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Muscle is one of the more complex structures in the body and many of the details of muscle function remain obscure.
Parts of a Muscle Fibre
-(note: the terms muscle fibre and muscle cell are used interchangeably)
-outer membrane (in muscle, called sarcolemma)
-contain many cell nuclei (each contain DNA)
-contain many mitochondrion (pl. = mitochondria) (in muscle, they are called sarcosomes)
-contain a large endoplasmic reticulum (in muscle, called a sarcoplasmic reticulum)
-contain thousands of inner strands called myofibrils (they make up the cytoplasm [in muscle, called sarcoplasm] of the cell).
-myofibrils contain units called sarcomeres
-sarcomeres link up end to end to form one myofibril
sarcomeres contain actin thin filaments and myosin thick filaments: together responsible for muscle contraction
-actin (thin filaments) and myosin (thick filaments) interact in the sliding-filament model (our current theory of muscle function).
-myosin heads briefly bind to actin to cause the contraction
-muscle is made up out of proteins (the meat we eat is animal muscle): myosin, actin, tropomyosin and troponin make up 75% of muscle. About 24 other proteins make up the rest of the protein found in muscle.
-some neuromuscular diseases involve problems with one of these proteins
-the number of muscle fibers a person has appears to be a genetic factor and is fixed at birth, but new myofibrils inside the fibers are created by exercise
Muscle Function
-motor nerve cells (motor neurons) in the CNS carry signals from the brain down the spinal cord and out to muscles
-some neuromuscular diseases involve problems with the motor neurons
-one motor neuron connects to a group of muscle fibers to make up one motor unit
-where the nerve contacts the muscle is a bridge called the neuromuscular junction
-the neuromuscular junction is a synapse: no direct connection between the nerve and muscle: signals are sent across a tiny gap by a neurotransmitter called acetylcholine (Ach)
-when an impulse reaches the junction, Ach is released, crosses the gap and contacts the muscle fiber. When enough Ach accumulates, the muscle fiber fires (muscle contracts).
-some neuromuscular diseases involve problems with this neurotransmitter connection
Muscle Energy
-Muscle energy is supplied by a complex series of biochemical reactions depending
upon the demands placed upon the muscle. There are three subsystems that all
use chemical molecules called adenosine triphosphate (ATP).
-1). the immediate source of energy for muscle contraction is created when myosin uses (chemically breaks down) ATP. A muscle fiber contains only enough ATP to power a few twitches (up to about 10 seconds worth of energy). (like a runner doing a 100 meter sprint).
-2). skeletal muscle fibers contain about 1% glycogen. The muscle fiber can degrade this glycogen by a chemical process (glycolysis). Glycolysis yields two molecules of ATP for each pair of lactic acid molecules produced. This process does not need oxygen and can function for up to about 90 seconds (like a swimmer doing a 400 meter race)
-3). for longer periods of exertion (like a marathon race), oxygen is needed. In this third process, called aerobic respiration, oxygen is supplied by the blood to the muscle. When oxygen is present, glucose can be completely broken down into carbon dioxide and water in a process called aerobic respiration. The glucose can come from three different places:
=remaining glycogen supplies in the muscles
=breakdown of the liver's glycogen into glucose, which gets to working muscle through the bloodstream
=absorption of glucose from food in the intestine, which gets to working muscle through the bloodstream
-aerobic respiration is required to meet the ATP needs of a muscle engaged in prolonged activity (thus causing more rapid and deeper breathing), and is also required afterwards to enable the body to resynthesize glycogen (deep breathing continues for a time after exercise is stopped).
Muscle Exercise
-when muscle works, the current theory is that there is mechanical damage and micro-tears occur in the muscle fibers
-satellite cells (each with one nucleus) are scattered along the outside of the muscle fiber
-muscle work creates micro-tears or tiny rips in the fibres, damage stimulates a growth factor and attracts satellite cells
-satellite cells incorporate themselves into the muscle fiber
-the satellite cells produce protein and give their nuclei to the muscle fiber
-over time, the muscle fiber collects more nuclei and, in addition, the fibre expands
-exercise adds to muscle mass by adding more myofibrils (no new muscle fibres are created)
-in addition to exercise, there is a normal balance between protein synthesis and protein breakdown in the muscle.
-muscle composition involves a complex control mechanism that depends upon a number of factors including, activity level, diet and internal biochemical regulation
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Muscle is among the strangest tissues in the human body. A single muscle cell consists of a membrane, many scattered nuclei that contain genes, and thousands of inner strands called myofibrils that constitute the cytoplasm of the cell. Sustained by the multiple nuclei, the cells can grow to be centimetres long.
Filling the inside of a muscle fiber, the myofibrils can be as long as the fiber and are the part that enables the cell to contract forcefully in response to nerve impulses. The actual contraction is accomplished by the myofibrils' tiny component units, which are called sarcomeres. They are linked end to end to make up a myofibril, which contracts when all of its sarcomeres do. Within each sarcomere are two filamentary proteins, called myosin and actin, whose interaction causes contraction. Basically, during contraction, a sarcomere shortens like a collapsing telescope, as the actin filaments at each end of a central myosin filament slide toward the myosin's center [see "The Mystery of Muscle," by Glenn Zorpette; Scientific American Presents: Men: The Scientific Truth about Their Work, Play, Health and Passions, Summer 1999].
Muscle cells, also known as fibers, cannot split themselves to form completely new fibers. So a muscle can become more massive only when its individual fibers become thicker. What causes this thickening is the creation of new myofibrils. In an extremely complex process that is still poorly understood, the mechanical stresses that exercise exerts on tendons and other structures connected to the muscle trigger many different biochemical pathways that ultimately cause the muscle cells to make more proteins. Enormous amounts of these proteins, chiefly myosin and actin, are needed as the cell produces additional myofibrils. To produce and support all this protein requires more nuclei. As muscle cells cannot divide, the new nuclei are donated by so-called satellite cells, which are scattered among the many nuclei on the surface of a skeletal muscle fiber. Satellite cells are largely separate from the muscle cell and, unlike it, have only the usual one nucleus apiece. Thus, they can replicate by dividing. Researchers now know that satellite cells proliferate in response to the stresses and wear and tear of exercise. As they multiply, some remain as satellites on the fiber, but others become incorporated into it. Their nuclei become indistinguishable from the muscle cell's other nuclei. With these additional nuclei, the fiber is able to churn out more proteins and create more myofibrils.
According to the prevailing theory, rigorous exercise inflicts tiny "microtears" in muscle fibers.
The damaged area attracts the satellite cells, which incorporate themselves into the muscle tissue and begin producing proteins to fill the gap.
Significantly, the number of nuclei passing from the satellite cells into the damaged area of the fiber is greater than the number of nuclei lost when the
gap opened up. As a result, in that part of the fiber, more protein can be produced and supported. Gradually, as more microtears are repaired in this manner,
the overall number of nuclei grows, as does the fiber itself.
In order to produce a protein, a muscle cell, like any cell in the body, must
have a "blueprint" to specify the order in which amino acids should be put together
to make the protein - that is, which protein will be created. This blueprint is
a gene in the cell's nucleus, and the process by which the information gets out
of the nucleus into the cytoplasm, where the protein will be made, starts with
transcription. It occurs in the nucleus when a gene's information (encoded in
DNA) is copied into a molecule called messenger RNA. The mRNA then carries this
information outside the nucleus to structures known as ribosomes, which assemble
amino acids into the protein - myosin or actin, say - specified by that gene.
This latter process is called translation. The source of biochemical complexity
in muscle enlargement is not really transcription or translation but rather what
precedes those processes: the many biochemical pathways that bring about transcription.
Researchers know of dozens of different key biochemicals that initiate or sustain
these pathways, and some suspect that there may actually be thousands. Most of
these biochemicals are proteins that fall into five basic categories: sex hormones,
like testosterone; thyroid hormones; insulin-like growth factors; fibroblast growth
factor; and myriad other proteins lumped under the general term transcription
factors. Some of these proteins are produced in organs such as the liver and circulate
throughout the body; others are created locally, in specific muscle tissue, in
response to exercise or stretching of that tissue.
These hormones, growth factors and transcription factors act in a variety of ways, often in conjunction with one another, to promote protein production. The many biochemical reactions are like a sprawling game with thousands of players, the goal being to get into the nucleus and, typically, to combine with a site on a chromosome known as a promoter region. This combination activates a nearby gene and triggers transcription.
As with any game, there are rules. Only the transcription factors, as their name implies, can get into the nucleus by themselves and activate genes. Hormones and growth factors spur transcription indirectly, usually in conjunction with transcription factors and other molecules called receptors. And one of the game's complexities is that sometimes transcription factors activate genes that produce more transcription factors. As an example of how a hormone works, take testosterone. Produced by the testes and carried by the blood, it can penetrate a muscle cell's outer membrane and get into the cytoplasm. There it combines with a receptor floating free in the cytoplasm. The complex then enters the nucleus and binds to a promoter region to activate a gene and initiate transcription. Because anabolic steroids are merely synthetic versions of testosterone, this pathway is the one they trigger and exploit to build muscle.
Other pathways are even more complex. Some crucial ones begin with the binding of growth factors, for instance, to receptors that poke through the surface membranes of cells. When the parts outside the cell bind to a specific molecule, the union activates a series of chemical reactions inside the cell. For example, the binding of a growth factor to its receptor activates cascades of enzymes, called kinases, that modify other proteins in the cytoplasm, which in turn bind to promoter regions on chromosomes and otherwise regulate the activity of genes. One of the most important growth factors is insulin-like growth factor-1 (IGF-1). During infancy and childhood, IGF-1 produced by the liver circulates throughout the body, rapidly expanding all the body's muscle fibers. The amount of this circulating, liver-produced IGF-1 eventually declines sharply, ending the early-life growth spurt. For muscle growth, the free ride is then over, and only exercise can add (and eventually, merely maintain) muscle mass. IGF-1 and other growth factors continue to play a major role, but they are released only locally in muscle during exercise or in response to injury.
Significantly, IGF-1 concentrations are high around the tiny tears in muscle fibers caused by exercise. Researchers believe that the growth factor plays a major role in attracting the satellite cells to the damaged area. End of Scientific American summary.
Image from the article. Click Here.
From: http://www.sciam.com/specialissues/0999bionic/0999zorpette.html
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How do muscles work?
In order to understand muscle contraction we need to know a little about muscle
cell structure. A skeletal muscle is made up of long muscle fibres (muscle cells)
which, in turn, are composed of bundles of myofibrils (myo = muscle, fibrils
are threadlike strands of proteins). Each myofibril consists of two kinds of
protein filament (sometimes called myofilaments) - thick filaments made of myosin
and thin filaments made of actin. Myofilaments do not extend the full length
of a muscle fibre; they are stacked together in compartments called sarcomeres.
Sarcomeres are separated from one another by narrow zones of dense material
called Z lines.
Overview: The myosin heads extend and retract to form what are called cross bridges. These bridges "walk" along the actin fibers like the legs of a caterpillar walking along the ground (or think of the action of a boat's oars in the water). When the heads grab the actin and a bridge is formed, it acts to shorten the actin fibre, producing a contraction of the length of the overall muscle fibre. Contraction is the only movement a muscle can make, it can only contract and relax back to its original position (it can't expand or push). It is thought that these repetitive sliding movements produce the muscle contractions.
Sliding of the filaments depends on the interaction of actin and myosin molecules.
Myosin filaments are long and thin with rounded "heads" projecting out at the
sides. The myosin "heads" bind with ATP converting it to ADP using the energy
to alter their shape. The energized myosin can then bind to actin molecules
at specific sites forming cross-bridges.
A skeletal muscle contracts only when stimulated by a motor neurone. At rest, myosin is prevented from binding with actin molecules by the protein tropomyosin. Troponin controls the position of tropomyosin on the thin actin filament (not shown on the above diagram - tropomyosin wraps around the actin fibre like a vine on a tree). However following stimulation by a motor nerve, acetylcholine diffuses from the neurone triggering the release of calcium ions into the sarcoplasm. Calcium ions bind to the troponin which then act on the tropomyosin molecule exposing the myosin-binding sites. Once the binding sites are open the myosin molecules form cross-bridges with the actin and the two filaments slide over one another (the cross-bridges act rather like oars on a rowing boat sweeping the myosin molecule forwards). During relaxation, an active transport system pumps calcium back into the sarcoplasmic reticulum for storage.
There are a number of proteins involved in the overall process of nerve to muscle communication and in muscle contraction and recovery. If any of these proteins is defective in some way, the muscle can't function properly. In most cases, a protein defect results from a genetic defect in the code that spells out the structure and function of the protein. The "size" and impact of the defect determine the muscle disease and symptoms seen. In minor defects, a long term impact is seen and muscle damage slowly accumulates over years.
Click here to see the diagram by Dr. Barber at Pikeville College, KY. (From the website: http://www.embl-heidelberg.de/CellBiophys/LocalProbes/motorproteins/myosin.html#microbiology)
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Muscle is an excitable tissue, meaning that it can be stimulated mechanically, chemically or electrically to produce an action potential. An action potential is an electrical change across a cell membrane due to changes in the conduction of ions across the membrane. Nervous tissue is also an excitable tissue. Muscle cells contain a contractile mechanism that is activated by action potentials. There are about 630 muscles in the human body. About 40% of the body is skeletal muscle, add another 5-10 % for cardiac and smooth muscle.
Contraction by a whole muscle:
Isometric versus Isotonic: Isotonic contractions are those when the tension on a muscle remains constant but the muscle shortens as in lifting a static amount of weight. Isometric muscle contractions occur when the muscle doesn't shorten as, for example when pushing against an immovable object like a wall. Isometric contraction differs from isotonic in that the myofibrils don't slide over each other much as force is developed. Sliding does occur in isotonic contractions and external work is performed.
Motor unit concept: The motor nerve and all the fibers it innervates is called the motor unit. The number of fibers is dependent on the necessity for fine control. In general, small muscles that react rapidly with fine control have one nerve and only a few muscle fibers. Those muscles that do not require fine control, such as the gastrocnemius (calf muscle), may have several hundred muscle fibers per motor unit.
Summation: The contraction of individual muscle fibers is all-or- none. Therefore, any graded response must come from the number of motor units stimulated at any one time. Summation is the adding together of individual muscle twitches to make a whole muscle contraction. This can be accomplished by increasing the number of motor units contracting at one time (spatial summation) or by increasing the frequency of contraction of individual muscle contractions (temporal summation). These processes almost always occur simultaneously within normal muscle contraction. Usually, individual motor units fire asynchronously.
All motor units are not created equal. Therefore one motor unit within a particular muscle may be as much as 50 times as strong as another. Smaller motor units are much more easily excited than larger ones because they are innervated by smaller nerve fibers that have a naturally lower threshold for excitation. In spatial summation motor units are recruited by increasing the strength of the stimulus thereby increasing the strength of the contraction.
In temporal or wave summation the rapidity of each motor units contraction increases such that one contraction isn't completely over when the stimulus for the next arrives. So the force generated in the first is added to that generated by the second, third and so on. When a muscle is stimulated at progressively greater frequencies, a frequency is finally reached at which the successive contractions fuse together and cannot be distinguished one from the other. The muscle then enters a long continual state of maximal contraction called tetany.
Muscle Fatigue: Prolonged strong contractions leads to fatigue of the muscle caused by the inability of the contractile and metabolic processes to supply adequately to maintain the work load. The nerve continues to function properly passing the action potential onto the muscle fibers but the contractions become weaker and weaker due to the lack of ATP.
Hypertrophy: Muscle hypertrophy (increase in muscle mass) is caused by forceful muscular activity. The diameters of individual fibers increase, nutrient and metabolic substances increase, mitochondria may increase, and the myofibrils also increase in size and number. Muscular hypertrophy increases the power for muscle contraction and nutritive mechanisms for motioning that increased power. Forceful muscle activity, above 75% of maximal, is necessary to produce hypertrophy which is why isometric exercise for even short periods of time can have profound effects on muscle mass. However, prolonged light exercise increases endurance, causing increases in oxidative enzymes, myoglobin, and even blood capillaries.
Atrophy: Muscle atrophy results when a muscle is not used for a length of time or is used for only weak contractions. For instance, atrophy occurs when limbs are put in casts. As little as one month of disuse can sometimes decrease the muscle size to one half normal. Damage to the nerve to a muscle results atrophy a well. If the damage is repaired in the first 3-4 months the muscle will regain full function. After four months muscle fibers will have degenerated to fibrous and fatty tissue.
Muscle Types and Mechanism of Contraction
Skeletal Muscle
Skeletal muscle makes up most of the body's muscle and does not contract without nervous stimulation. It is under voluntary control and lacks anatomic cellular connections between fibers. The fibers (cells) are multinucleated and appear striated due to the arrangement of actin and myosin protein filaments. Each fiber is a single cell, long, cylindric and surrounded by a cell membrane. The muscle fibers contain many myofibrils that are made of myofilaments. These myofilaments are made of the contractile proteins. The key proteins in muscle contraction are myosin, actin, tropomyosin and troponin.
Skeletal muscle fibers have differences in metabolic and contractile properties. Type I fibers are mostly found in the muscle for posture as in the long muscles of the back. These are also called red muscles because the fibers contain many mitochondria that give the muscle more of a dark reddish hue. White muscles contain mostly Type IIB fibers and are specialized for fast, fine movements as in the muscles that move the eye or some hand muscles. The differences in fiber type occur because of differences in amino acid composition of the skeletal proteins without a change in biologic activity. Various forms of the proteins can be expressed thus determining the functional characteristics of each muscle. Changes in muscle function can be caused by alterations in activity (training), hormonal environment (steroids), or innervation. Skeletal muscle can undergo a limited regeneration in case of injury via satellite cells that are located on the periphery of the muscle fiber. These cells may be active in muscle hypertrophy as well. Contractile Proteins
Skeletal muscle is composed of cells, called fibers, that are specialized to contract or shorten in length. Each fiber is made of smaller subunits called myofibrils that are composed of contractile proteins called myosin and actin which are responsible for muscle contraction at the molecular level. These contractile protein filaments are also called thick (myosin) and thin (actin) filaments. These filaments interdigitate such that the proteins can interact. The myosin filaments have what are called cross bridges that stick out from the filament to interact with the actin filaments during contraction. Imagine a set of golf clubs held together by their shafts with the heads radiating out around the shafts. This is a visual picture of what the thick filaments look like. Because the clubs have different length shafts the heads stick out at different places along the cluster. The myosin filaments look like this on both ends of a long filament that is made of some 200 myosin protein molecules. This structure allows the myosin filament to pull the actin filaments from both directions thus shortening the fiber.
The actin filaments are composed of two strands of protein that are woven together as one. The actin filaments are anchored to Z lines that make the boundaries of the functional unit of muscle contraction called the sarcomere. There are many sarcomeres in a muscle fiber and Z lines are continuous across muscle fibers.
Sliding Filament Theory:
Muscle contraction occurs by a sliding filament mechanism whereby the sarcomeres shorten (the Z-lines come closer together) by the action of the actin filaments sliding over the myosin filaments. Myosin filaments may look somewhat like a golf club but they are not inflexible. In fact, muscle contraction would be impossible if the myosin molecules did not have a "hinge" along the shaft that allows for a ratchet movement of the head. The force behind muscle contraction is the ratchet movement of these tiny myosin heads toward the center of their sarcomere. This ratchet movement occurs many times during a muscle contraction.
The thin filaments are actually composed of more than just actin which forms the backbone of the filament. Two other proteins are part of the thin filaments, tropomyosin and troponin. Along the actin filaments there are active sites where myosin attaches during contraction. These active sites are covered in the relaxed state by tropomyosin so that contraction cannot occur. Troponin is a complex of three submits having different affinities. One has an affinity for actin, another for tropomyosin and a third for calcium. Troponin molecules are positioned along the actin- tropomyosin filaments and act to position the tropomyosin filaments over the active sites on the actin filaments. When calcium is present it binds to the troponin which changes in shape causing the movement of tropomyosin off the active sites so that myosin and actin can interact and muscle contraction can occur. When the active sites are uncovered the myosin heads bind to the sites which initiates a movement of the head toward the center of the sarcomere thus pulling the actin along and shortening the sarcomere. Each one of the myosin heads is thought to operate independently of the others, each attaching and pulling in a continuous alternating ratchet cycle until the calcium is removed and the active sites are covered up again.
Muscle contraction requires a great deal of energy. Energy is required to break the bond between the myosin head and the actin active sites as well as for removal of calcium from the cytoplasm by the use of a special pump within the sarcoplasmic reticulum. When the myosin head is tilted forward, after the power stroke, a binding site for ATP (the chief energy currency of the cell) is exposed. The breakdown of ATP to ADP releases the head from the actin filament and cocks it for the next ratchet power stroke.
Energy Sources
Energy is required for muscle contraction. At rest and during light exercise, muscles use lipids as their energy source. The use of carbohydrate becomes more important as the intensity of exercise increases. The breakdown of glucose to water and carbon dioxide generates energy that is transferred to regenerate phosphorylcreatine and ATP. When oxygen supplies are inadequate this process is short circuited and a metabolite (lactic acid) of one of the products builds up in the muscle. This is called anaerobic metabolism (glycolysis) and is a normal process that can occur prior to the oxidative breakdown of glucose. The lactate builds up in the muscles causing a change in pH that inhibits enzyme activity. After the exercise, an oxygen debt exists in that oxygen must be used to convert the lactate into carbon dioxide and water and replenish energy stores. Short intense exercise utilizes anaerobic metabolic mechanisms more than more sustained activities. For example, in a 100 m dash 85% of the energy is derived from anaerobic means while in a mile run only 20% is generated anaerobically.
Excitation-Contraction Coupling:
Contraction in skeletal muscle begins with an action potential in the muscle fiber. This causes the release of calcium from the sacroplasmic reticulum. The action potential in the muscle fiber begins after it is excited by interaction with a large insulated (myelinated) nerve fiber. The point of contact of the nerve and muscle is called the neuromuscular junction which is normally located in the middle of the muscle fiber. Therefore an action potential initiated here spreads toward the ends of the fiber making it possible for all sarcomeres to contract at the same time. Skeletal muscle has an adaptation that allows the action potential to spread deep within the fiber. The T or transverse tubules are internal extensions of the sarcolemma that penetrate through the fiber such that action potentials in the t-tubules cause the release of calcium from the nearby sarcoplasmic reticulum in the immediate vicinity of the myofibrils.
The sarcoplasmic reticulum contains calcium ions in very high concentration that are released when the adjacent T-tubule is excited. Pumps within the walls of the sarcoplasmic reticulum return the calcium within the cytoplasm to levels below those needed to activate the contractile process.
Neuromuscular Junction:
The association of the motor nerve and the muscle fiber occurs at the neuromuscular junction. Here, the neuron ends in a terminal button that contains small vesicles filled with the neurotransmitter acetylcholine. When an action potential reaches the terminal button the vesicles are released and the acetylcholine diffuses across a narrow space to bind to receptors on the muscle fiber cell membrane. When the acetylcholine binds to the receptors, the local permeability of the muscle cell membrane is altered so that an action potential is initiated on the muscle cell. This action potential then spreads over the muscle cell membrane and T-tubule system to initiate the contractile process. An enzyme called acetylcholinesterase is present within the neuromuscular junction to break down the acetylcholine and remove the stimulus to contract.
Smooth Muscle:
Smooth muscle is found in the walls of blood vessels, tubular organs such as the stomach and uterus, the iris, or associated with the hair follicles. It exists in the body as multiunit or visceral smooth muscle. It is not under voluntary control, each cell has one nucleus and it is displays automaticity in the visceral form. In multiunit smooth muscle each cell exists as a discreet independent unit that is innervated by a single nerve ending. Visceral smooth muscle exists as a sheet or bundle of fibers that are intimately connected by junctions that allow ions to flow freely and it therefore performs as a syncytium. Therefore, when one portion of visceral smooth muscle is stimulated the action potential spreads to all other fibers.
Most of the same contractile proteins are present and active in smooth muscle contraction but they are not arranged as microscopically visible parallel myofilaments as in skeletal muscle. The contractile mechanism is very similar to skeletal muscle except that the myosin of smooth muscle only interacts with actin when it has been phosphorylated. In smooth muscle calcium binds to a protein called calmodulin and the complex then interacts with an enzyme that adds a phosphate group to myosin thus activating it.
In smooth muscle, T-tubules are absent, the sarcoplasmic reticulum is poorly developed and the calcium pump is present but it is slower acting. Because of these differences in the contractile mechanism and machinery, smooth muscle takes about 30 times as long to contract and relax as does skeletal muscle and it does this while using much less energy. Elaborate neuromuscular junctions are not present in smooth muscle. Often neurotransmitter is released only in close proximity to the muscle such that the neurotransmitter, which may be acetylcholine or norepinephrine, must diffuse to the muscle cells to interact with receptors on the cell membrane. Either of these neurotransmitters may be excitatory or inhibitory depending on the receptors present on that particular smooth muscle cell. Because smooth muscle has spontaneous activity, neuronal input only serves to modify that activity rather than initiating it as in skeletal muscle. Local tissue factors, hormones and mechanical stretch can cause action potentials and thus contraction in smooth muscle. Smooth muscle is capable of active regeneration after injury.
Cardiac Muscle:
The heart is made of specialized muscle tissue with some similarities to both smooth and skeletal muscle. It is involuntary and mononucleate as is smooth muscle. Cardiac muscle is striated like skeletal muscle which means that it has microscopically visible myofilaments arranged in parallel with the sarcomere structure described above. These filaments slide along each other during the process of contraction in the same manner as occurs in skeletal muscle.
Cardiac muscle fibers branch and have a single nucleus per cell. Another difference in cardiac muscle is the presence of intercalated discs that are specialized connections between one cardiac muscle cell and another. These tight connections allow for almost completely free movement of ions so that action potentials can freely pass from one cell to another. This makes cardiac muscle tissue a functional syncytium. When one cell is excited the resultant action potential is spread to all of them. This is an important feature in that it allows the atrial or ventricular muscle to contract as one to forcefully pump blood. Action potentials in cardiac muscle are also specialized to maximize the pumping function of the heart. They last 10 to 30 times as long as those of skeletal muscle and cause a correspondingly increased period of contraction. Cardiac muscle had long been said to have no regenerative capacity beyond early childhood. Recently, however, evidence has been found to debunk this statement. There is strong evidence that human heart muscle regenerates to some degree by myocyte replication after cardiac injury.
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There are a number of excellent web pages available. Please see them for more in-depth material.
http://www.daviddarling.info/encyclopedia/S/skeletal_muscle_groups.html
http://www.daviddarling.info/encyclopedia/M/muscular_system.html
http://www.daviddarling.info/encyclopedia/M/muscle_contraction.html
Upper Extremity Muscle Atlas: http://www.rad.washington.edu/atlas/extpollbrevis.html
http://www.indstate.edu/thcme/mwking/muscle.html#intro
http://www.mpimf-heidelberg.mpg.de/~holmes/muscle/muscle1.html
Muscle Physiology Lab at the University of California, San Diego.
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Muscle tissue -- constitutes the bulk of the carcass of meat animals.
Skeletal muscle -- of principal interest to the meat industry. Muscle that is attached directly or indirectly to the skeleton.
Cardiac muscle -- muscle of the heart. Differentiated by the presence of intercalated disks.
Smooth muscle -- located in arteries and the lymph system as well as the digestive and reproduction systems. No real ordered
myofibrils and thus nonstriated appearance.
Skeletal muscle fiber terms
Sarcolemma -- membrane surrounding the muscle fiber.
Transverse tubules -- portion of the sarcoplasmic reticulum that stores and releases calcium during contraction and relaxation.
Myoneural junction -- where motor nerve endings terminate on the sarcolemma.
Motor end plate -- structure present at the myoneural junction that forms a small mound on the surface of the muscle fiber
Sarcoplasm -- cytoplasm of muscle fibers.
Nuclei -- "brain" of the cell. Muscle fibers contain many nuclei.
Myofibrils -- long, thin, cylindrical rods that run within and parallel to the long axis of the muscle
fiber.
Myofilaments -- comprised of thick and thin filaments. The thick are comprised of myosin and the thin are comprised of actin,
troponin, and tropomyosin.
Sarcomere -- the basic contractile unit of the muscle. Has Z-lines on either end along with A-band and two 1/2 I-bands.
Z-disk ultrastructure -- comprised of Z filaments. These are the connecting units between sarcomeres.
Proteins of the myofilament -- primarily actin and myosin (65% of total), but also include tropomyosin and troponin within the thin filament, C protein (which surrounds the myosin filaments to form the thick filaments), desmin (which encircles the Z disks and radiate out to connect adjacent myofibrils
Sarcoplasmic reticulum and T tubules -- membranous system of tubules and cisternae (flattened reservoirs for Ca++) that forms closely meshed network around each myofibril.
Mitochondria -- "powerhouse of the cell." Provides the cell with chemical energy.
Lysosomes -- small vesicles located in the sarcoplasm that contain a large number of enzymes collectively capable of digesting the cell and its contents. The best known of these are the cathepsins.
Golgi complex -- many of these are located in the muscle fiber and serve the same purpose as those in regular cells.
Connective tissue
Extracellular substance -- varies from a soft jelly to a tough fibrous mass.
Connective tissue proper -- fibrous connective tissue that surrounds muscles, muscle bundles and muscle fibers.
Supportive connective tissues -- bone and cartilage.
Ground substance -- viscous solution containing soluble glycoproteins (carbohydrate containing proteins) where the extracellular fibers are embedded.
Extracellular fibers -- Primarily comprised of collagen, elastin, and reticulin.
Adipose tissue
White versus brown fat -- most of adipose tissue in meat animals is white fat. Brown fat is mostly present in animals at birth.
Bone
Diaphysis -- long, central shaft of the bone.
Epiphyses -- enlargements on the ends of bones.
Periosteum -- thin membrane connective tissue covering of bone.
Articular cartilage -- present on the ends (joint) of bones. Comprised of hyaline cartilage.
Epiphyseal plate -- cartilaginous region separating the diaphysis and epiphysis.
Above from: http://savell-j.tamu.edu/structure.html
Size
Maximus=largest
Minimus=smallest
Longus=longest
Brevis=shortest
Number of origins
Biceps=two origins
Triceps=three origins
Quadriceps=four origins
Relative shape
Deltoid=triangular
Trapezius=trapezoid
Serratus=saw-toothed
Rhomboideus=rhomboid or diamond-shaped
Classification of Muscle Actions
-abductor = moves body part out
-adductor = draws body part in
-extensor = opens joint out (increases the angle at a joint)
-flexor = closes joint (decreases the angle at a joint)
-levator = raises a body part - upward movement
-depressor = lowers a body part - downward movement
-pronator = turns the palm downward
-supinator = turns the palm upward or anteriorly
-rotator = moves a bone around its longitudinal axis
-sphincter (constrictor) = decreases the size of an opening
-tensor = makes a body part more rigid
Muscles that cause a joint to move away are abductors. Abduction refers to movement of a limb away from the central line of the body. Muscles that carry out this type of movement are called "abductor muscles."
Muscles that cause a joint to move back are adductors. Adductor muscles move a limb toward the central line of the body.
Muscles that cause a joint to extend are extensors. Muscle extension occurs when the angle between the bones is increased - as when the arm is extended in a handshake. An extensor is any muscle serving to extend a bodily part.
Muscles that cause a joint to bend are flexors. A flexor muscle is one which decreases the angle between two bones, as in bending the arm at the elbow; raising the leg toward the stomach as in kicking a football; or bringing the lower leg up toward the thigh.
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I highly recommend the reader investigates the outstanding site on musculature and the descriptions available on Wikipedia at the following link: http://en.wikipedia.org/wiki/List_of_muscles_of_the_human_body
-Pectoralis major = adducts humerus (long bone of the arm, extending from shoulder to elbow.)
-Rectus Abdominus = produces trunk motions
-Trapezius = elevates and rotates scapula (the shoulder blade bone)
-Latissimus dorsi = rotates humerus
from: http://www.landholt.com/3d/leg_muscles/
-Sartorius = flexes hip and knee-Deltoid = abducts arm
-Biceps brachii = flexes forearm, supinates (turns or rotates) the forearm so that the palm faces up or forward.
-Triceps brachii = extends forearm
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There are several excellent web sites listing and showing all of the muscles.
Here is a comprehensive site:
http://www.meddean.luc.edu/lumen/MedEd/GrossAnatomy/ From there, click on master muscle list.
The Hosford Muscle Tables (a comprehensive site):
http://www.ptcentral.com/muscles/
LUMEN's Master Muscle List (a comprehensive site): http://www.meddean.luc.edu/lumen/MedEd/GrossAnatomy/dissector/muscles/mus_ue.html
I highly recommend the reader investigates the outstanding site on musculature and the descriptions available on Wikipedia at the following link: http://en.wikipedia.org/wiki/List_of_muscles_of_the_human_body
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An excellent book on muscles for the "general reader" has recently come out:
Prime Mover: A Natural History of Muscle
by Steven Vogel, Annette Deferrari (Illustrator) 2001 W.W. Norton Company; ISBN 0393021262
Here is a book review from Amazon.com
Beneath the skin of a human being's inner upper arm, some metaphorically minded ancient Greek once observed, lives a little mouse. In Latin, this imagined creature, evident in the bump of the biceps, was called musculus, the origin of our word muscle. It's a staggeringly complex animal, we learn from this vivid exploration of the muscular world--one that requires much care and feeding, and that repays that attention with endless, efficient energy.
Biologist and bioengineer Steven Vogel takes us deep within our bodies, observing humansand other animals at rest and work to show how muscles expand and (sort of) contract, how our proprioceptive system coordinates that motion, how bodily mass relates to metabolism, and many other matters. Muscle is, of course, meat, and Vogel closes his book with a discussion of why meat has so long been prized in the human diet--and why today we can do without it and still keep the motor running.
Vogel's book is a fine example of how complex science can be made comprehensible to nonspecialists--and just the thing for a budding physiologist. --Gregory McNamee
A comprehensive textbook of muscles and their pathology (geared towards the expert):
Karpati, G., Hilton-Jones, D., Griggs, R. C. (Eds) (Seventh Edition) (2001). Disorders of Voluntary Muscle. Cambridge U. K.: Cambridge University Press.
From Book News, Inc. A comprehensive reference-text on disorders of muscle for clinicians, first published in 1964 and most recently in 1988. The structure of the previous edition is retained, with sections devoted respectively to anatomy, physiology, and biochemistry; pathology; clinical problems in neuromuscular disease; and electrodiagnosis. This updated edition adds two co-editors, George Karpati and David Hilton-Jones. Among the changes in this edition are new chapters on the cell biology of muscle; the molecular biology of muscle; the light microscopic morphological abnormalities in skeletal muscle disease; metabolic and endocrine myopathies; mitochondrial and lipid storage diseases of muscle; and myasthenia and related disorders.
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Most of this information is generic and can be found in most high school textbooks. The primary sources this material is based on are:
Encyclopaedia Britannica. http://www.britannica.com/
American Heritage Collegiate Dictionary. (via http://www.bartleby.com )
Columbia Encyclopaedia. (via http://www.bartleby.com )
Gray's Anatomy. (via http://www.bartleby.com )
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