Chapter 5 Muscle
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Microanatomy of Muscles
Microanatomy of Muscles Anatomy & Physiology Class Three Main Muscle Types Objectives: By the end of this presentation you will have the information to: 1. Describe the 3 main types of muscles. 2. Detail the functions of the muscle system. 3. Correctly label the parts of a myocyte (muscle cell) 4. Identify the levels of organization in a skeletal muscle from organ to myosin. 5. Explain how a muscle contracts utilizing the correct terminology of the sliding filament theory. 6. Contrast and compare cardiac and smooth muscle with skeletal muscle. Major Functions: Muscle System 1. Moving the skeletal system and posture. 2. Passing food through the digestive system & constriction of other internal organs. 3. Production of body heat. 4. Pumping the blood throughout the body. 5. Communication - writing and verbal Specialized Cells (Myocytes) ~ Contractile Cells Can shorten along one or more planes because of specialized cell membrane (sarcolemma) and specialized cytoskeleton. Specialized Structures found in Myocytes Sarcolemma: The cell membrane of a muscle cell Transverse tubule: a tubular invagination of the sarcolemma of skeletal or cardiac muscle fibers that surrounds myofibrils; involved in transmitting the action potential from the sarcolemma to the interior of the myofibril. Sarcoplasmic Reticulum: The special type of smooth endoplasmic Myofibrils: reticulum found in smooth and a contractile fibril of skeletal muscle, composed striated muscle fibers whose function mainly of actin and myosin is to store and release calcium ions. Multiple Nuclei (skeletal) & many mitochondria Skeletal Muscle - Microscopic Anatomy A whole skeletal muscle (such as the biceps brachii) is considered an organ of the muscular system. Each organ consists of skeletal muscle tissue, connective tissue, nerve tissue, and blood or vascular tissue. -
Genetic Mutations and Mechanisms in Dilated Cardiomyopathy
Genetic mutations and mechanisms in dilated cardiomyopathy Elizabeth M. McNally, … , Jessica R. Golbus, Megan J. Puckelwartz J Clin Invest. 2013;123(1):19-26. https://doi.org/10.1172/JCI62862. Review Series Genetic mutations account for a significant percentage of cardiomyopathies, which are a leading cause of congestive heart failure. In hypertrophic cardiomyopathy (HCM), cardiac output is limited by the thickened myocardium through impaired filling and outflow. Mutations in the genes encoding the thick filament components myosin heavy chain and myosin binding protein C (MYH7 and MYBPC3) together explain 75% of inherited HCMs, leading to the observation that HCM is a disease of the sarcomere. Many mutations are “private” or rare variants, often unique to families. In contrast, dilated cardiomyopathy (DCM) is far more genetically heterogeneous, with mutations in genes encoding cytoskeletal, nucleoskeletal, mitochondrial, and calcium-handling proteins. DCM is characterized by enlarged ventricular dimensions and impaired systolic and diastolic function. Private mutations account for most DCMs, with few hotspots or recurring mutations. More than 50 single genes are linked to inherited DCM, including many genes that also link to HCM. Relatively few clinical clues guide the diagnosis of inherited DCM, but emerging evidence supports the use of genetic testing to identify those patients at risk for faster disease progression, congestive heart failure, and arrhythmia. Find the latest version: https://jci.me/62862/pdf Review series Genetic mutations and mechanisms in dilated cardiomyopathy Elizabeth M. McNally, Jessica R. Golbus, and Megan J. Puckelwartz Department of Human Genetics, University of Chicago, Chicago, Illinois, USA. Genetic mutations account for a significant percentage of cardiomyopathies, which are a leading cause of conges- tive heart failure. -
Muscle Physiology Dr
Muscle Physiology Dr. Ebneshahidi Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Skeletal Muscle Figure 9.2 (a) Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Functions of the muscular system . 1. Locomotion . 2. Vasoconstriction and vasodilatation- constriction and dilation of blood vessel Walls are the results of smooth muscle contraction. 3. Peristalsis – wavelike motion along the digestive tract is produced by the Smooth muscle. 4. Cardiac motion . 5. Posture maintenance- contraction of skeletal muscles maintains body posture and muscle tone. 6. Heat generation – about 75% of ATP energy used in muscle contraction is released as heat. Copyright. © 2004 Pearson Education, Inc., publishing as Benjamin Cummings . Striation: only present in skeletal and cardiac muscles. Absent in smooth muscle. Nucleus: smooth and cardiac muscles are uninculcated (one nucleus per cell), skeletal muscle is multinucleated (several nuclei per cell ). Transverse tubule ( T tubule ): well developed in skeletal and cardiac muscles to transport calcium. Absent in smooth muscle. Intercalated disk: specialized intercellular junction that only occurs in cardiac muscle. Control: skeletal muscle is always under voluntary control‚ with some exceptions ( the tongue and pili arrector muscles in the dermis). smooth and cardiac muscles are under involuntary control. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Innervation: motor unit . a) a motor nerve and a myofibril from a neuromuscular junction where gap (called synapse) occurs between the two structures. at the end of motor nerve‚ neurotransmitter (i.e. acetylcholine) is stored in synaptic vesicles which will release the neurotransmitter using exocytosis upon the stimulation of a nerve impulse. Across the synapse the surface the of myofibril contains receptors that can bind with the neurotransmitter. -
Physiologist Physiologist
Published by The American Physiological Society Integrating the Life Sciences from Molecule to Organism The PhysiologistPhysiologist Generating Support for Science INSIDE in the 111th Congress Rebecca Osthus APS Science Policy Analyst APS The 2008 election cycle brings a new is somewhat more promising. There is a administration to Washington, DC this plan to double the agency’s budget over Bylaw Changes January and also ushers in the 111th the next several years as part of the p. 240 Congress. With many new Members of America COMPETES Act, but so far Congress in both the House of yearly increases have not lived up to Representatives and the Senate, now is the goals laid out by Congress. Annual Meeting of the time for APS members to reach out Lawmakers are also making deci- the Nebraska and communicate the importance of sions about what regulations govern Physiological supporting biomedical research the use of animals in research, whether through strong federal funding and federally funded scientists should con- Society sound policy making. While scientists tinue to consult for and own stock in p. 243 carry out research in labs across the pharmaceutical and biotechnology com- country, many decisions are being made in APS Membership Washington, DC that Statistics will affect how they do p. 244 their jobs. The current fiscal cri- sis means that it is Starting a Lab: more important than How to Develop a ever before to make a strong case for federal Budget and Buy investment in research. Equipment Since the completion of p. 252 the doubling of the NIH budget, yearly increas- es have failed to keep Congress Extends pace with inflation, Current Levels of causing success rates for extramural grants Research Funding to fall into the teens. -
Loss of Mouse Cardiomyocyte Talin-1 and Talin-2 Leads to Β-1 Integrin
Loss of mouse cardiomyocyte talin-1 and talin-2 leads PNAS PLUS to β-1 integrin reduction, costameric instability, and dilated cardiomyopathy Ana Maria Mansoa,b,1, Hideshi Okadaa,b, Francesca M. Sakamotoa, Emily Morenoa, Susan J. Monkleyc, Ruixia Lia, David R. Critchleyc, and Robert S. Rossa,b,1 aDivision of Cardiology, Department of Medicine, University of California at San Diego School of Medicine, La Jolla, CA 92093; bCardiology Section, Department of Medicine, Veterans Administration Healthcare, San Diego, CA 92161; and cDepartment of Molecular Cell Biology, University of Leicester, Leicester LE1 9HN, United Kingdom Edited by Kevin P. Campbell, Howard Hughes Medical Institute, University of Iowa, Iowa City, IA, and approved May 30, 2017 (received for review January 26, 2017) Continuous contraction–relaxation cycles of the heart require ognized as key mechanotransducers, converting mechanical per- strong and stable connections of cardiac myocytes (CMs) with turbations to biochemical signals (5, 6). the extracellular matrix (ECM) to preserve sarcolemmal integrity. The complex of proteins organized by integrins has been most CM attachment to the ECM is mediated by integrin complexes commonly termed focal adhesions (FA) by studies performed in localized at the muscle adhesion sites termed costameres. The cells such as fibroblasts in a 2D environment. It is recognized that ubiquitously expressed cytoskeletal protein talin (Tln) is a compo- this structure is important for organizing and regulating the me- nent of muscle costameres that links integrins ultimately to the chanical and signaling events that occur upon cellular adhesion to sarcomere. There are two talin genes, Tln1 and Tln2. Here, we ECM (7, 8). -
Postmortem Changes in the Myofibrillar and Other Cytoskeletal Proteins in Muscle
BIOCHEMISTRY - IMPACT ON MEAT TENDERNESS Postmortem Changes in the Myofibrillar and Other C'oskeletal Proteins in Muscle RICHARD M. ROBSON*, ELISABETH HUFF-LONERGAN', FREDERICK C. PARRISH, JR., CHIUNG-YING HO, MARVIN H. STROMER, TED W. HUIATT, ROBERT M. BELLIN and SUZANNE W. SERNETT introduction filaments (titin), and integral Z-line region (a-actinin, Cap Z), as well as proteins of the intermediate filaments (desmin, The cytoskeleton of "typical" vertebrate cells contains paranemin, and synemin), Z-line periphery (filamin) and three protein filament systems, namely the -7-nm diameter costameres underlying the cell membrane (filamin, actin-containing microfilaments, the -1 0-nm diameter in- dystrophin, talin, and vinculin) are listed along with an esti- termediate filaments (IFs), and the -23-nm diameter tubu- mate of their abundance, approximate molecular weights, lin-containing microtubules (Robson, 1989, 1995; Robson and number of subunits per molecule. Because the myofibrils et al., 1991 ).The contractile myofibrils, which are by far the are the overwhelming components of the skeletal muscle cell major components of developed skeletal muscle cells and cytoskeleton, the approximate percentages of the cytoskel- are responsible for most of the desirable qualities of muscle eton listed for the myofibrillar proteins (e.g., myosin, actin, foods (Robson et al., 1981,1984, 1991 1, can be considered tropomyosin, a-actinin, etc.) also would represent their ap- the highly expanded corollary of the microfilament system proximate percentages of total myofibrillar protein. of non-muscle cells. The myofibrils, IFs, cell membrane skel- eton (complex protein-lattice subjacent to the sarcolemma), Some Important Characteristics, Possible and attachment sites connecting these elements will be con- Roles, and Postmortem Changes of Key sidered as comprising the muscle cell cytoskeleton in this Cytoskeletal Proteins review. -
Disease-Proportional Proteasomal Degradation of Missense Dystrophins
Disease-proportional proteasomal degradation of missense dystrophins Dana M. Talsness, Joseph J. Belanto, and James M. Ervasti1 Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota–Twin Cities, Minneapolis, MN 55455 Edited by Louis M. Kunkel, Children’s Hospital Boston, Harvard Medical School, Boston, MA, and approved September 1, 2015 (received for review May 5, 2015) The 427-kDa protein dystrophin is expressed in striated muscle insertions or deletions (indels) represent ∼7% of the total DMD/ where it physically links the interior of muscle fibers to the BMD population (13). When indel mutations cause a frameshift, they extracellular matrix. A range of mutations in the DMD gene encod- can specifically be targeted by current exon-skipping strategies (15). ing dystrophin lead to a severe muscular dystrophy known as Du- Patients with missense mutations account for only a small percentage chenne (DMD) or a typically milder form known as Becker (BMD). of dystrophinopathies (<1%) (13), yet they represent an orphaned Patients with nonsense mutations in dystrophin are specifically tar- subpopulation with an undetermined pathomechanism and no cur- geted by stop codon read-through drugs, whereas out-of-frame de- rent personalized therapies. letions and insertions are targeted by exon-skipping therapies. Both The first missense mutation reported to cause DMD was L54R treatment strategies are currently in clinical trials. Dystrophin mis- in ABD1 of an 8-y-old patient (16). Another group later reported sense mutations, however, cause a wide range of phenotypic se- L172H, a missense mutation in a structurally analogous location of verity in patients. The molecular and cellular consequences of such ABD1 (17), yet this patient presented with mild symptoms at 42 mutations are not well understood, and there are no therapies spe- years of age. -
Costamere Protein Expression and Tissue Composition of Rotator Cuff Muscle After Tendon Release in Sheep
Zurich Open Repository and Archive University of Zurich Main Library Strickhofstrasse 39 CH-8057 Zurich www.zora.uzh.ch Year: 2018 Costamere protein expression and tissue composition of rotator cuff muscle after tendon release in sheep Ruoss, Severin ; Möhl, Christoph B ; Benn, Mario C ; von Rechenberg, Brigitte ; Wieser, Karl ; Meyer, Dominik C ; Gerber, Christian ; Flück, Martin Abstract: Previous studies suggested that degradation of contractile tissue requires cleavage of the costamere, a structural protein complex that holds sarcomeres in place. This study examined if costamere turnover is affected by a rotator cuff tear in a previously established ovine model. We found theactivity of focal adhesion kinase (FAK), a main regulator of costamere turnover, was unchanged at 2 weeks but decreased by 27% 16 weeks after surgical release of the infraspinatus tendon. This was accompanied by cleavage of the costamere protein talin into a 190 kDa fragment while full length talin remained un- changed. At 2 weeks after tendon release, muscle volume decreased by 17 cm from an initial 185 cm(3) , the fatty tissue volume was halved, and the contractile tissue volume remained unchanged. After 16 weeks, the muscle volume decreased by 36 cm(3) , contractile tissue was quantitatively lost, and the fat content increased by 184%. Nandrolone administration mitigated the loss of contractile tissue by 26% and prevented fat accumulation, alterations in FAK activity, and talin cleavage. Taken together, these findings imply that muscle remodeling after tendon release occurs in two stages. The early decreaseof muscle volume is associated with reduction of fat; while, the second stage is characterized by substantial loss of contractile tissue accompanied by massive fat accumulation. -
Titin Force Is Enhanced in Actively Stretched Skeletal Muscle
© 2014. Published by The Company of Biologists Ltd | The Journal of Experimental Biology (2014) 217, 3629-3636 doi:10.1242/jeb.105361 RESEARCH ARTICLE Titin force is enhanced in actively stretched skeletal muscle Krysta Powers1, Gudrun Schappacher-Tilp2, Azim Jinha1, Tim Leonard1, Kiisa Nishikawa3 and Walter Herzog1,* ABSTRACT Aubert, 1952; Edman et al., 1978; Edman et al., 1982; Morgan, 1994; The sliding filament theory of muscle contraction is widely accepted Herzog et al., 2006; Leonard and Herzog, 2010). This property, as the means by which muscles generate force during activation. termed residual force enhancement, provides a direct challenge to the Within the constraints of this theory, isometric, steady-state force sliding filament-based cross-bridge theory. produced during muscle activation is proportional to the amount of Residual force enhancement has been observed in vivo and down filament overlap. Previous studies from our laboratory demonstrated to the sarcomere level (Abbott and Aubert, 1952; Edman et al., enhanced titin-based force in myofibrils that were actively stretched 1982; Herzog and Leonard, 2002; Leonard et al., 2010; Rassier, to lengths which exceeded filament overlap. This observation cannot 2012). There are three main filaments at the sarcomere level that be explained by the sliding filament theory. The aim of the present contribute to force production in muscle: the thick (myosin), the thin study was to further investigate the enhanced state of titin during (actin), and the titin filaments. The thick filament is composed active stretch. Specifically, we confirm that this enhanced state of primarily of the protein myosin, and the thin filament is composed force is observed in a mouse model and quantify the contribution of of actin and regulatory proteins. -
Biomechanics of Skeletal Muscle
BiomechanicsBiomechanics ofof SkeletalSkeletal MuscleMuscle www.fisiokinesiterapia.biz ContentsContents I.I. CompositionComposition && structurestructure ofof skeletalskeletal musclemuscle II.II. MechanicsMechanics ofof MuscleMuscle ContractionContraction III.III. ForceForce productionproduction inin musclemuscle IV.IV. MuscleMuscle remodelingremodeling V.V. SummarySummary 2 MuscleMuscle types:types: –– cardiaccardiac muscle:muscle: composescomposes thethe heartheart –– smoothsmooth muscle:muscle: lineslines hollowhollow internalinternal organsorgans –– skeletalskeletal (striated(striated oror voluntary)voluntary) muscle:muscle: attachedattached toto skeletonskeleton viavia tendontendon && movementmovement SkeletalSkeletal musclemuscle 4040--45%45% ofof bodybody weightweight –– >> 430430 musclesmuscles –– ~~ 8080 pairspairs produceproduce vigorousvigorous movementmovement DynamicDynamic && staticstatic workwork –– Dynamic:Dynamic: locomotionlocomotion && positioningpositioning ofof segmentssegments –– Static:Static: maintainsmaintains bodybody postureposture 3 I.I. CompositionComposition && structurestructure ofof skeletalskeletal musclemuscle Structure & organization • Muscle fiber: long cylindrical multi-nuclei cell 10-100 μm φ fiber →endomysium → fascicles → perimysium → epimysium (fascia) • Collagen fibers in perimysium & epimysium are continuous with those in tendons • {thin filament (actin 5nm φ) + thick filament (myosin 15 nm φ )} → myofibrils (contractile elements, 1μm φ) →muscle fiber 4 5 6 BandsBands ofof myofibrilsmyofibrils -
Skeletal Muscle Tissue and Muscle Organization
Chapter 9 The Muscular System Skeletal Muscle Tissue and Muscle Organization Lecture Presentation by Steven Bassett Southeast Community College © 2015 Pearson Education, Inc. Introduction • Humans rely on muscles for: • Many of our physiological processes • Virtually all our dynamic interactions with the environment • Skeletal muscles consist of: • Elongated cells called fibers (muscle fibers) • These fibers contract along their longitudinal axis © 2015 Pearson Education, Inc. Introduction • There are three types of muscle tissue • Skeletal muscle • Pulls on skeletal bones • Voluntary contraction • Cardiac muscle • Pushes blood through arteries and veins • Rhythmic contractions • Smooth muscle • Pushes fluids and solids along the digestive tract, for example • Involuntary contraction © 2015 Pearson Education, Inc. Introduction • Muscle tissues share four basic properties • Excitability • The ability to respond to stimuli • Contractility • The ability to shorten and exert a pull or tension • Extensibility • The ability to continue to contract over a range of resting lengths • Elasticity • The ability to rebound toward its original length © 2015 Pearson Education, Inc. Functions of Skeletal Muscles • Skeletal muscles perform the following functions: • Produce skeletal movement • Pull on tendons to move the bones • Maintain posture and body position • Stabilize the joints to aid in posture • Support soft tissue • Support the weight of the visceral organs © 2015 Pearson Education, Inc. Functions of Skeletal Muscles • Skeletal muscles perform -
Sodium Dysregulation Coupled with Calcium Entry Leads to Muscular
Sodium dysregulation coupled with calcium entry leads to muscular dystrophy in mice A dissertation submitted to the Division of Research and Advanced Studies Of the University of Cincinnati In partial fulfillment of the Requirements for the degree of DOCTOR OF PHILOSOPHY (Ph.D.) In the department of Molecular and Developmental Biology of the College of Medicine 2014 Adam R. Burr B.S. University of Minnesota, 2007 i Abstract Duchenne Muscular Dystrophy (DMD) and many of the limb girdle muscular dystrophies form a family of diseases called sarcoglycanopathies. In these diseases, mutation of any of a host of membrane and membrane associated proteins leads to increased stretch induced damage, aberrant signaling, and increased activity of non-specific cation channels, inducing muscle necrosis. Due to ongoing necrosis, DMD follows a progressive clinical course that leads to death in the mid-twenties. This course is slowed only modestly by high dose corticosteroids, which cause a plethora of harsh side effects. Targeted therapies are needed to ameliorate this disease until a more permanent therapy such as replacement of the mutated gene can be routinely performed. Here, we identified sodium calcium exchanger 1 (NCX1) as a potential therapeutic target. We started from the observation that sodium calcium exchanger 1 (NCX1) was upregulated during the necrotic phase of the disease in Sgcd-/- mice, which have similar pathology and mechanism of disease to boys with DMD. To test the causal effect of NCX1 overexpression on disease, we generated mice that overexpress NCX1 specifically in skeletal muscle. By Western blotting and immunofluorescence, we showed that NCX1 transgenic mice express more NCX1 protein in a similar localization pattern as endogenous NCX1.