eccentric training) are known to strongly impact the maximum elongation capacity of muscles in vivo (i.e., maximum joint range of motion), largely by increasing our ability to tolerate higher stretch loads. However, only small effects are observed in the passive stiffness of the muscle-tendon unit (MTU) or the muscle itself, although a reduction in muscle stiffness has been observed in the plantar flexors after both stretching and eccentric exercise interventions. No changes have yet been observed in viscoelastic properties such as the MTU stress-relaxation response, although a minimum of evidence indicates that hysteresis during passive stretch-relaxation cycles may be reduced by muscle stretching training. Importantly, data exist for relatively few muscle groups, and little is known about the effects of age and sex on the adaptive process of passive mechanical properties. Despite the significant research effort afforded to understanding the effects of altered physical activity patterns on the maximum range of motion at some joints, further information is needed before it will be possible to develop targeted physical activity interventions with the aim of evoking specific changes in passive mechanical properties in individuals or in specific muscles and muscle groups.
42
Laws, Nicola, and Andrew Hoey. "Progression of kyphosis in mdx mice." Journal of Applied Physiology 97, no. 5 (November 2004): 1970–77. http://dx.doi.org/10.1152/japplphysiol.01357.2003.
Анотація:
Spinal deformity in the form of kyphosis or kyphoscoliosis occurs in most patients with Duchenne muscular dystrophy (DMD), a fatal X-linked disorder caused by an absence of the subsarcolemmal protein dystrophin. Mdx mice, which also lack dystrophin, show thoracolumbar kyphosis that progresses with age. We hypothesize that paraspinal and respiratory muscle weakness and fibrosis are associated with the progression of spinal deformity in this mouse model, and similar to DMD patients there is evidence of altered thoracic conformation and area. We measured kyphosis in mdx and age-matched control mice by monthly radiographs and the application of a novel radiographic index, the kyphotic index, similar to that used in boys with DMD. Kyphotic index became significantly less in mdx at 9 mo of age (3.58 ± 0.12 compared with 4.27 ± 0.04 in the control strain; P ≤ 0.01), indicating more severe kyphosis, and remained less from 10 to 17 mo of age. Thoracic area in 17-mo-old mdx was reduced by 14% compared with control mice ( P ≤ 0.05). Peak tetanic tension was significantly lower in mdx and fell 47% in old mdx latissimus dorsi muscles, 44% in intercostal strips, and 73% in diaphragm strips ( P ≤ 0.05). Fibrosis of these muscles and the longissimus dorsi, measured by hydroxyproline analysis and histological grading of picrosirius red-stained sections, was greater in mdx ( P < 0.05). We conclude that kyphotic index is a useful measure in mdx and other kyphotic mouse strains, and assessment of paralumbar and accessory respiratory muscles enhance understanding of spinal deformity in muscular dystrophy.
43
Murphy, Kate T., Annabel Chee, Ben G. Gleeson, Timur Naim, Kristy Swiderski, René Koopman, and Gordon S. Lynch. "Antibody-directed myostatin inhibition enhances muscle mass and function in tumor-bearing mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 3 (September 2011): R716—R726. http://dx.doi.org/10.1152/ajpregu.00121.2011.
Анотація:
Cancer cachexia describes the progressive skeletal muscle wasting and weakness in many cancer patients and accounts for >20% of cancer-related deaths. We tested the hypothesis that antibody-directed myostatin inhibition would attenuate the atrophy and loss of function in muscles of tumor-bearing mice. Twelve-week-old C57BL/6 mice received a subcutaneous injection of saline (control) or Lewis lung carcinoma (LLC) tumor cells. One week later, mice received either once weekly injections of saline (control, n = 12; LLC, n = 9) or a mouse chimera of anti-human myostatin antibody (PF-354, 10 mg·kg−1·wk−1, LLC+PF-354, n = 11) for 5 wk. Injection of LLC cells reduced muscle mass and maximum force of tibialis anterior (TA) muscles by 8–10% ( P < 0.05), but the muscle atrophy and weakness were prevented with PF-354 treatment ( P > 0.05). Maximum specific (normalized) force of diaphragm muscle strips was reduced with LLC injection ( P < 0.05) but was not improved with PF-354 treatment ( P > 0.05). PF-354 enhanced activity of oxidative enzymes in TA and diaphragm muscles of tumor-bearing mice by 118% and 89%, respectively ( P < 0.05). Compared with controls, apoptosis that was not of myofibrillar or satellite cell origin was 140% higher in TA muscle cross sections from saline-treated LLC tumor-bearing mice ( P < 0.05) but was not different in PF-354-treated tumor-bearing mice ( P > 0.05). Antibody-directed myostatin inhibition attenuated the skeletal muscle atrophy and loss of muscle force-producing capacity in a murine model of cancer cachexia, in part by reducing apoptosis. The improvements in limb muscle mass and function highlight the therapeutic potential of antibody-directed myostatin inhibition for cancer cachexia.
44
Balakrishnan, Rekha, Satvik Mareedu, and Gopal J. Babu. "Reducing sarcolipin expression improves muscle metabolism in mdx mice." American Journal of Physiology-Cell Physiology 322, no. 2 (February 1, 2022): C260—C274. http://dx.doi.org/10.1152/ajpcell.00125.2021.
Анотація:
Duchenne muscular dystrophy (DMD) is an inherited muscle wasting disease. Metabolic impairments and oxidative stress are major secondary mechanisms that severely worsen muscle function in DMD. Here, we sought to determine whether germline reduction or ablation of sarcolipin (SLN), an inhibitor of sarco/endoplasmic reticulum (SR) Ca2+ ATPase (SERCA), improves muscle metabolism and ameliorates muscle pathology in the mdx mouse model of DMD. Glucose and insulin tolerance tests show that glucose clearance rate and insulin sensitivity were improved in the SLN haploinsufficient mdx ( mdx:sln+/−) and SLN-deficient mdx ( mdx:sln−/−) mice. The histopathological analysis shows that fibrosis and necrosis were significantly reduced in muscles of mdx:sln+/− and mdx:sln−/− mice. SR Ca2+ uptake, mitochondrial complex protein levels, complex activities, mitochondrial Ca2+ uptake and release, and mitochondrial metabolism were significantly improved, and lipid peroxidation and protein carbonylation were reduced in the muscles of mdx:sln+/− and mdx:sln−/− mice. These data demonstrate that reduction or ablation of SLN expression can improve muscle metabolism, reduce oxidative stress, decrease muscle pathology, and protects the mdx mice from glucose intolerance.
45
Remels, A. H. V., H. R. Gosker, R. C. J. Langen, and A. M. W. J. Schols. "The mechanisms of cachexia underlying muscle dysfunction in COPD." Journal of Applied Physiology 114, no. 9 (May 1, 2013): 1253–62. http://dx.doi.org/10.1152/japplphysiol.00790.2012.
Анотація:
Pulmonary cachexia is a prevalent, debilitating, and well-recognized feature of COPD associated with increased mortality and loss of peripheral and respiratory muscle function. The exact cause and underlying mechanisms of cachexia in COPD are still poorly understood. Increasing evidence, however, shows that pathological changes in intracellular mechanisms of muscle mass maintenance (i.e., protein turnover and myonuclear turnover) are likely involved. Potential factors triggering alterations in these mechanisms in COPD include oxidative stress, myostatin, and inflammation. In addition to muscle wasting, peripheral muscle in COPD is characterized by a fiber-type shift toward a more type II, glycolytic phenotype and an impaired oxidative capacity (collectively referred to as an impaired oxidative phenotype). Atrophied diaphragm muscle in COPD, however, displays an enhanced oxidative phenotype. Interestingly, intrinsic abnormalities in (lower limb) peripheral muscle seem more pronounced in either cachectic patients or weight loss-susceptible emphysema patients, suggesting that muscle wasting and intrinsic changes in peripheral muscle's oxidative phenotype are somehow intertwined. In this manuscript, we will review alterations in mechanisms of muscle mass maintenance in COPD and discuss the involvement of oxidative stress, inflammation, and myostatin as potential triggers of cachexia. Moreover, we postulate that an impaired muscle oxidative phenotype in COPD can accelerate the process of cachexia, as it renders muscle in COPD less energy efficient, thereby contributing to an energy deficit and weight loss when not dietary compensated. Furthermore, loss of peripheral muscle oxidative phenotype may increase the muscle's susceptibility to inflammation- and oxidative stress-induced muscle damage and wasting.
46
Lionikas, A., D. A. Blizard, G. S. Gerhard, D. J. Vandenbergh, J. T. Stout, G. P. Vogler, G. E. McClearn, and L. Larsson. "Genetic determinants of weight of fast- and slow-twitch skeletal muscle in 500-day-old mice of the C57BL/6J and DBA/2J lineage." Physiological Genomics 21, no. 2 (April 14, 2005): 184–92. http://dx.doi.org/10.1152/physiolgenomics.00209.2004.
Анотація:
C57BL/6J (B6) and DBA/2J (D2) strains and two derivative populations, BXD recombinant inbred strains (BXD RIs) and B6D2F2, were used to explore genetic basis for variation in muscle weight at 500 days of age. In parallel with findings in 200-day-old mice (Lionikas A, Blizard DA, Vandenbergh DJ, Glover MG, Stout JT, Vogler GP, McClearn GE, and Larsson L. Physiol Genomics 16: 141–152, 2003), weight of slow-twitch soleus, mixed gastrocnemius, and fast-twitch tibialis anterior (TA) and extensor digitorum longus (EDL) muscles was 13–22% greater ( P < 0.001) in B6 than in D2. Distribution of BXD RI strain means indicated that genetic influence on muscle weight (strain effect P < 0.001, all muscles) was of polygenic origin, and effect of genetic factors differed between males and females (strain-by-sex interaction: P < 0.01 for soleus, EDL; P < 0.05 for TA, gastrocnemius). Linkage analyses in B6D2F2population identified QTL affecting muscle weight on Chr 1, 2, 6, and 9. Pleiotropic influences were observed for QTL on Chr 1 (soleus, TA), 2 (TA, EDL, gastrocnemius), and 9 (soleus, TA, EDL) and were not related to muscle type (fast/slow-twitch) or function (flexor/extensor). Effect of QTL on Chr 9 on soleus muscle was male specific. QTL on Chr 2 and 6 were previously observed at 200 days of age, whereas QTL on Chr 1 and 9 are novel muscle weight QTL. In summary, muscle weight in B6/D2 lineage is affected by a polygenic system that has variable influences at different ages, between males and females, and across muscles in a manner independent of muscle type.
47
Arnold, J. S., A. J. Thomas, and S. G. Kelsen. "Length-tension relationship of abdominal expiratory muscles: effect of emphysema." Journal of Applied Physiology 62, no. 2 (February 1, 1987): 739–45. http://dx.doi.org/10.1152/jappl.1987.62.2.739.
Анотація:
The present study examined the active and passive length-tension relationship of the abdominal expiratory muscles in vitro during electrically stimulated contractions. Studies were performed on isolated strips of transverse abdominis and external oblique muscle from nine adult hamsters with normal lung function. The effect of chronic hyperinflation on the two muscles was assessed in eight hamsters with elastase-induced emphysema. In normal animals the maximal active tension per cross-sectional area (Po) was equal in the two muscles. The absolute muscle fiber length at which Po occurred (Lo) was less for the external oblique than the transverse abdominis and the length-tension curve operated at shorter fiber lengths. However, the change in tension produced by an increase or decrease in muscle length expressed in relative terms (i.e., as %Lo) was greater for the transverse abdominis than the external oblique. Mean total lung capacity of emphysematous animals was 198% of control. Po of the transverse abdominis and external oblique were the same in emphysematous and control animals. However, Lo and the length-tension curve of the transverse abdominis occurred at shorter fiber lengths in emphysematous animals because of a reduction in the number of sarcomeres in series along the fiber. The length-tension curve and the number of sarcomeres in the external oblique was the same in emphysematous and control animals. These results in normal animals indicate that the magnitude of the change in active and passive tension produced by a change in muscle length differs in the transverse abdominis and external oblique. Moreover, chronic hyperinflation of the thorax produced by elastase injection alters the length-tension relationships of some but not all the expiratory muscles.
48
Wang, Wei, Dingding Shen, Lilei Zhang, Yanan Ji, Lai Xu, Zehao Chen, Yuntian Shen, et al. "SKP-SC-EVs Mitigate Denervated Muscle Atrophy by Inhibiting Oxidative Stress and Inflammation and Improving Microcirculation." Antioxidants 11, no. 1 (December 28, 2021): 66. http://dx.doi.org/10.3390/antiox11010066.
Анотація:
Denervated muscle atrophy is a common clinical disease that has no effective treatments. Our previous studies have found that oxidative stress and inflammation play an important role in the process of denervated muscle atrophy. Extracellular vesicles derived from skin precursor-derived Schwann cells (SKP-SC-EVs) contain a large amount of antioxidants and anti-inflammatory factors. This study explored whether SKP-SC-EVs alleviate denervated muscle atrophy by inhibiting oxidative stress and inflammation. In vitro studies have found that SKP-SC-EVs can be internalized and caught by myoblasts to promote the proliferation and differentiation of myoblasts. Nutrient deprivation can cause myotube atrophy, accompanied by oxidative stress and inflammation. However, SKP-SC-EVs can inhibit oxidative stress and inflammation caused by nutritional deprivation and subsequently relieve myotube atrophy. Moreover, there is a remarkable dose-effect relationship. In vivo studies have found that SKP-SC-EVs can significantly inhibit a denervation-induced decrease in the wet weight ratio and myofiber cross-sectional area of target muscles. Furthermore, SKP-SC-EVs can dramatically inhibit highly expressed Muscle RING Finger 1 and Muscle Atrophy F-box in target muscles under denervation and reduce the degradation of the myotube heavy chain. SKP-SC-EVs may reduce mitochondrial vacuolar degeneration and autophagy in denervated muscles by inhibiting autophagy-related proteins (i.e., PINK1, BNIP3, LC3B, and ATG7). Moreover, SKP-SC-EVs may improve microvessels and blood perfusion in denervated skeletal muscles by enhancing the proliferation of vascular endothelial cells. SKP-SC-EVs can also significantly inhibit the production of reactive oxygen species (ROS) in target muscles after denervation, which indicates that SKP-SC-EVs elicit their role by upregulating Nrf2 and downregulating ROS production-related factors (Nox2 and Nox4). In addition, SKP-SC-EVs can significantly reduce the levels of interleukin 1β, interleukin-6, and tumor necrosis factor α in target muscles. To conclude, SKP-SC-EVs may alleviate the decrease of target muscle blood perfusion and passivate the activities of ubiquitin-proteasome and autophagy-lysosome systems by inhibiting oxidative stress and inflammatory response, then reduce skeletal muscle atrophy caused by denervation. This study not only enriches the molecular regulation mechanism of denervated muscle atrophy, but also provides a scientific basis for SKP-SC-EVs as a protective drug to prevent and treat muscle atrophy.
49
Radak, Z., K. Asano, M. Inoue, T. Kizaki, S. Oh-Ishi, K. Suzuki, N. Taniguchi, and H. Ohno. "Superoxide dismutase derivative reduces oxidative damage in skeletal muscle of rats during exhaustive exercise." Journal of Applied Physiology 79, no. 1 (July 1, 1995): 129–35. http://dx.doi.org/10.1152/jappl.1995.79.1.129.
Анотація:
A superoxide dismutase derivative (SM-SOD) that circulates and is bound to albumin with a half-life of 6 h was injected intraperitoneally into rats before exhaustive treadmill running to study its antioxidant scavenging capacity in the plasma and soleus and tibialis muscles. The exercise induced a marked increase in xanthine oxidase activity in plasma and an increase in thiobarbituric acid-reactive substances in the plasma as well as in the soleus and tibialis muscles of nonadministered rats immediately after the exercise. The immunoreactive content and activity of both SOD isoenzymes (Cu,Zn-SOD and Mn-SOD) of the nonadministered rats increased in the soleus and tibialis muscles immediately after running. SM-SOD treatment definitely attenuated the degree of the increase in thiobarbituric acid-reactive substances and xanthine oxidase in all samples examined immediately after exercise. Glutathione peroxidase activity significantly increased in the soleus muscle of nonadministered rats 1 day after running, whereas catalase activity remained unchanged throughout the experimental period. These results suggest that a single bout of exhaustive exercise induces oxidative stress in skeletal muscle of rats and that this oxidative stress can be attenuated by exogenous SM-SOD.
50
Himori, Koichi, Daisuke Tatebayashi, Yuki Ashida та Takashi Yamada. "Eccentric training enhances the αB-crystallin binding to the myofibrils and prevents skeletal muscle weakness in adjuvant-induced arthritis rat". Journal of Applied Physiology 127, № 1 (1 липня 2019): 71–80. http://dx.doi.org/10.1152/japplphysiol.00102.2019.
Анотація:
Patients with rheumatoid arthritis (RA) frequently suffer from muscle weakness. We examined whether eccentric training prevents skeletal muscle weakness in adjuvant-induced arthritis (AIA) rat, a widely used animal model for RA. AIA was induced in the knees of Wistar rats by injection of complete Freund’s adjuvant. To induce eccentric contractions (ECCs), neuromuscular electrical stimulation (45 V) was applied to the plantar flexor muscles simultaneously with forced dorsiflexion of the ankle joint (0–40°) and was given every 6 s. ECC exercise was applied every other day for a total of 11 sessions and consisted of 4 sets of 5 contractions. There was a significant reduction in in vitro maximum Ca2+-activated force in skinned fibers in gastrocnemius muscle from AIA rats. These changes were associated with reduced expression levels of contractile proteins (i.e., myosin and actin), increased levels of inflammation redox stress-related biomarkers (i.e., TNF-α, malondialdehyde-protein adducts, NADPH oxidase 2, and neuronal nitric oxide synthase), and autolyzed active calpain-1 in AIA muscles. ECC training markedly enhanced the steady-state levels of αB-crystallin, a small heat shock protein, and its binding to the myofibrils and prevented the AIA-induced myofibrillar dysfunction, reduction in contractile proteins, and inflammation-oxidative stress insults. Our findings demonstrate that ECC training preserves myofibrillar function without muscle damage in AIA rats, which is at least partially attributable to the protective effect of αB-crystallin on the myofibrils against oxidative stress-mediated protein degeneration. Thus ECC training can be a safe and effective intervention, counteracting the loss of muscle strength in RA patients. NEW & NOTEWORTHY Eccentric contractions (ECCs) are regarded as an effective way to increase muscle strength. No studies, however, assess safety and effectiveness of ECC training on muscle weakness associated with rheumatoid arthritis. Here, we used adjuvant-induced arthritis (AIA) rats to demonstrate that ECC training prevents intrinsic contractile dysfunction without muscle damage in AIA rats, which may be attributed to the protective effect of αB-crystallin on the myofibrils against inflammation-oxidative stress insults.