Muscles and Muscle Tissue PDF

Muscles and Muscle Tissue In t his c hapter , you will learn that Muscles use actin and myosin molecules to convert the energy of ATP into force I ..., beginning w ith Overview of muscle types, special characteristics, and functions ..., next exploring I ..., and investigating "' I ...,...

Muscles and Muscle Tissue In t his c hapter , you will learn that Muscles use actin and myosin molecules to convert the energy of ATP into force I ..., beginning w ith Overview of muscle types, special characteristics, and functions ..., next exploring I ..., and investigating "' I ..., ..., and asking then asking 9.2 and then exploring • .J, • and How does smooth muscle differ from skelet al muscle? • r .J, - and - -finally, - -exploring - - - ., Developmental Aspects of L and - - - - - - - - ...J and CAREER CONNECTION and O Watch a video to learn how the chapter content is used in a real health ca re setting. Go to Mastering A&P® > Study A rea > Animations and Videos or use quick access URL https://goo.gl/88srfV 279 280 UNIT 2 Covering, Support, and Movement of the Body Card iac Muscle Because f lexing muscles look like mice scurrying beneath the skin, some scientist long ago dubbed them muscles, from the Latin nius meaning "little mouse." Indeed, we tend to think of the rippl ing muscles of professional boxers or weight lifters when we hear the word 111uscle. But muscle is also the dominant tissue in the heart and in the walls of other hollow organs. In all its forms, muscle tissue makes up nearly half the body's mass. Muscles are distinguished by their ability to transfonn chemical energy (ATP) into directed mechanical energy. In so doing, they become capable of exerting force. Cardiac muscle tissue occurs only in the heart, where it constitutes the bulk of the heart walls. Li ke skeletal muscle cells, cardiac muscle cells are striated, but cardiac muscle is not voluntary. Indeed, it can and does contract without being stimulated by the nervous sys tem. Most of us have no consc ious control over how fast our heart beats. • Key words to remember for cardiac muscle are cardiac, striGirvcleated ated, and involuntary. ↓ Cardiac muscle usually contracts at a fairly steady rate set by the heart's pacemaker, but neural controls allow the heart to speed up for brief periods, as whe n you race across the te nnis court to make that overhead smash. There are three types of muscle tissue Smooth Muscle Learning Outcomes Smooth muscle tissue is found in the walls of hollow visceral organs, such as the stomach, urinary bladder, and respiratory passages. Its role is to force flu ids and other substances through internal body channels. Smooth muscle also forms valves to regulate the passage of substances through internal body openings, d ilates and constricts the pupils of your eyes, and forms the arrector pili muscles attached to hair follicles. L ike skele ta l muscle, smooth muscle consists of elongated cells, but smooth muscle has no striations. Like cardiac muscle, smooth muscle is not subject to voluntary control. Its contractions are slow and sustained. II- Com pare and contrast the three basic types of muscle tissue. II- List fo ur important functions of muscle t issue. Types of Muscle Tissue Chapter 4 introduced the three types of muscle tissue-skeletal, cardiac, and snwoth ( <1111 pp. 138- 140). In this chapter, we first examine the structure and function of skeletal muscle. Then we consider smooth muscle more briefly, largely by comparing it \Vith skeletal muscle. We describe cardiac muscle in detail in Chapter 18, but for easy comparison, Table 9.3 on pp. 312-3 13 summarizes the characteristics of all three muscle types. Let's introduce some term inology before we describe each type of muscle. • We can describe smooth muscle tissue as visceral, non.striated, and involuntary. named in muscles "Sarcoplasmic • Skeletal and smooth muscle cells (but not card iac muscle cells) are elongated, and are called muscl e fibers. endoplasmic • reticulum" Characteristics of Muscle Tissue a ⑤ Whenever you see the prefixes 1nyo or 1nys (both are word What enables ,nuscle tissue to perform its duties? Four special important characteristics are key. mousin (Contractical facilitate between reticular is roots meaning "muscle") or sarco (flesh), the reference is to muscle. For example, the plasma me,nbrane of muscle cells is called the sarcolem111a (sar"ko-Jem'ah), literally, "muscle" (sarco) "husk" (lemma), and muscle cell cytoplasm is called sa rcoplas,n. Okay, Jet's get to it. Skeletal Muscle having Since[a actin and -> is essential and its • Excitability, also termed responsiveness, is the ability of a cell to receive and respond to a stimulus by changing its membrane potential. In the case of muscle, the stimulus is usually a chemical-for example, a neurotransmitter released by a be nerve cell. e recenters that bind technics stored there of recessed Slower ↑ large Arclecules agg are an membranes I > the ability to ofeffort, and the S contract will require certain amount ability of the sells to utilize ATD. whererates the ATR • Contr actility is the ab ility to shorten forcibly when adequately stimulated. T his ability sets muscle apart from all other tissue types. MadiateourrepbetweenIrelaxedoverloopsanerlur • Extensibility is the ability to extend or stretch. Muscle cells shorten when contract ing, but they can be stretc hed, even beyond their rest ing le ngth, when relaxed. back Skeletal 1nuscle tissue is packaged into the skeletal ,nuscles, from organs that attach toelongated and cover the skeleton. Skeletal muscle represent fibers are the lo ngest muscle cells and have obvious stripes the alligme< Relaxed restiny length Myo filamentscalled striations. Al though it is often activated by reflexes, • Elas ticity is the ability of a muscle cell to recoil and resume muscle is called voluntary 111uscle because it is the only actie/musin skeletal its resting length after stretching. heart amount of ATP getting cells type subj ect to conscious control. trop I there's consequences. like recoil if dfaster to its of the sufficient on in tropomyosin • When you think of skeletal muscle tissue, the key words to time keep in mind are skeletal, striated, and voluntary. Without and multi muscle exercise for long period of excessive not restiny nucleated and resume after contraction Muscle Functions or proper Skeletal muscle is responsible for overall body mobility. It can intake, Muscles perform at least four important functions for the all three contract rapidly, but it tires easily and n1ust rest after short periods eventually body: get of activity. Nevertheless, it can exert tremendous power. Skeletal Muscle • Produce movement. Skeletal ,nuscles are responsible for all muscle is also remarkably adaptable. For example, your forearm fatigue. locomotion and manipulation. They e nable you to respond muscles can exert a force of a fraction of an ounce to pick up a quickly to jump out of the way of a car, direct your eyes, and paper clip--0r a force of about 6 pounds to pick up this book! smile or frown. On Will muscle cells May go through the cellular components or acids generated when muscle cell dont have enough (they will be able ATR to contract but there will be a drawback) in the muscle function usofto ions Masks in summary Skeletal long, muscles # stricted, Multialted Smooth ↓ key : term "spindle shape from its muscles toT end packed making together closely :stricted, veinin and connected interculated discs more name cardiac muscle with (has * ** (specialized functions I for fast communication because heart muscles contract constantly, ( sheets than one) Sympathetic and nervous Control few With out you knowing Smooth and Cardin muscle ~athelete system unconsciously desirable more parasympathetic has one which or - engage all A they specific part on enlarging it work body building of muscles Chapter 9 Muscles and Muscle Tissue brokhwlard -> S contraction Since skeleful completely disagrees about that muscles Blood courses through your body because of the rhythmically beating cardiac muscle of your heart and the smooth muscle in the walls of your blood vessels, which helps maintain blood pressure. Smooth muscle in organs of the digestive, uri nary, and reproductive tracts propels substances (foodstuffs, uri ne, semen) through the organs and along the tract. Since they're the flesh of the called body • Ma inta in posture a nd bod y position. We are rarely aware of the skeletal muscles that maintain body posture. Yet these muscles function almost continuously, maki ng o ne tiny adj ustment after another to cou nteract the never-ending dow nward pull of slain, there layers, (epidermis, dermis, gravity. Whenever hypodermis/adipose) there's muscle, face, skeletal muscles you see are the even • Sta bilize joints. Even as they pull o n bones to cause movement, they strengthen and stabilize the joints of the skeleton. elbow, knee, wrists. Support by skeletal muscles, facilitate joint Contract d & Kinetic d beat movement (a) • Generate heat. Muscles generate heat as they contract, which plays a role in mainvasoconstriction taining normal body temperature. vasodilation - - - mediated by muscles Check Your Understanding 1. When describing muscle, what does "striated" mean ? 2. At right are photomicrographs of three types of muscle tissue (introduced in Chapter 4). For each, identify the type of muscle, state whether it is striated, whether it is volunta ry, and its major location. Create a short table that summarizes this information. -- - -··-· -------------===="'"'- For answers, see Answers Appendix. A skeletal muscle is made up of muscle fibers, nerves, blood vessels, and connective tissues (b) Learning Outcome ll> Describe t he g ross struct ure of a skeletal muscle. is migue individually separate Each skeletal muscle is a d iscrete organ, made up of several ki nds of tissues. Skeletal muscle fibers predominate, but blood vessels, nerve fibers, and substantial amounts of all con nective tissue are also present. We can easily examine a skeletal muscle 's shape and found there its attachments in the body without a microscope. in Nerve and Blood Supply nerve end waste managment accomplishingaftermuscle contractas -> ~ In general, one nerve, one artery, and o ne or more veins serve each muscle. These structures all enter or exit near the central part of the muscle and branch profusely through its con nective tissue sheaths (described below). Unlike cells of cardiac and smooth muscle tissues, which can contract without nerve stirn ulation, every skeletal rnuscle fiber is supplied with a nerve ending that controls its activity. Skeletal muscle has a rich blood supply. This is understandable because contracting muscle fibers use huge amounts of energy and require almost continuous delivery of oxygen and nutrients via the arteries. Musc le cells also give off large amounts of metabolic wastes that must be removed through veins if contraction is to remain effic ient. Capillaries, the smal lest of the body's blood vessels, take a Jong and winding path through muscle, and have numerous cross-links, features that accommodate changes in muscle length . They straighten when the muscle stretches and contort when the muscle contracts. Connective Tissue Sheaths In an intact muscle, there are several different connective tissue sheaths. Together these sheaths support each cell and reinforce and hold together the muscle, preventing the bulging muscles from bursting duri ng exceptionally strong contractions. (c) • - 281 outer & pi: 282 UNIT 2 Covering, Support, and Movement of the Body peri: around endo: inside Connecting Skeletal muscle S d needs a tendon Epim sium ↓ .~ -Muscle fiber in middle of a fascicle (b) separated bY ..-- - - - - -- S Blood vessel around Sheet covering the bridles of the muscle muscles & Pimy Sirm fascicles (Portion) perimysium (Coveringfusicleare s endomysium between (Covering the musefibers musclefibers ,.,-- Endomysium (between individual muscle fibers) Muscle fiber covering (a) muscle dense irregular t < C.t separating fasicles ↑ Figure 9.1 Connective tissue sheaths of ske letal muscle: epimysium, perimysium, (fascicle outerlayer and endomysium. (b) Photomicrograph of a cross section of part of a skeletal muscle (30X). separating muscle fibers Attachments Let's consider these connective tissue sheaths from external to internal (see Figure 9 .1 and the top three rows of • Epimysium. The epimysiu1n (ep''i-mis' e-um; "outside the muscle") is an "overcoat" of dense irregular connective tissue that surrounds the whole muscle. Sometimes it ble nds with the deep fascia that lies bel\veen neighbori ng muscles or the superficial fascia deep to the skin (~ p. 151). as epi my Swim • Endomys ium. The endo1nysium (en"do-mis'e-um; "within the muscle") is a wispy sheath of con nective tissue that surrounds each individual muscle fiber. It consists of fine areolar connective tissue. As shown in Figure 9. l , all of these connective tissue sheaths are continuous with one another as well as with the tendons that join muscles to bones. When muscle fibers contract, they pull o n these sheaths, which transmit the pulling force to the bone to be moved. The sheaths contribute somewhat to the natural elasticity of muscle tissue, and also provide routes for the entry and exit of the blood vessels and nerve fibers that serve the rnuscle. your ever hand muscles you're you have (Connection movingones of attainment and Recall from Chapter 8 that most skele tal muscles span joints and attach to bones (or other structures) in at least two places. When a muscle co ntracts, the movab le bone, the muscle's insertion, moves toward the immovable or Jess movable bone, the rnuscle's origin. In the muscles of the limbs, the origin typiknown cally lies prox irnal to the insertion. Muscle attachments, whether orig in or insertion, may be d irect or indirect. Table 9.1 ) . • Pe rimysium a nd fascicles. Within each skeletal muscle, the muscle fibers are grouped into fascicles (fas'T-klz; "bund les") that resemble bundles of st icks. Surrounding each fascicle is a layer of dense irregular connective tissue called perimysium (per''i-mis' e-um; "around the muscle"). ↳ same When Origin is Origin from f shoulder plates o elbow ↓ & insertion to be the proximal to the insertion layer of the muscle outer most • In direct, or fleshy, attachments, the epimysium of the muscle is fused to the periosteum of a bone or perichondrium of layer layer a cartilage. tillage directly • In indirect attachn1ents, the rn uscle's connective tissue wrapS pings extend beyond the muscle either as a ropelike tendon from outer must of the Must Common d said Uc need 7o know more than that bon Outer most car of the (Figure 9. Ia) or as a sheetlike a poneurosis (ap"o-nu-ro' sis) (see Figure l 0. l 2a on p. 347). The tendo n or a po neurosis anchors the muscle to the connective tissue covering of a skeletal element (bone or cartilage) or to the fascia of other On muscles. Ind irect attac hments are much more commo n because of thei r durability and small size. Tendons are mostly tough collagen fibers, which can withstand the abrasion of rough bony projections that would tear apart the more delicate muscle tissues. Because of their relatively small size, more tendons tha n from muscle to bone/curtillage to muscle tendons aP onerosis to bone/cartillage S 283 Chapter 9 Muscles and Muscle Tissue Table 9.1 Structure and Organizational Levels of Skeletal Muscle STRUCT URE AND ORGANIZATIONAL LEVEL Muscle (organ) Contain many muscle bliegel, and neuromuscular junctions A muscle consists of hundreds to tho usands of muscle cells, plus connective t issue wrappings, blood vessels, and nerve fibers. to be establishanatomres forbers were Muscle I Pristing I ⑤@ fascicles DESCRIPTION we expect Epimysium CONNECTIVE TISSUE WRAPPINGS or Covered externally by the epimysium each muscle hisfusicles Fascicle (a portion of the muscle) G Part of fascicle 1----: A fascicle is a discrete bundle of muscle cells, segregated from the rest of the muscle by a connective tissue sheath. UC @S bentle fam I Contain hundreds muscle Muscle fiber Muscle fiber (cell) Muscle enclosed b represents -> S endemyscie and under in Surcolemma fibers by muscle new the Part of muscle fiber G fiber in Myofibril a cell membrane membrane, has Stimelesting affect Within muscle Surro unded by endomysium cell Should be (wrapped of A muscle fiber is an elongated multi nucleate cell; it has a banded (striated) appearance. Nucleus - - by muscle Likers fascicle perimyrsin cell of each Surro unded by perimysium sad components, enclosing them estorage mere ensuringas and moveunce every by inside all cellular enter to layers 7-table and side to inner way of it by f twirle nerve layers R releasing All to receptors enter to and F-tubule and side SR signal high ↓ Sucroplasm d to inner Cytoplasm ways of muscle - organelle Myofibrils are rodlike contractile elements s.6.4.0y etc lot that occupy most of the muscle cell volume. Sacromeres Composed of sarcomeres arranged end to end, they appear banded, and bands of adj acent myofibrils are alig ned. Myofibril (complex o rganelle composed of bundles of myofilaments) - a each myofibril Will Contain Many sucremeres Contracting Unit in one & any given muscle Sarcomere cell of the most important cellular component Sarcomere (a segment of a myofibril) A sarcomere is the contractile un it, composed of myofilaments made up of contractile proteins. Sarcomere / actin Thin (actin) filament one of Thick filament Myrsin Thick (myosin) filament Myofilament, or filament (extended macromolecular structure) them should have the ability to breakdown AtP needs support from an enzyme that Can Convert Atr poit & represent - S represent or when muscles sent wasting S release energy -> major Changes happen ADR to Contractile myofilaments are of two typesthick and thin. Thick f ilaments contain bundled myosin molecules; th in fi laments contain actin molecules (plus other proteins). The slid ing of the thin f ilaments past the thick filaments produces muscle shortening. Elastic filaments (not shown here) provide elastic recoil when tension is released and help maintain myofilament o rganization. it won't be able to contract Ca27 Compare fa of fiber 284 UNIT 2 Covering, Support, and Movement of the Body fiber, the dark A bands and light I bands are nearly perfectly aligned, giving the cell its striated appearance. As illustrated in Figure 9.2c: fleshy muscles can pass over a joint-so tendons also conserve space. Check Your Understanding • Each dark A bru1d has a lighter region in its midsection called the H zone (H for helle; "bright"). 3. How does the term epimysium relate to the role and position of th is connective tissue sheath? What is the difference between a tendon 4. and a ligament? (Hint: See Chapter 4, p. 133.) • Each H zone is bisected vert ically by a dark line called the M line (M for middle) formed by molecules of the prote in myomes1n. -==---------" For answers, see Answers Appendix. • Each light I band also has a midline interruption, a darker area called the Z disc (or Z line). Skeletal muscle fibers contain calcium-regulated molecular motors Sarcomeres has to have the ability to store and release calcin, and rsetlements The region of a myofibril between two successive Z discs is a need to know the sa rcomer e (sar'ko-mer; "muscle segment"). Averaging 2 µm Learning Outcomes for units to II- Describe the microscopic structure a nd functional roles of contract Jong, a sarcomere is the smallest contractile un it of a muscle the functional unit of skeletal muscle. It contains an A t he myofibrils, sa rcoplasmic reticu lum, a nd T tubules of (overlapbetweenfiberS band flanked by half ru1 I band at each end. Within each myofiskeletal muscle fibers. bril, the sarcomeres align end to e nd like boxcars in a train. II- Describe the slid ing filament model of muscle contraction. to breakdown ATP to go back to normal all one component act in Each skeletal muscle fiber is a Jong cylindrical cell with mul tiple oval nuclei j ust beneath its sarcole1nma or plasma membrane (Figure 9 .2b). Skeletal muscle fibers are huge cells. Their d iruneter typically ranges from JO to JOO µm-up to ten times that of an average body cell-ru1d their length is phenomenal, some up to 30 cm Jong. T he ir large size ru1d multiple nuclei are not surprising once you learn that hundreds of embryonic cells fuse to produce each fiber. Sa r coplasm , the cytoplasm of a muscle cell, is similar to the cytoplasm of o ther cells, but it contains u nusually large amounts of glycosomes (granules of stored glycogen that provide glucose during muscle cell activity for AT P production) and 1nyoglobin, a red pigment that stores oxygen. Myoglobin is similar to hemoglobin, the pigment that transports oxygen in blood. In add ition to the usual organelles, a muscle cell contains three specialized structures: myofibrils, sarcoplasm ic ret iculum, and T tubules. Let's look at these structures rnore closely because they play important roles in muscle contraction. Myofibrils Many myofibrils necromuscularjunction will have the nerve Myofilaments If we examine the bandi ng pattern of a rnyofibril at the molecular level, we see that it arises from orderly arrru1gement of even smaller structures within the sarcomeres. These smaller structures, the 1n yofila1nents or fila,nents, are the muscle equivalents of the actin-contain ing microfilruuents and myosin motor prote ins described in Chapter 3 ( <Ill p. 88). As you will recall, the proteins actin and myosin play a role in motility and shape change in virtually every cell in the body. This property reaches its highest development in the contractile muscle fibers. There are two types of contractile myofilaments in a sarcomere: • The central thick filaments containing myosin (red) extend the entire length of the A band (Figure 9 .2c and d). They are ↳ connected in the middle of the sarcomere at the M line. arrangment • The more lateral thin fila,n ents containing actin (blue) extend across the I band and partway into the A band. The Z disc, a protein sheet, anchors the thi n filaments. We describe the third type of myofilament, the elastic fila,11e11t, in the next section. terminals A close look at myofibril arrangement and banding patterns A single muscle fiber contains hundreds to thousands of rod- maybe reveals that: like myofibr ils that run parallel to its length (Figure 9.2b). The • A hexagonal arrangement of six thin filaments surrounds each elements myofibrils, each 1-2 µm in diameter, are so densely packed in inside? thick filruuent, and three thick filaments enclose each thin filathe fiber that mitochondria and other organelles appear to be inside ment. This is shown in Figure 9.2e (far right), which shows a fusicles plante 80% of celsqueezed between them. They account for about cross section of a sarcomere in ru1 area where thick and thi n elements. lular volume. they contract filaments overlap. Myofibrils are made up of a chain of sarcomeres linked • The H zone of the A band appears Jess dense because the end to end. Sarco,neres (shown in Figure 9.2c and decribed thin fila,nents do not extend into this region. shortly) contain even smaller rodlike structures called r11yojila• The M line in the center of the H zo ne is sl ightly darker ,11ents. Table 9. 1 (bottom three rows; p. 283) summarizes these because of the fine protein strands there that hold adjacent system structures. thick filaments together. Stimulating S somewhere near, so is it going to penetrate through the C.T? along with Scrollema? or Medinte the whole are of all same time. S nerves one Striations fiber and stimulation goes deeper of muscle into the fibers Striations, a repeat ing series of dark and light bands, are evident along the length of each myofibri l. In an intact muscle • The myofilaments are he ld in alignment at the Z discs and the M lines, and are anchored to the sarcolemma at the Z discs. layers -> sacromere 285 Chapter 9 Muscles and Muscle Tissue (a) Photomicrograph of portio ns of two muscle fibers (700 X). Notice the striations (alternating dar1< and light bands). ... ............ . . I (b) Diagram of part of a muscle fiber showing the myofibrils. One myofibril extends from the cut end of the fiber. ------------------'.,,. Dark A band Light I band Nucleus , ---- - I Thin (actin) , , - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -' filament , , ' z disc z disc I (c) Small part of one myofibril enlarged to show the myofilaments responsible for the banding pattern. Each sarcomere extends from one Z disc to the next. Thick (myosin) filament I I ---------' • Overlap cross Zdisc (d) Enlargement of one sarcomere (sectioned lengthwise). I Part in h I band I band A band contraction, 1 - + - - - - Sarcomere - - - + -:' the M line ' -:::--~~t~::~!~~!i~=~=- other. M line •----------- each A goes absent - • r.h, 111 - -" · ~ - -~ !:::!!!!!!::j~ ' ••••• •••• I band thin filaments only Hzone thick filaments only Figure 9.2 Microscopic anatomy of a skeletal muscle fi ber. - ~fii4.- ~D~~~~- - (e) Cross sections of a sarcomere cut through in different locations. - '' ~ ~ Thin (actin) filament Elastic (titin) filaments ~ - - Thick (myosin) filament L- ~ ~ , - - Myosin filament ~ - - Actin filament -' - M line thick filaments linked by accessory proteins Outer edge of A band thick and thin filaments overlap UNIT 2 Covering, Support, and Movement of the Body 286 Longit udinal section of filaments within one sarcomere of a myofibril Zd~ r1-i r1-i .........--:-_Ill= .................... In the center of the sarcomere, the thick filaments lack myosin heads. Myosin heads are present only in areas of myosin-actin overlap. Thick filament Thin filament Each thick filament consists of many myosin molecules whose heads protrude at opposite ends of the filament A thin filament consists of two strands of actin subunits twisted into a helix plus two types of regulatory proteins (troponin and tropomyosin). Portion of a thick filament Portion of a thin filament - inhibitory Myosin h e a d ~ Tropomyosin - Proteins to move it facilitate Contraction returning Actin it to relaxing Cr State sirding releasein Actin-binding sites Tail ATPbinding site break I •- ~ ~ - Myosinbinding sites Flexible hinge region down AT4 Actin subunits Myosin molecule for Overlap Figure 9.3 Composit ion of th ick and t hin filaments. Contraction from CNS Motor nervous nevretrani & ng chemical opened ↓ junction between terminus S. end and Sacrofema -> M olecular Composition of Myofilament s Muscle contraction depends on the rn yosin- and actin-containing myofilaments. As noted earlier, thick filaments are composed pri marily of the protein myosin. Each myosin molecule consists of six polypeptide chains: two heavy (high-molecular-weight) fast is with by ACH. Casensed by opened by irns opposite, eliminate muscle cells Voltage gated Channels (Figure 9.3) . The globular heads, each associated with t\vo light chains, are the "business end" of myosin. During contraction, they link the Sudden - burst alot in Slow myoglobin one ↓ use energy fairly to slowly - "One submit" Cholding twitch and make it Act) action potential chai ns and four light chains. The heavy chains twist together to form myosin 's rodlike ta il, and each heavy chai n ends in a globular head that is attached to the tail via a flex ible hinge faster dealing needs and return free Ca twitch much when Creturning gated In Channels synapse last long Onl less infust twitch we sends of f of energy like jump 0, or Vcc ATP contracts and returns it Scentures actin gets "musked" to prevent contraction for and "relaxing" State in exac a -> What protein for muscle needed to be inactivated contraction? (Sliding theory Traponin orthosin b d Chapte r 9 Muscles and Muscle Tissue - needed to its blocking (a 287 binding be inactivated site, in order to expose it to facilitate Contraction th ick a nd thin filaments together, forming cr oss bridges, and swivel around their point of attachment, acting as motors to generate force. Myosin itself splits ATP (acts as an ATPase) and uses the released energy to drive movement. Each th ick filament contains about 300 myosin molecules bundled together, with their tails form ing the central part of the thick filament and the ir heads facing oul\vard at the e nd of each molecule (Figure 9 .3). As a result, the central portion of a thick filament (in the H zone) is smooth, but its ends are studded with a staggered array of myosin heads. The thin filaments are composed chiefly of the protein a ctin (blue in Figure 9.3). Actin has kid ney-sh aped polypeptide subunits, called globular acti11 or G actin. Each G actin has a ,nyosin-binding site (or active site) to which the myosin heads attach during contraction. G actin subunits polymerize into long acti n filaments called fila,11e111ous, or F, actin. l\vo intemvined actin filaments, resembl ing a twisted double strand of pearls, form the backbone of each thin filament (Figure 9.3). Thin fila,ne nts also contai n several regulatory proteins. .---""'- HOMEOSTATIC ..., A IMBALANCE 9.1 Praten or ↑ or gene mutated develops muscle weakness girls Y CLINICAi! 1l1e term muscnlar dystrophy refers to a group of inherited muscledestroying diseases that generally appear duri ng childhood. The affected muscles initially enlarge due to deposits of fat and connective tissue, but the muscle fibers atrophy and degenerate. The most common and serious form is Duchenne muscular d ystrophy (DMD), which is inherited as a sex-linked reces s ive disease. It is expressed almost exclusively in males (one in every 3600 male births) and is diagnosed when the boy is between 2 and 7 years old (Figure 9.4). Active, normalappeari ng boys become clumsy and fall frequently as their skeletal muscles weaken. The disease progresses relentlessly from the extrem ities upward, fi nally affecting the head and chest muscles, and cardiac muscle. The weakness continues to progress, but with supportive care, DMD patients are living into their 30s and beyond. • Polypeptide strands of tropon1yosi11 (tro"po- mi 'o-sin), a rodshaped protein, spiral about the actin core and help stiffen and stabi lize it. Successive tropomyosin molecules are arranged end to e nd along the acti n filaments, and in a relaxed muscle fiber, they block myosin-binding sites on actin so that myosin heads o n the thick filaments can not bi nd to the thin filaments. • Troponin (tro' po-nin), the other maj or prote in in thin filaments, is a globular protei n with three polypeptide subunits (Figure 9.3). One subu nit attaches troponi n to actin. Another subunit binds tropomyosin and helps position it on actin. The third subunit binds calcium ions. Both troponin and tropomyosin help control the myosin-actin interactions involved in contraction. Several other proteins help form the structure of the myofibril. • The elastic filament we referred to earlier is composed of the giant protein titin (Figure 9.2d). Titin extends from the Z disc to the thick filament, and then runs within the thick filament (forming its core) to attach to the M line. It holds the thick filaments in place, maintai ning the organization of the A band, and helps the muscle cell spring back into shape after stretching. (The part of the titin that spans the I bands is extensible, unfolding when the muscle stretches and recoiling when the tension is released.) Titin does not res ist stretching in the ordinary range of extension, but it stiffens as it uncoils, helping the muscle resist excess ive stretching, which might pull the sarcomeres apart. • Another important structural protein is d ystrophin, wh ich links the thin filaments to the integral proteins of the sarcolemma (\vhich in turn are anchored to the extracellular matrix). • Other proteins that b ind filaments or sarcomeres together and rnai ntain their alignment include 11ebulin, myo,nesin, and C proteins. Intermediate (desmin) filaments extend from the Z disc and connect each myofibril to the next throughout the width of the rn uscle cell. Figure 9.4 A boy w it h Duchenne muscular d ystro phy (DMD). Physiotherapy can help maintain mobility. DMD is caused by a defective gene for dystrophin, the cytoplasmic protei n described above. Dystrophin links the cytoskeleton to the extracellular matrix and, like a girder, helps stabilize the sarcolemma. The fragile sarcolemma of DMD patients tears during contraction, allowing entry of excess Ca2 + , which damages the contractile fibers . Inflammatory cells (macrophages and lymphocytes) accurnulate in the surrounding connective tissue. As the regenerative capacity of the muscle is lost, damaged cells undergo apoptosis, and muscle mass drops. There is still no cure for DMD. Current treatments are aimed at preventing or reducing spine and joint deformities and helping those with DMD remain mobile as long as possible. Two newly-approved drugs may broaden the treatment options for certai n patients. • •• • • should have 2 mutated x Y bays only on e no proper Muscle contruction Cardins, respiratory failure UNIT 2 Covering, Support, and Movement of the Body 288 I band Part of a skeletal muscle fiber (cell) I Z disc r A band I band H zone Z disc Myofibril -,-,;.,;=:....::'-,--,,...;.,;.,;~ ~,,..,:;~-'-- -• T tubule ~ ~.,..,..-- - -• Terminal cisterns of the SR (2) Sarcolemma I Figure 9.5 Relationship of t he sarcoplasm ic reticu lum and T t ubules t o myofibrils of skeletal muscle. The tubules of the SR (blue) fuse to form the saclike terminal cisterns next to the A·I junctions. The T tubules (gray) are inward invaginations of the sarcolemma that run deep into the cell between the terminal Sarcoplasmic Reticulum and T Tubules Skeletal muscle fibers contain two sets of intracell ular tubules that help regulate muscle co ntraction: (1) the sarcoplasmic reticulum and (2) T tubules. Sa rco p lasm ic Re t icu lum S hown in blue in Figure 9 . 5, the sa r coplas mic reticulum (SR) is an elaborate smooth e ndopl asm ic reticulum. The SR regulates intracell ular levels of ionic calcium. It stores calcium and releases it on demand when the muscle fiber is stimulated of her to contract. As you will see, calcium provides the final "go" signal for contraction. Interconnecting tubules of SR surround each myofibril the way the sleeve of a loosely knitted sweater surrounds your arm. Most SR tubules run longitudinally along the myofibril, commun icating with each o ther at the H zone. Others called terrn in al cisten1s ("end sacs") form larger, perpendicular cross channels at the A band-I band junctions, and they always occur in pairs. Closely associated with the SR are large numbers of mitochondria and glycogen granules, both involved in producing the energy used during contraction. AR T Tubu les At each A band-I band j unction, the sarcolemma of the muscle cell protrudes deep into the cell interior, forming an elongated tube called the T tub ule (T for "transverse"), shown in gray in Transverse to all fibril space cisterns. (See detailed view in Focus Figure 9.2, pp. 294- 295.) Sites of close contact of these three elements (terminal cistern, T tubule, and terminal cistern) are called triads. Figure 9.5 . The lunien (cav ity) of the T tubule is co ntinuous with the extracellular space. As a result, T tubules trernendously increase the muscle fiber's surface area. This allows changes in the membrane potential to rapidly penetrate deep into the muscle fiber. Along its length, each T tubule runs betv,een the paired terminal cisterns of the SR, forming triads (Figure 9.5), successive groupings of the three membranous structures (terminal cistern, T tubule, and termi nal cistern). As they pass from one myofibril to the next, the T tubules also encircle each sarcomere. Muscle contrac tion is ultimately controll ed by nerveinitiated electrical impulses that travel along the sarcolemma. Because T tubules are cont inuations of the sarcolemma, they conduct impulses to the deepest regions of the muscle cell and every sarcomere. These impulses trigger the release of calcium from the adjacent term inal cisten1s. Th ink of the T tubules as a rap id commun ication or messaging system that ensures that every myofibril in the muscle fiber contracts at virtually the same time. Triad Relationsh ips The roles of the T tubules and SR in providing signals for contraction are tightly lin ked. At the triads, membrane-spanning proteins from the T tubules and SR link together across the gap between the two membranes. • The protruding integral proteins of the T tubule act as voltage sensors. Chapte r 9 Muscles and Muscle Tissue • The integral proteins of the SR form gated channels through which the term inal cisterns release Ca2 + (see top right of Focus Figure 9.2 on p. 295). 289 1 Fully relaxed sarcomere of a muscle fiber - Sliding Filament Model of Contraction We almost always think "shortening" when we hear the word contraction , but to physiologists contraction refers only to the activation of myosin' s cross bridges, \vhich are the forcegenerat ing sites. Shortening only occurs if the cross bridges generate enough tension on the thin filaments to exceed the forces that oppose shortening, such as when you lift a bowling ball. Contraction ends when the cross bridges become inactive, the tension declines, and the muscle fiber relaxes. In a relaxed muscle fiber, the thin and thick filaments overlap only at the ends of the A band (Figure 9.6 G)). T he sliding fila1nent model of contr action states that during contraction, the thin filaments slide past the thick ones so that the actin and myosin filaments overlap to a greater degree. Neither the thick nor the thin filaments change length during contraction. Here's how it works: • When the nervous system stimulates muscle fibers, the myosin heads on the thick filaments latch onto myosin-binding sites on actin in the thin filaments, and the sliding begins. • These cross bridge attachments form and break several times during a contract ion, acting like tiny ratchets to generate tension and propel the thin filaments toward the center of the sarcomere. • As this event occurs simultaneously in sarcomeres throughout the cell, the muscle cell shortens. At the microscopic level, the following th ings occur as a muscle cell shortens: • The I bands shorten. • The distance between successive Z discs shortens. As the thin filaments slide centrally, the Z discs to which they attach are pulled toward the M line (Figure 9.6 @). • The H zones disappear. • The contiguous A bands move closer together, but their length does not change. Check Your Understanding 5. Name proteins a, b, c, and d. Which protein can act as an enzyme to hydrolyze (split) ATP? Wh ich bi nds Ca2 +? Wh ich must move out of the way in order for cross bridges to form? 6. Which region or organelle-cytosol, mitochondrion, or SRcontains the highest concentration of calcium ions in a resting muscle fiber? Which structure provides the ATP needed for muscle activity? • ,ti!• ....... y y ..~ '' -----' z • H z ' A @ Fully contracted sarcomere of a muscle fiber y .' .... ' z ••'' A ' .. y z ,- I • Fi gure 9.6 Sliding filament model of contraction. At full contraction, the Z discs approach the thick filaments and the thin filaments overlap each other. The photomicrographs (top view in G) and@) show enlargements of 33,000x . 7. l•);W/1 Draw four thick fi laments in each of two columns. Add a column of fou r thi n filaments between the th ick filaments, as they would appear in a relaxed myofibril. Then add two more col umns, each with four th in filaments, on the left and right sides of the original drawing. Label an A ba nd, an I band, and an H zone. Draw and label an M line and a Z disc. 8. Consider a phosphorus atom that is part of the membrane of the sarcoplasmic reticulum in the biceps muscle of your arm. Using the levels of structu ral organization (described in Chapter 1), name in order the structu re that corresponds to each level of organ ization. Begin at the atomic level (the phosphorus atom) and end at the organ system level. - - - - - - - - - - For answers, see Answers Appendix. 290 UNIT 2 Covering, Support, and Movement of the Body Ill Motor neurons stimulate skeletal muscle fibers to contract Learning Outcomes II- Explain how muscle fibers a re stimulated to contract by describing events that occur at the neu rom uscula r junction. II- Follow the events of excitation-contraction coupling that lead to cross bridge activity. II- Describe the steps of a cross bridge cycle. The sliding filament model tells us that myofilaments slide past each other as the sarcomeres contract. In this module, we will see exactly how th is happens. But before we begin, Jet's fill in some background information that will help you understand this topic, and then look at the big picture of how muscle contraction works. Background and Overview changes in the membrane potential (as we will see shortly). Receptors for acetylcholine are an example of this class. An ACh receptor is a single protein in the plasma membrane that is both a receptor and an ion channel. • Volta ge-gated ion channels open or close in respo nse to c hanges in membrane potential. They underlie all action potentials. In skeletal muscle fibers, the initial change in me,nbrane potential is created by chemically gated channels. In other words, chemically gated ion channels cause a small local depoVoltage-gated ion larh.ation (a decrease in the mem- channel brane potential) that then triggers the voltage-gated ion channels to create an action potential. (We will describe ion channels in more detail in Chapter 11.) Ion Channels Rapidly changing the membrane potential in neurons and muscle cells requires the opening and closing of membrane channel proteins that allow certain ions to pass across the membrane (<Ill p. 70). The movement of ions through these ion channels changes the Chemical messenger membrane voltage. 1\vo classes of ion (e.g., ACh) c hannels are important for exc itation and contraction of skeletal ,nuscle: Anatomy of Motor Neuro ns and t he Neurom uscu la r Junct ion Mo tor neurons that activate skeletal muscle fibers are called so,natic ,notor neurons, or nu>lor neurons of the somatic (voluntary) nervous syste,n (Figure 9.7). These neurons reside in the spinal cord (except for those that supply the muscles of the head and neck). Each neuro n has a Jong threadlike extension called an axon that extends from the cell body in the spinal cord to the muscle fiber it serves (<Ill see Chapter 4, p. 140, to review the parts of a neuron). These axons exit the spinal cord and pass throughout the body bundled together as nerves. The axon of each motor neuron branches profusely as it enters the ,nuscle so that it can innervate ,nultiple ,nuscle fibers. When it reaches a muscle fiber, each axon divides agai n, giving off several short, curling branches that collectively form an oval neuromuscular junction, or m otor end plate, with a single muscle fiber. Each muscle fiber has o nly one neuromuscular junction, located approx imately midway along its length. The end of the axon, called the axon ter1ninal, and the muscle fiber are exceedingly close (50-80 nm apart), but they remain separated by a space, the synaptic cleft (Figure 9.7), which is filled with a gel-like extracellular substance rich in glycoproteins and collagen fibers. Within the mou ndlike axon terminal are syna ptic vesicles, small membranous sacs contai ning the neurotransmitter acetylcholine. The trough-like part of the muscle fiber's sarcolemma that helps form the neuromuscular j unction is highly folded. These junctional folds provide a large surface area for the thousands of ACh receptors located there. To summarize, the neuromuscular junction is like a sandw ich: It is made up of part of a neuron (the axon term inals), part of a muscle cell (the junctional fol ds), and the "filler" between them (the synaptic cleft). • Chemically gated ion channels are opened by chemical messengers (e.g., neurotransmitters). This class of ion channel creates small local The Big Picture Figure 9.7 presents an overview of skeletal muscle contraction and divides this process into four groups of steps. We will Remember that skeletal muscle contractions are voluntary. For example, you decide when you want to co ntract your biceps muscle to pick up your cell phone. Making that decision involves many neurons in your brain, but the contraction of a skeletal muscle ultimately comes down to activating a few ,notor neurons in the sp inal cord. Motor neurons are the way that the nervous system connects wi th skeletal muscles and "tells" the,n to contract. Both neurons and muscles are excitable cells. That is, they respond to external stimuli by changing their resting membrane pote ntial. (Remember that all cells have a resting membrane potential, \vhich is a vol tage across the plasma membrane; <Ill pp. 79-80.) These changes in membrane potential act as signals. One type of electrical signal is called an action potential (AP ; sometimes called a nerve i,npulse). An AP is a large c hange in membrane pote ntial that spreads rapidly over Jo ng distances within a cell. Generally, APs don't spread from cell to cell. For this reason, the signal has to be converted to a c hemical signal-a chemical messenger called a neurotrans1niller (<Ill p. 81 ) that diffuses across the small gap between excitable cells to start the signal again. The neurotransmitter that motor neurons use to "tell" skeletal muscle to contract is acetylcholine (as"e-til-ko' len), or ACh. H ↓ With we can the cell Chemically gated ion channel enter Grvg) botox: temper mini Humbing (Bufiber) marrona prevents eyes of (K -3kSley Plurisis: Units C Mecotonic receptors after binding action potential spreads muscles fiber on the into the and into swhichContraction recessa binding contraction at all car all crass etc) motor units that are the muscle spas: managed A - no !useof muscularaction aretened Ache (after number of We all release Fluid Strength is by determined ↳ ori Palaisis Chapter 9 Muscles and Muscl e Tissue you Brain------ & 291 would expect least the Spinal cord---.._ reshold Minimum - - - - -Axon of \ motor neuron Charge enough for intake a The neuromuscular junction is the region where the motor neuron contacts the skeletal muscle. It consists of multiple axon terminals and the underlying junctional folds of the sarcolemma. a lot --- -- -- -- of Sequence of events leading to contraction: Axon of motor neuron A motor neuron fires an action potential (AP) down its axon. Ca The motor neuron's axon terminal releases acetylcholine (ACh) into the synaptic cleft. neuromuscular junction (see Focus Figure 9.1) voltage Ca EPP With - will be stimuli ACH AP in sarcolemma travels down T tubules. @ Excitation- explore each group of steps in more detail in the rest of this module: Sarcoplasmic reticulum releases Ca2 •. contraction coupling (see Focus Figure 9.2) binding site to be shown for - - allows Ca2 • binds to troponin, which shifts tropomyosin to uncover the myosin-binding sites on actin. Myosin heads bind actin . (see Focus Figure 9.3) actin Muscle fiber excitation. The EPP triggers an action potential that travels across the entire sarcolemma (see Figure 9.8 on p. 293). @ Excitation-contraction coupli ng (see Focus Figure 9.2 on pp. 294-295). The AP in the sarcolemma propagates along the T tubules and causes release of Ca2 + frorn the tenninal cisten1s of the SR. Ca2 + is the final trigger for contraction. It is the internal messenger that links the AP to contraction. Ca2 + binds to troponin and this causes the myosin-binding sites on actin to be exposed so that myosin heads can bind to actin. © Cross bridge cycling (see Focus Figure 9.3 on p. 297). The muscle contracts as a result of a repeating cycle of steps that cause myofilaments to slide relative to each other. vel my as in Contraction occurs via cross bridge cycling. Myo filaments overlap Figure 9.7 Overview of skeletal muscle contraction. Events at t he neuromuscular junction (see Focus Figure 9.1 on p. 292). The rnotor neuron releases ACh that stimulates the skeletal muscle fiber, causing a local depolarization (decrease in membrane potential) called an end plale potential (EPP). @ far myosin to kind on © Cross bridge cycle Cytoplasm of skeletal muscle fiber c->--Junctional folds of the sarcolemma G) the actin ~ to release The local depolarization (EPP) triggers an AP in the adjacent sarcolemma. S release ACh binding causes a local depolarization called an end plate potential (EPP). released @Muscle fiber excitation (see Figure 9.8) Ca enters to active energy ACh binds receptors on the junctional folds of the sarcolemma . enter inSM - need Outside ++f t gated Channels ACI G) Events at the Muscle Axon terminal of motor neuron sensed by voltage ------ When a nerve impulse reaches a Watch a 3·D an imat ion of t his process: MasteringA&P" > neuromuscular junction, acetylcholine (ACh) St udy Area > Animations & Videos > A&P Flix is released. Upon binding to sarcolemma "' receptors, ACh causes a change in sarcolemma ··~ - - - Axon of motor neuron permeability leading to a change in Action - - - -"....,. membrane potential. potential (AP) Axon terminal of neuromuscular junction I Sarcolemma of I the muscle fiber r J G) Action potentia l arrives at axon terminal of motor neuron. @ Voltage-gated Ca 2• channels open . Ca2• enters the axon terminal, moving down its electrochemica l gradient. Synaptic vesicle containing ACh the resides of ALI @ Ca 2• entry causes ACh (a neurotransmitter) to be released by exocytosis. © ACh d iffuses across the synaptic cleft and binds to ACh sarcolemma receptors on the sarcolemma. Sarcoplasm of muscle fiber @ ACh b ind ing opens chemically gated ion channels that allow simultaneous passage of Na• into the muscle fiber and-> K• out of action the muscle fiber. More Na• ions potential enter than K• ions exit, which produces a local change in the membrane potential called the end plate potential. @ ACh effects are term inated by its breakdown in the synaptic 1 - - - - - - - --1-----< cleft by acetylcholinesterase and diffusion away from the j unction. 292 _,,-; - - Postsynaptic membrane ion channel opens; ions pass. /"'"1-- Ion channel closes; ions cannot pass. Chapte r 9 Muscles and Muscle Tissue Open voltagegated Na+ channel ACh-containing synaptic vesicle Axon terminal of neuromuscular junction No -> entering Na~ 293 Closed voltagegated K + channel ..)v..J..) de Polarization Na5 K Wave of depolarization after ACH bind to receptors Q) An end plate potential (EPP) is generated at the - depolarization Walls -> occur neuromuscular junction (see Focus Figure 9.1). The EPP causes a wave of depolarization that spreads to the adjacent sarcolemma. @Depolarization: Generating and propagating an action potential (AP). Depolarization of the sarcolemma opens voltage-gated sodium channels. Na+ enters, following its elect rochemical gradient. At a certain membrane voltage, an AP is generated (initiated). The AP spreads to adjacent areas of the sarcolemma and opens voltage-gated Na+ channels there, propagating the AP. The AP propagates along the sarcolemma in all directions, just like ripples from a pebble dropped in a pond. ! Fig ure 9.8 Summa ry of events in the generation and propagation of an action potential in a skeletal muscle fiber. Open voltageClosed voltagegated Na+ channel gated K+ channel + ..) Na ..J..) ..).., Events at the Neuromuscular Junction +++ +++++ How does a motor neuron stimulate a skeletal muscle fiber? Focus on Events at the Neurornuscular Junction (Focus Figure 9.1) covers this process step by step. Study th is figure before continuing. The resul t of the events at the neuromuscular junction is a transient change in membrane poten tial that causes the interior C Complete an interactive of the sarcolemma to become Jess tutorial: MasteringA&P " > negative (a depolarization). This Study Area > Interactive local depolarization is called an Physiology end p la te potential (EP P). The EPP spreads to the adjacent sarcolemma and triggers an AP there. After ACh binds to the ACh receptors, its effects are quickly terminated by acetylcholinesterase (as"e-t il-ko"lin-es' ter-as), an enzyme located in the synaptic cleft. Acetylchol inesterase breaks down ACh to its building blocks, acetic acid and choline. Removing ACh prevents continued muscle fiber contraction in the absence of adclitional nervous syste,n stimulation. auto .- HOMEOSTATIC ~-.,.Ji~ IMBALANCE 9 . 2 immene: attack immone normal cells attackingit receptors, spasm repular: Zution K 00 0 leaving = - ++++ @ Repolarization: Restoring t he sarcolemma to its init ial polarized state (negative inside, posit ive outside). The repolarization wave is also a consequence of opening and closing ion channels-voltage-gated Na+ channels close and voltage-gated K + channels open. The potassium ion concentration is substantially higher inside the cell than in the extracellular fluid, so K + diffuses out of the muscle fiber. This restores the negatively charged conditions inside that are characteristic of a sarcolemma at rest. Generation of an Action Potential across the Sarcolemma Now let's consider the electrical events that trigger an action potential along the sarcolemma. An action potential is the result of a predictable sequence of electrical changes. Once in itiated, an action potential sweeps along the entire surface of the sarcoJemma. Three steps are involved in triggering and then propagating an action potential. These three steps-generation of an end plate potential followed by action potential depolarization and repolarization-are shown in Fig ure 9.8. A tracing of the Many toxins, drugs, and diseases interfere with events at the tone neuromuscular junction. For example, myasthenia gravis (asthen = weakness; gravi = heavy), a disease characterized by drooping upper eyelids, difficulty swallowing and talking, and generalized muscle weakness, involves a shortage of ACh autain menusmust appearmuuscurses, trams, hornoueet receptors. Myasthenia gravis is an autoi,nmune disease in which can the immune system destroys ACh receptors. •• •• • with end up Candiovascular and respiratory failure (Texr co111i11ues on p. 296.) Excitation-contraction (E-C) coupling is the sequence of events by which transmission of an action potential along the sarcolemma leads to the sliding of myofilaments. Watch a 3-D animation of this process: MastcringA&P" > Study Area> An imations & Videos> A&P Flix Setting the stage The events at the neuromuscular junction (NMJ) set the stage for E-C coupling by providing excitation. Released acetylcholine binds to receptor proteins on the sarcolemma and triggers an action potential in a muscle fiber. terminal and sacrolemn tagether & Axon terminal of motor neu ron at NMJ / after pre Action potential is generated the Ap triggers (a voltage gates to open in the Sarcolemma SR to release to 2 Muscle fiber 294 Ca +~ ~··· .. : ......... " ~ ._.., " " ~..,..»~···· feelingin for contraction Steps in E-C Coupling: Sarcolemma I G) The action potential (AP) propagates - + - - - - - - - - - - - - - - - - - - - - --< along t he sarcolemma and down t he T t ubules. ;a~;=~~~' . . _ ! 1 @ calcium ions are released. Transmission of th e AP along t he T tubules of t he triads causes t he voltage-sensit ive t ubule proteins to change shape. This shape chan ge opens the Ca2• release cha nnels in the terminal cisterns of the sarcoplasmic reticulum (SR), allowing Ca2• t o flow into t he cytosol. Cyte plasm . .. ___ --. . --. . ------c • .. -----2+• a • • • • • •• • • • • -- within organneles like inside .... ----- • • • • • • • • • • sacromeres • Tropomyosin blocking myosin-binding sites "=c----------~ • • • • • _ - Ca • • ••• •• • • •• • • • • • • - excitors Contraction Myosin hibitory relaxin @ calcium b inds to t roponin and the blocking action of Removes &removes ,,---------------------1 tropomyosin. When Ca2• binds, 2 • in -> ⑧ S - ~ ~ tropo nin changes shape, exposing myosin-bind ing sites o n t he t hin f ilaments. Myosin-binding sites exposed and ready for myosin binding ! Myosin __,,,/ cross bridge The aftermath When the muscle AP ceases, the voltage-sensitive tubule proteins return to their original shape, closing the Ca2+ release channels of the SR. Ca2+ levels in the sarcoplasm fall as Ca2+ is continually pumped back into the SR by active transport. Without Ca2+, the blocking action of tropomyosin is restored, myosin-actin interaction is inhibited, and relaxation occurs. Each time an AP arrives at the neuromuscular junction, the sequence of E-C coupling is repeated. © Cont raction begins: Myosin binding to actin forms cross bridges and contraction (cross bridge cycling) begins. At this point E-C coupling is over. A reaching 1. the tubule 2. In released voltage by sensitive proteins (Releasertram SM) 3. Calcrim Binds troponin to mask and expose the 4. binding off sites for myosin heads Contraction, Cross Bridge, Overlay the "Mask" 295 296 UNIT 2 Covering, Support, and Movement of the Body 14"leaving -rustity entering -- +30 > E .; --.. ..8. 0 ↓Na ↑ increasing + Depolarizatio n due to Na• entry c: .. .J::j E Repolarizat ion due to K• exit Na• channels open :; K• channels closed - 90 0 5 10 15 Calcrim Binds troponin and expose the Na• channels close, K• channels open c: .. Muscle Fiber Contraction: Cross Bridge Cycling 20 Tim e (ms) Figure 9.9 Record ing of an action potential (AP) in a mu scle fibe r. An AP is a brief change in membrane potential. resu lting membrane potential changes is shown in Figure 9.9 . We will describe action potentials in more detail in Chapter 11. During repolarization, a muscle fiber is said to be in a refractor y pe riod, because the cell cannot be stimulated again until repolarization is complete. Note that repolarization restores only the electrical conditions of the resting (polarized) state. The ATP-dependent Na +. K+ pump restores the ionic conditions of the resting state, but thousands of action potentials can occur before ionic imbalances interfere with contractile activity. Once ini tiated, the action potential is unstoppable. It ul timately results in contraction of the muscle fiber. Although the actio n pote ntial itself lasts o nly a few mill iseconds (ms), the contraction phase of a muscle fiber may persist for I 00 ms or more and far outlasts the electrical event that triggers it. Excitation-Contraction Coupling Excita tion-con