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Nearly half of body's mass

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1 Nearly half of body's mass
Muscle Tissue Nearly half of body's mass Transforms chemical energy (ATP) to directed mechanical energy  exerts force Three types Skeletal Cardiac Smooth Myo, mys, and sarco - prefixes for muscle © 2013 Pearson Education, Inc.

2 Types of Muscle Tissue Skeletal muscles
Organs attached to bones and skin Elongated cells called muscle fibers Striated (striped) Voluntary (i.e., conscious control) Contract rapidly; tire easily; powerful Require nervous system stimulation © 2013 Pearson Education, Inc.

3 Types of Muscle Tissue Cardiac muscle
Only in heart; bulk of heart walls Striated Can contract without nervous system stimulation Involuntary © 2013 Pearson Education, Inc.

4 Types of Muscle Tissue Smooth muscle
In walls of hollow organs, e.g., stomach, urinary bladder, and airways Not striated Can contract without nervous system stimulation Involuntary © 2013 Pearson Education, Inc.

5 Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (1 of 4)
© 2013 Pearson Education, Inc.

6 Special Characteristics of Muscle Tissue
Excitability (responsiveness or irritability): ability to receive and respond to stimuli Contractility: ability to shorten forcibly when stimulated Extensibility: ability to be stretched Elasticity: ability to recoil to resting length © 2013 Pearson Education, Inc.

7 Four important functions
Muscle Functions Four important functions Movement of bones or fluids (e.g., blood) Maintaining posture and body position Stabilizing joints Heat generation (especially skeletal muscle) Additional functions Protects organs, forms valves, controls pupil size, causes "goosebumps" © 2013 Pearson Education, Inc.

8 Each muscle served by one artery, one nerve, and one or more veins
Skeletal Muscle Each muscle served by one artery, one nerve, and one or more veins Enter/exit near central part and branch through connective tissue sheaths Every skeletal muscle fiber supplied by nerve ending that controls its activity Huge nutrient and oxygen need; generates large amount of waste © 2013 Pearson Education, Inc.

9 Connective tissue sheaths of skeletal muscle
Support cells; reinforce whole muscle External to internal Epimysium: dense irregular connective tissue surrounding entire muscle; may blend with fascia Perimysium: fibrous connective tissue surrounding fascicles (groups of muscle fibers) Endomysium: fine areolar connective tissue surrounding each muscle fiber © 2013 Pearson Education, Inc.

10 Figure 9.1 Connective tissue sheaths of skeletal muscle: epimysium, perimysium, and endomysium.
Bone Perimysium Tendon Endomysium Muscle fiber in middle of a fascicle Blood vessel Perimysium wrapping a fascicle Endomysium (between individual muscle fibers) Muscle fiber Fascicle Perimysium © 2013 Pearson Education, Inc.

11 Skeletal Muscle: Attachments
Attach in at least two places Insertion – movable bone Origin – immovable (less movable) bone Attachments direct or indirect Direct—epimysium fused to periosteum of bone or perichondrium of cartilage Indirect—connective tissue wrappings extend beyond muscle as ropelike tendon or sheetlike aponeurosis © 2013 Pearson Education, Inc.

12 Microscopic Anatomy of A Skeletal Muscle Fiber
Long, cylindrical cell 10 to 100 µm in diameter; up to 30 cm long Multiple peripheral nuclei Sarcolemma = plasma membrane Sarcoplasm = cytoplasm Glycosomes for glycogen storage, myoglobin for O2 storage Modified structures: myofibrils, sarcoplasmic reticulum, and T tubules © 2013 Pearson Education, Inc.

13 Densely packed, rodlike elements ~80% of cell volume
Myofibrils Densely packed, rodlike elements ~80% of cell volume Contain sarcomeres - contractile units Sarcomeres contain myofilaments Exhibit striations - perfectly aligned repeating series of dark A bands and light I bands © 2013 Pearson Education, Inc.

14 Sarcolemma Mitochondrion Dark A band Light I band Nucleus
Figure 9.2b Microscopic anatomy of a skeletal muscle fiber. Diagram of part of a muscle fiber showing the myofibrils. One myofibril extends from the cut end of the fiber. Sarcolemma Mitochondrion Myofibril Dark A band Light I band Nucleus © 2013 Pearson Education, Inc.

15 Striations H zone: lighter region in midsection of dark A band where filaments do not overlap M line: line of protein myomesin bisects H zone Z disc (line): coin-shaped sheet of proteins on midline of light I band that anchors thin filaments and connects myofibrils to one another Thick filaments: run entire length of an A band Thin filaments: run length of I band and partway into A band Sarcomere: region between two successive Z discs © 2013 Pearson Education, Inc.

16 Smallest contractile unit (functional unit) of muscle fiber
Sarcomere Smallest contractile unit (functional unit) of muscle fiber Align along myofibril like boxcars of train Contains A band with ½ I band at each end Composed of thick and thin myofilaments made of contractile proteins © 2013 Pearson Education, Inc.

17 Z disc H zone Z disc I band A band I band M line Sarcomere
Figure 9.2c Microscopic anatomy of a skeletal muscle fiber. Thin (actin) filament Z disc H zone Z disc 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 band A band I band M line Sarcomere © 2013 Pearson Education, Inc.

18 one sarcomere (sectioned length- wise). Notice the myosin heads on
Figure 9.2d Microscopic anatomy of a skeletal muscle fiber. Sarcomere Thin (actin) filament Z disc M line Z disc Enlargement of one sarcomere (sectioned length- wise). Notice the myosin heads on the thick filaments. Elastic (titin) filaments Thick (myosin) filament © 2013 Pearson Education, Inc. 18

19 Myofibril Banding Pattern
Orderly arrangement of actin and myosin myofilaments within sarcomere Actin myofilaments = thin filaments Extend across I band and partway in A band Anchored to Z discs Myosin myofilaments = thick filaments Extend length of A band Connected at M line © 2013 Pearson Education, Inc.

20 Ultrastructure of Thick Filament
Composed of protein myosin Each composed of 2 heavy and four light polypeptide chains Myosin tails contain 2 interwoven, heavy polypeptide chains Myosin heads contain 2 smaller, light polypeptide chains that act as cross bridges during contraction Binding sites for actin of thin filaments Binding sites for ATP ATPase enzymes © 2013 Pearson Education, Inc.

21 Ultrastructure of Thin Filament
Twisted double strand of fibrous protein F actin F actin consists of G (globular) actin subunits G actin bears active sites for myosin head attachment during contraction Tropomyosin and troponin - regulatory proteins bound to actin © 2013 Pearson Education, Inc.

22 Portion of a thick filament Portion of a thin filament
Figure 9.3 Composition of thick and thin filaments. Longitudinal section of filaments within one sarcomere of a myofibril Thick filament Thin filament 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 oppositeends 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 Myosin head Tropomyosin Troponin Actin Actin-binding sites Heads Tail ATP- binding site Active sites for myosin attachment Actin subunits Flexible hinge region Myosin molecule Actin subunits © 2013 Pearson Education, Inc.

23 Structure of Myofibril
Elastic filament Holds thick filaments in place; helps recoil after stretch; resists excessive stretching Dystrophin Links thin filaments to proteins of sarcolemma Nebulin, myomesin, C proteins bind filaments or sarcomeres together; maintain alignment © 2013 Pearson Education, Inc.

24 Sarcoplasmic Reticulum (SR)
Network of smooth endoplasmic reticulum surrounding each myofibril Most run longitudinally Pairs of terminal cisternae form perpendicular cross channels Functions in regulation of intracellular Ca2+ levels Stores and releases Ca2+ © 2013 Pearson Education, Inc.

25 Continuations of sarcolemma Lumen continuous with extracellular space
T Tubules Continuations of sarcolemma Lumen continuous with extracellular space Increase muscle fiber's surface area Penetrate cell's interior at each A band–I band junction Associate with paired terminal cisterns to form triads that encircle each sarcomere © 2013 Pearson Education, Inc.

26 Part of a skeletal muscle fiber (cell) I band A band I band Z disc
Figure 9.5 Relationship of the sarcoplasmic reticulum and T tubules to myofibrils of skeletal muscle. Part of a skeletal muscle fiber (cell) I band A band I band Z disc H zone Z disc M line Sarcolemma Myofibril Triad: • T tubule • Terminal cisterns of the SR (2) Sarcolemma Tubules of the SR Myofibrils Mitochondria © 2013 Pearson Education, Inc.

27 T tubules conduct impulses deep into muscle fiber; every sarcomere
Triad Relationships T tubules conduct impulses deep into muscle fiber; every sarcomere Integral proteins protrude into intermembrane space from T tubule and SR cistern membranes–act as voltage sensors SR foot proteins: gated channels that regulate Ca2+ release from SR cisterns © 2013 Pearson Education, Inc.

28 Sliding Filament Model of Contraction
Generation of force Does not necessarily cause shortening of fiber Shortening occurs when tension generated by cross bridges on thin filaments exceeds forces opposing shortening © 2013 Pearson Education, Inc.

29 Sliding Filament Model of Contraction
In relaxed state, thin and thick filaments overlap only at ends of A band Sliding filament model of contraction During contraction, thin filaments slide past thick filaments  actin and myosin overlap more Occurs when myosin heads bind to actin  cross bridges © 2013 Pearson Education, Inc.

30 Sliding Filament Model of Contraction
Myosin heads bind to actin; sliding begins Cross bridges form and break several times, ratcheting thin filaments toward center of sarcomere Causes shortening of muscle fiber Pulls Z discs toward M line I bands shorten; Z discs closer; H zones disappear; A bands move closer (length stays same) © 2013 Pearson Education, Inc.

31 Fully relaxed sarcomere of a muscle fiber
Figure 9.6 Sliding filament model of contraction. Slide 2 1 Fully relaxed sarcomere of a muscle fiber Z H Z I A I © 2013 Pearson Education, Inc. 31

32 Fully contracted sarcomere of a muscle fiber
Figure 9.6 Sliding filament model of contraction. Slide 3 2 Fully contracted sarcomere of a muscle fiber Z Z I A I © 2013 Pearson Education, Inc. 32

33 Fully relaxed sarcomere of a muscle fiber
Figure 9.6 Sliding filament model of contraction. Slide 4 1 Fully relaxed sarcomere of a muscle fiber Z H Z I A I 2 Fully contracted sarcomere of a muscle fiber Z Z I A I © 2013 Pearson Education, Inc. 33

34 Physiology of Skeletal Muscle Fibers
For skeletal muscle to contract Activation (at neuromuscular junction) Must be nervous system stimulation Must generate action potential in sarcolemma Excitation-contraction coupling Action potential propagated along sarcolemma Intracellular Ca2+ levels must rise briefly © 2013 Pearson Education, Inc.

35 Action potential (AP) arrives at axon
Figure 9.7 The phases leading to muscle fiber contraction. Action potential (AP) arrives at axon terminal at neuromuscular junction ACh released; binds to receptors on sarcolemma Phase 1 Motor neuron stimulates muscle fiber (see Figure 9.8). Ion permeability of sarcolemma changes Local change in membrane voltage (depolarization) occurs Local depolarization (end plate potential) ignites AP in sarcolemma AP travels across the entire sarcolemma AP travels along T tubules Phase 2: Excitation-contraction coupling occurs (see Figures 9.9 and 9.11). SR releases Ca2+; Ca2+ binds to troponin; myosin-binding sites (active sites) on actin exposed Myosin heads bind to actin; contraction begins © 2013 Pearson Education, Inc.

36 The Nerve Stimulus and Events at the Neuromuscular Junction
Skeletal muscles stimulated by somatic motor neurons Axons of motor neurons travel from central nervous system via nerves to skeletal muscle Each axon forms several branches as it enters muscle Each axon ending forms neuromuscular junction with single muscle fiber Usually only one per muscle fiber © 2013 Pearson Education, Inc.

37 Action potential arrives at axon terminal of motor neuron. 1
Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 2 Action potential arrives at axon terminal of motor neuron. 1 Synaptic vesicle containing ACh Axon terminal of motor neuron Synaptic cleft Fusing synaptic vesiclesa ACh Junctional folds of sarcolemma Sarcoplasm of muscle fiber © 2013 Pearson Education, Inc. 37

38 Action potential arrives at axon terminal of motor neuron. 1
Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 3 Action potential arrives at axon terminal of motor neuron. 1 Synaptic vesicle containing ACh Voltage-gated Ca2+ channels open. Ca2+ enters the axon terminal moving down its electochemical gradient. 2 Axon terminal of motor neuron Synaptic cleft Fusing synaptic vesiclesa ACh Junctional folds of sarcolemma Sarcoplasm of muscle fiber © 2013 Pearson Education, Inc. 38

39 Action potential arrives at axon terminal of motor neuron. 1
Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 4 Action potential arrives at axon terminal of motor neuron. 1 Synaptic vesicle containing ACh Voltage-gated Ca2+ channels open. Ca2+ enters the axon terminal moving down its electochemical gradient. 2 Axon terminal of motor neuron Synaptic cleft Fusing synaptic vesiclesa Ca2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. 3 ACh Junctional folds of sarcolemma Sarcoplasm of muscle fiber © 2013 Pearson Education, Inc. 39

40 Action potential arrives at axon terminal of motor neuron. 1
Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 5 Action potential arrives at axon terminal of motor neuron. 1 Synaptic vesicle containing ACh Voltage-gated Ca2+ channels open. Ca2+ enters the axon terminal moving down its electochemical gradient. 2 Axon terminal of motor neuron Synaptic cleft Fusing synaptic vesiclesa Ca2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. 3 ACh Junctional folds of sarcolemma ACh diffuses across the synaptic cleft and binds to its receptors on the sarcolemma. 4 Sarcoplasm of muscle fiber © 2013 Pearson Education, Inc. 40

41 channels in the receptors that allow simultaneous passage of
Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 6 ACh binding opens ion channels in the receptors that allow simultaneous passage of Na+ into the muscle fiber and K+ out of the muscle fiber. More Na+ ions enter than K+ ions exit, which produces a local change in the membrane potential called the end plate potential. 5 Postsynaptic membrane ion channel opens; ions pass. © 2013 Pearson Education, Inc. 41

42 Acetylcholinesterase
Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 7 ACh effects are terminated by its breakdown in the synaptic cleft by acetylcholinesterase and diffusion away from the junction. 6 ACh Degraded ACh Acetylcholinesterase Ion channel closes; ions cannot pass. © 2013 Pearson Education, Inc. 42

43 Neuromuscular Junction (NMJ)
Situated midway along length of muscle fiber Axon terminal and muscle fiber separated by gel-filled space called synaptic cleft Synaptic vesicles of axon terminal contain neurotransmitter acetylcholine (ACh) Junctional folds of sarcolemma contain ACh receptors NMJ includes axon terminals, synaptic cleft, junctional folds © 2013 Pearson Education, Inc.

44 Events at the Neuromuscular Junction
Nerve impulse arrives at axon terminal  ACh released into synaptic cleft ACh diffuses across cleft and binds with receptors on sarcolemma  Electrical events  generation of action potential PLAY A&P Flix™: Events at the Neuromuscular Junction © 2013 Pearson Education, Inc.

45 Destruction of Acetylcholine
ACh effects quickly terminated by enzyme acetylcholinesterase in synaptic cleft Breaks down ACh to acetic acid and choline Prevents continued muscle fiber contraction in absence of additional stimulation © 2013 Pearson Education, Inc.

46 The aftermath Actin Troponin Tropomyosin blocking active sites Myosin
Figure 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. Slide 6 Actin Troponin Tropomyosin blocking active sites Myosin The aftermath © 2013 Pearson Education, Inc.

47 The aftermath Actin Troponin Tropomyosin blocking active sites Myosin
Figure 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. Slide 7 Actin Troponin Tropomyosin blocking active sites Myosin Calcium binds to troponin and removes the blocking action of tropomyosin. When Ca2+ binds, troponin changes shape, exposing binding sites for myosin (active sites) on the thin filaments. 3 Active sites exposed and ready for myosin binding The aftermath © 2013 Pearson Education, Inc.

48 The aftermath Actin Troponin Tropomyosin blocking active sites Myosin
Figure 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. Slide 8 Actin Troponin Tropomyosin blocking active sites Myosin Calcium binds to troponin and removes the blocking action of tropomyosin. When Ca2+ binds, troponin changes shape, exposing binding sites for myosin (active sites) on the thin filaments. 3 Active sites exposed and ready for myosin binding Contraction begins: Myosin binding to actin forms cross bridges and contraction (cross bridge cycling) begins. At this point, E-C coupling is over. 4 Myosin cross bridge The aftermath © 2013 Pearson Education, Inc.

49 A&P Flix™: Excitation-contraction coupling.
Figure 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. Slide 9 Steps in E-C Coupling: Sarcolemma The action potential (AP) propagates along the sarcolemma and down the T tubules. 1 Voltage-sensitive tubule protein T tubule PLAY Ca2+ release channel Calcium ions are released. Transmission of the AP along the T tubules of the triads causes the voltage-sensitive tubule proteins to change shape. This shape change opens the Ca2+ release channels in the terminal cisterns of the sarcoplasmic reticulum (SR), allowing Ca2+ to flow into the cytosol. 2 Terminal cistern of SR A&P Flix™: Excitation-contraction coupling. Actin Troponin Tropomyosin blocking active sites Myosin Calcium binds to troponin and removes the blocking action of tropomyosin. When Ca2+ binds, troponin changes shape, exposing binding sites for myosin (active sites) on the thin filaments. 3 Active sites exposed and ready for myosin binding Contraction begins: Myosin binding to actin forms cross bridges and contraction (cross bridge cycling) begins. At this point, E-C coupling is over. 4 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. © 2013 Pearson Education, Inc.

50 Role of Calcium (Ca2+) in Contraction
At low intracellular Ca2+ concentration Tropomyosin blocks active sites on actin Myosin heads cannot attach to actin Muscle fiber relaxed © 2013 Pearson Education, Inc.

51 Role of Calcium (Ca2+) in Contraction
At higher intracellular Ca2+ concentrations Ca2+ binds to troponin Troponin changes shape and moves tropomyosin away from myosin-binding sites Myosin heads bind to actin, causing sarcomere shortening and muscle contraction When nervous stimulation ceases, Ca2+ pumped back into SR and contraction ends © 2013 Pearson Education, Inc.

52 Continues as long as Ca2+ signal and adequate ATP present
Cross Bridge Cycle Continues as long as Ca2+ signal and adequate ATP present Cross bridge formation—high-energy myosin head attaches to thin filament Working (power) stroke—myosin head pivots and pulls thin filament toward M line © 2013 Pearson Education, Inc.

53 Cross Bridge Cycle Cross bridge detachment—ATP attaches to myosin head and cross bridge detaches "Cocking" of myosin head—energy from hydrolysis of ATP cocks myosin head into high-energy state © 2013 Pearson Education, Inc.

54 A&P Flix™: The Cross Bridge Cycle
Figure The cross bridge cycle is the series of events during which myosin heads pull thin filaments toward the center of the sarcomere. Slide 6 Actin Ca2+ Thin filament PLAY Myosin cross bridge Thick filament A&P Flix™: The Cross Bridge Cycle Myosin Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming a cross bridge. 1 ATP hydrolysis Cocking of the myosin head. As ATP is hydrolyzed to ADP and Pi, the myosin head returns to its prestroke high-energy, or “cocked,” position. * 4 The power (working) stroke. ADP and Pi are released and the myosin head pivots and bends, changing to its bent low-energy state. As a result it pulls the actin filament toward the M line. 2 In the absence of ATP, myosin heads will not detach, causing rigor mortis. *This cycle will continue as long as ATP is available and Ca2+ is bound to troponin. Cross bridge detachment. After ATP attaches to myosin, the link between myosin and actin weakens, and the myosin head detaches (the cross bridge “breaks”). 3 © 2013 Pearson Education, Inc.

55 Homeostatic Imbalance
Rigor mortis Cross bridge detachment requires ATP 3–4 hours after death muscles begin to stiffen with weak rigidity at 12 hours post mortem Dying cells take in calcium  cross bridge formation No ATP generated to break cross bridges © 2013 Pearson Education, Inc.


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