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PowerPoint ® Lecture Slides prepared by Barbara Heard, Atlantic Cape Community College C H A P T E R © 2013 Pearson Education, Inc.© Annie Leibovitz/Contact.

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Presentation on theme: "PowerPoint ® Lecture Slides prepared by Barbara Heard, Atlantic Cape Community College C H A P T E R © 2013 Pearson Education, Inc.© Annie Leibovitz/Contact."— Presentation transcript:

1 PowerPoint ® Lecture Slides prepared by Barbara Heard, Atlantic Cape Community College C H A P T E R © 2013 Pearson Education, Inc.© Annie Leibovitz/Contact Press Images 9 Muscles and Muscle Tissue: Part A

2 © 2013 Pearson Education, Inc. 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

3 © 2013 Pearson Education, Inc. 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

4 © 2013 Pearson Education, Inc. Types of Muscle Tissue Cardiac muscle –Only in heart; bulk of heart walls –Striated –Can contract without nervous system stimulation –Involuntary –More details in Chapter 18

5 © 2013 Pearson Education, Inc. 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

6 © 2013 Pearson Education, Inc. Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (1 of 4)

7 © 2013 Pearson Education, Inc. Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (2 of 4)

8 © 2013 Pearson Education, Inc. Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (3 of 4)

9 © 2013 Pearson Education, Inc. Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (4 of 4)

10 © 2013 Pearson Education, Inc. 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

11 © 2013 Pearson Education, Inc. 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"

12 © 2013 Pearson Education, Inc. 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

13 © 2013 Pearson Education, Inc. Skeletal Muscle 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

14 © 2013 Pearson Education, Inc. Figure 9.1 Connective tissue sheaths of skeletal muscle: epimysium, perimysium, and endomysium. Bone Tendon Epimysium Perimysium Endomysium Muscle fiber in middle of a fascicle Blood vessel Perimysium wrapping a fascicle Endomysium (between individual muscle fibers) Muscle fiber Perimysium Fascicle

15 © 2013 Pearson Education, Inc. 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

16 © 2013 Pearson Education, Inc. Table 9.1 Structure and Organizational Levels of Skeletal Muscle (1 of 3)

17 © 2013 Pearson Education, Inc. Table 9.1 Structure and Organizational Levels of Skeletal Muscle (2 of 3)

18 © 2013 Pearson Education, Inc. Table 9.1 Structure and Organizational Levels of Skeletal Muscle (3 of 3)

19 © 2013 Pearson Education, Inc. 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 O 2 storage Modified structures: myofibrils, sarcoplasmic reticulum, and T tubules

20 © 2013 Pearson Education, Inc. 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

21 © 2013 Pearson Education, Inc. 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 Nucleus Light I band Dark A band

22 © 2013 Pearson Education, Inc. 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

23 © 2013 Pearson Education, Inc. 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

24 © 2013 Pearson Education, Inc. Figure 9.2c Microscopic anatomy of a skeletal muscle fiber. 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. Thin (actin) filament Z discH zoneZ disc Thick (myosin) filament I band A band I bandM line Sarcomere

25 © 2013 Pearson Education, Inc. Figure 9.2d Microscopic anatomy of a skeletal muscle fiber. Enlargement of one sarcomere (sectioned length- wise). Notice the myosin heads on the thick filaments. Z disc Sarcomere M lineZ disc Thin (actin) filament Elastic (titin) filaments Thick (myosin) filament

26 © 2013 Pearson Education, Inc. 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

27 © 2013 Pearson Education, Inc. 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

28 © 2013 Pearson Education, Inc. 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

29 © 2013 Pearson Education, Inc. 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 ATP- binding site Heads Tail Flexible hinge region Myosin molecule Actin subunits Active sites for myosin attachment Figure 9.3 Composition of thick and thin filaments.

30 © 2013 Pearson Education, Inc. Structure of Myofibril Elastic filament –Composed of protein titin –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

31 © 2013 Pearson Education, Inc. 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 Ca 2+ levels –Stores and releases Ca 2+

32 © 2013 Pearson Education, Inc. 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

33 © 2013 Pearson Education, Inc. Figure 9.5 Relationship of the sarcoplasmic reticulum and T tubules to myofibrils of skeletal muscle. Part of a skeletal muscle fiber (cell) Myofibril Sarcolemma I bandA bandI band Z discH zoneZ disc M line Sarcolemma Triad: T tubule Terminal cisterns of the SR (2) Tubules of the SR Myofibrils Mitochondria

34 © 2013 Pearson Education, Inc. 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 Ca 2+ release from SR cisterns

35 © 2013 Pearson Education, Inc. 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

36 © 2013 Pearson Education, Inc. 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

37 © 2013 Pearson Education, Inc. 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)

38 © 2013 Pearson Education, Inc. Figure 9.6 Sliding filament model of contraction. Slide 1 Fully contracted sarcomere of a muscle fiber 1 2 Fully relaxed sarcomere of a muscle fiber Z HZ II A Z Z I I A

39 © 2013 Pearson Education, Inc. Figure 9.6 Sliding filament model of contraction. Slide 2 1 Fully relaxed sarcomere of a muscle fiber Z H Z I I A

40 © 2013 Pearson Education, Inc. Figure 9.6 Sliding filament model of contraction. Slide 3 2 Fully contracted sarcomere of a muscle fiber ZZ II A

41 © 2013 Pearson Education, Inc. Figure 9.6 Sliding filament model of contraction. Slide 4 Fully contracted sarcomere of a muscle fiber 1 2 Fully relaxed sarcomere of a muscle fiber Z HZ II A Z Z I I A

42 © 2013 Pearson Education, Inc. 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 Ca 2+ levels must rise briefly

43 © 2013 Pearson Education, Inc. Phase 1 Motor neuron stimulates muscle fiber (see Figure 9.8). Phase 2: Excitation-contraction coupling occurs (see Figures 9.9 and 9.11). Action potential (AP) arrives at axon terminal at neuromuscular junction ACh released; binds to receptors on sarcolemma 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 SR releases Ca 2+ ; Ca 2+ binds to troponin; myosin-binding sites (active sites) on actin exposed Myosin heads bind to actin; contraction begins Figure 9.7 The phases leading to muscle fiber contraction.

44 © 2013 Pearson Education, Inc. 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

45 © 2013 Pearson Education, Inc. Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 1 Action potential (AP) Myelinated axon of motor neuron Axon terminal of neuromuscular junction Sarcolemma of the muscle fiber Synaptic vesicle containing ACh Synaptic cleft Junctional folds of sarcolemma Sarcoplasm of muscle fiber Postsynaptic membrane ion channel opens; ions pass. Ion channel closes; ions cannot pass. Action potential arrives at axon terminal of motor neuron. Voltage-gated Ca 2+ channels open. Ca 2+ enters the axon terminal moving down its electochemical gradient. Ca 2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. ACh diffuses across the synaptic cleft and binds to its receptors on the sarcolemma. 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. ACh effects are terminated by its breakdown in the synaptic cleft by acetylcholinesterase and diffusion away from the junction. Axon terminal of motor neuron Fusing synaptic vesicles Degraded ACh ACh Acetylcho- linesterase ACh

46 © 2013 Pearson Education, Inc. Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 2 Synaptic vesicle containing ACh Synaptic cleft Axon terminal of motor neuron Fusing synaptic vesiclesa ACh Junctional folds of sarcolemma Sarcoplasm of muscle fiber Action potential arrives at axon terminal of motor neuron. 1

47 © 2013 Pearson Education, Inc. Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 3 Synaptic vesicle containing ACh Synaptic cleft Axon terminal of motor neuron Fusing synaptic vesiclesa ACh Junctional folds of sarcolemma Sarcoplasm of muscle fiber Action potential arrives at axon terminal of motor neuron. Voltage-gated Ca 2+ channels open. Ca 2+ enters the axon terminal moving down its electochemical gradient. 1 2

48 © 2013 Pearson Education, Inc. Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 4 Synaptic vesicle containing ACh Synaptic cleft Axon terminal of motor neuron Fusing synaptic vesiclesa ACh Junctional folds of sarcolemma Sarcoplasm of muscle fiber Action potential arrives at axon terminal of motor neuron. Voltage-gated Ca 2+ channels open. Ca 2+ enters the axon terminal moving down its electochemical gradient. Ca 2+ entry causes ACh (a neurotransmitter) to be released by exocytosis

49 © 2013 Pearson Education, Inc. Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 5 Synaptic vesicle containing ACh Synaptic cleft Axon terminal of motor neuron Fusing synaptic vesiclesa ACh Junctional folds of sarcolemma Sarcoplasm of muscle fiber Action potential arrives at axon terminal of motor neuron. Voltage-gated Ca 2+ channels open. Ca 2+ enters the axon terminal moving down its electochemical gradient. Ca 2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. ACh diffuses across the synaptic cleft and binds to its receptors on the sarcolemma

50 © 2013 Pearson Education, Inc. Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 6 Postsynaptic membrane ion channel opens; ions pass. 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

51 © 2013 Pearson Education, Inc. 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 Degraded ACh ACh Acetylcholinesterase Ion channel closes; ions cannot pass.

52 © 2013 Pearson Education, Inc. Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 8 Action potential (AP) Myelinated axon of motor neuron Axon terminal of neuromuscular junction Sarcolemma of the muscle fiber Synaptic vesicle containing ACh Synaptic cleft Junctional folds of sarcolemma Sarcoplasm of muscle fiber Postsynaptic membrane ion channel opens; ions pass. Ion channel closes; ions cannot pass. Action potential arrives at axon terminal of motor neuron. Voltage-gated Ca 2+ channels open. Ca 2+ enters the axon terminal moving down its electochemical gradient. Ca 2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. ACh diffuses across the synaptic cleft and binds to its receptors on the sarcolemma. 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. ACh effects are terminated by its breakdown in the synaptic cleft by acetylcholinesterase and diffusion away from the junction. Axon terminal of motor neuron Fusing synaptic vesicles Degraded ACh ACh Acetylcho- linesterase ACh

53 © 2013 Pearson Education, Inc. 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

54 © 2013 Pearson Education, Inc. 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

55 © 2013 Pearson Education, Inc. Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Action potential (AP) Myelinated axon of motor neuron Axon terminal of neuromuscular junction Sarcolemma of the muscle fiber Synaptic vesicle containing ACh Synaptic cleft Junctional folds of sarcolemma Sarcoplasm of muscle fiber Postsynaptic membrane ion channel opens; ions pass. Ion channel closes; ions cannot pass. Action potential arrives at axon terminal of motor neuron. Voltage-gated Ca 2+ channels open. Ca 2+ enters the axon terminal moving down its electochemical gradient. Ca 2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. ACh diffuses across the synaptic cleft and binds to its receptors on the sarcolemma. 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. ACh effects are terminated by its breakdown in the synaptic cleft by acetylcholinesterase and diffusion away from the junction. Axon terminal of motor neuron Fusing synaptic vesicles Degraded ACh ACh Acetylcho- linesterase ACh

56 © 2013 Pearson Education, Inc. 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

57 © 2013 Pearson Education, Inc. Generation of an Action Potential Resting sarcolemma polarized –Voltage across membrane Action potential caused by changes in electrical charges Occurs in three steps –End plate potential –Depolarization –Repolarization

58 © 2013 Pearson Education, Inc. Generation of an Action Potential Across the Sarcolemma End plate potential (local depolarization) –ACh binding opens chemically (ligand) gated ion channels –Simultaneous diffusion of Na+ (inward) and K + (outward) –More Na + diffuses in, so interior of sarcolemma becomes less negative –Local depolarization = end plate potential

59 © 2013 Pearson Education, Inc. Events in Generation of an Action Potential Depolarization - generation and propagation of an action potential (AP) –End plate potential spreads to adjacent membrane areas –Voltage-gated Na + channels open –Na + influx decreases membrane voltage toward critical voltage called threshold –If threshold reached, AP initiated –Once initiated, is unstoppable  muscle fiber contraction

60 © 2013 Pearson Education, Inc. Events in Generation of an Action Potential AP spreads across sarcolemma  Voltage-gated Na + channels open in adjacent patch, causing it to depolarize to threshold

61 © 2013 Pearson Education, Inc. Events in Generation of an Action Potential Repolarization – restoring electrical conditions of RMP –Na + channels close and voltage-gated K + channels open –K + efflux rapidly restores resting polarity –Fiber cannot be stimulated - in refractory period until repolarization complete –Ionic conditions of resting state restored by Na + -K + pump

62 © 2013 Pearson Education, Inc. Figure 9.9 Summary of events in the generation and propagation of an action potential in a skeletal muscle fiber. Slide 1 Open Na + channel Na + Closed K + channel K+K+ Action potential Axon terminal of neuromuscular junction ACh-containing synaptic vesicle Ca 2+ Synaptic cleft Wave of depolarization An end plate potential is generated at the neuromuscular junction (see Figure 9.8). Depolarization: Generating and propagating an action potential (AP). The local depolarization current spreads to adjacent areas of the sarcolemma. This opens voltage-gated sodium channels there, so Na + enters following its electrochemical gradient and initiates the AP. The AP is propagated as its local depolarization wave spreads to adjacent areas of the sarcolemma, opening voltage-gated channels there. Again Na+ diffuses into the cell following its electrochemical gradient. Repolarization: Restoring the sarcolemma to its initial polarized state (negative inside, positive outside). Repolarization occurs as Na + channels close (inactivate) and voltage-gated K + channels open. Because K + concentration is substantially higher inside the cell than in the extracellular fluid, K + diffuses rapidly out of the muscle fiber Closed Na + channel Open K + channel Na + K+K+ −  −  −  −  −  −  −  − −  −  −  −  − −  −  −  −  −  −  −  −  −  −     −  −  −  −  −  −  −  − −  −  −  −−  −  −  −  −  −  −  −

63 © 2013 Pearson Education, Inc. Figure 9.9 Summary of events in the generation and propagation of an action potential in a skeletal muscle fiber. Slide 2 Axon terminal of neuromuscular junction ACh-containing synaptic vesicle Ca 2+ Synaptic cleft Wave of depolarization An end plate potential is generated at the neuromuscular junction (see Figure 9.8). 1

64 © 2013 Pearson Education, Inc. Figure 9.9 Summary of events in the generation and propagation of an action potential in a skeletal muscle fiber. Slide 3 Open Na + channel Na + Closed K + channel K+K+ Action potential Axon terminal of neuromuscular junction ACh-containing synaptic vesicle Ca 2+ Synaptic cleft Wave of depolarization An end plate potential is generated at the neuromuscular junction (see Figure 9.8). Depolarization: Generating and propagating an action potential (AP). The local depolarization current spreads to adjacent areas of the sarcolemma. This opens voltage-gated sodium channels there, so Na + enters following its electrochemical gradient and initiates the AP. The AP is propagated as its local depolarization wave spreads to adjacent areas of the sarcolemma, opening voltage-gated channels there. Again Na+ diffuses into the cell following its electrochemical gradient. 1 2 −  −  −  −  −  −  −  − −  −  −  −  − −  −  −  −  −  −  −  −  −  −  

65 © 2013 Pearson Education, Inc. Figure 9.9 Summary of events in the generation and propagation of an action potential in a skeletal muscle fiber. Slide 4 Open Na + channel Na + Closed K + channel K+K+ Action potential Axon terminal of neuromuscular junction ACh-containing synaptic vesicle Ca 2+ Synaptic cleft Wave of depolarization An end plate potential is generated at the neuromuscular junction (see Figure 9.8). Depolarization: Generating and propagating an action potential (AP). The local depolarization current spreads to adjacent areas of the sarcolemma. This opens voltage-gated sodium channels there, so Na + enters following its electrochemical gradient and initiates the AP. The AP is propagated as its local depolarization wave spreads to adjacent areas of the sarcolemma, opening voltage-gated channels there. Again Na+ diffuses into the cell following its electrochemical gradient. Repolarization: Restoring the sarcolemma to its initial polarized state (negative inside, positive outside). Repolarization occurs as Na + channels close (inactivate) and voltage-gated K + channels open. Because K + concentration is substantially higher inside the cell than in the extracellular fluid, K + diffuses rapidly out of the muscle fiber Closed Na + channel Open K + channel Na + K+K+ −  −  −  −  −  −  −  − −  −  −  −  − −  −  −  −  −  −  −  −  −  −     −  −  −  −  −  −  −  − −  −  −  −−  −  −  −  −  −  −  −

66 © 2013 Pearson Education, Inc. Figure 9.10 Action potential tracing indicates changes in Na + and K + ion channels. Membrane potential (mV) – Depolarization due to Na + entry Na + channels close, K + channels open Repolarization due to K + exit K + channels closed Na + channels open Time (ms)

67 © 2013 Pearson Education, Inc. Excitation-Contraction (E-C) Coupling Events that transmit AP along sarcolemma lead to sliding of myofilaments AP brief; ends before contraction –Causes rise in intracellular Ca 2+ which  contraction Latent period –Time when E-C coupling events occur –Time between AP initiation and beginning of contraction

68 © 2013 Pearson Education, Inc. Events of Excitation-Contraction (E-C) Coupling AP propagated along sarcomere to T tubules Voltage-sensitive proteins stimulate Ca 2+ release from SR –Ca 2+ necessary for contraction

69 © 2013 Pearson Education, Inc. Figure 9.11 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 1 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. Synaptic cleft Axon terminal of motor neuron at NMJ Action potential is generated ACh Muscle fiber T tubule Terminal cistern of SR Triad One sarcomere One myofibril Sarcolemma The action potential (AP) propagates along the sarcolemma and down the T tubules. 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. Steps in E-C Coupling: Terminal cistern of SR Ca 2+ release channel Voltage-sensitive tubule protein T tubule Sarcolemma Calcium binds to troponin and removes the blocking action of tropomyosin. When Ca 2+ binds, troponin changes shape, exposing binding sites for myosin (active sites) on the thin filaments. Contraction begins: Myosin binding to actin forms cross bridges and contraction (cross bridge cycling) begins. At this point, E-C coupling is over. The aftermath When the muscle AP ceases, the voltage-sensitive tubule proteins return to their original shape, closing the Ca 2+ release channels of the SR. Ca 2+ levels in the sarcoplasm fall as Ca 2+ is continually pumped back into the SR by active transport. Without Ca 2+, 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. Myosin cross bridge Active sites exposed and ready for myosin binding Myosin Tropomyosin blocking active sites Actin Troponin

70 © 2013 Pearson Education, Inc. Figure 9.11 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 2 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. Synaptic cleft Axon terminal of motor neuron at NMJ Action poten- tial is generated Muscle fiber T tubule Terminal cistern of SR Triad One sarcomere One myofibril Sarcolemma ACh

71 © 2013 Pearson Education, Inc. Figure 9.11 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 3 The action potential (AP) propagates along the sarcolemma and down the T tubules. 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. Steps in E-C Coupling: Terminal cistern of SR Ca 2+ release channel Voltage-sensitive tubule protein T tubule Sarcolemma Calcium binds to troponin and removes the blocking action of tropomyosin. When Ca 2+ binds, troponin changes shape, exposing binding sites for myosin (active sites) on the thin filaments. Contraction begins: Myosin binding to actin forms cross bridges and contraction (cross bridge cycling) begins. At this point, E-C coupling is over. The aftermath When the muscle AP ceases, the voltage-sensitive tubule proteins return to their original shape, closing the Ca 2+ release channels of the SR. Ca 2+ levels in the sarcoplasm fall as Ca 2+ is continually pumped back into the SR by active transport. Without Ca 2+, 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. Myosin cross bridge Active sites exposed and ready for myosin binding Myosin Tropomyosin blocking active sites Actin Troponin

72 © 2013 Pearson Education, Inc. Figure 9.11 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 4 The action potential (AP) propagates along the sarcolemma and down the T tubules. Steps in E-C Coupling: Terminal cistern of SR Ca 2+ release channel Voltage-sensitive tubule protein T tubule Sarcolemma 1

73 © 2013 Pearson Education, Inc. Figure 9.11 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 5 The action potential (AP) propagates along the sarcolemma and down the T tubules. Steps in E-C Coupling: Terminal cistern of SR Ca 2+ release channel Voltage-sensitive tubule protein T tubule Sarcolemma Calcium ions are released. 1 2

74 © 2013 Pearson Education, Inc. Figure 9.11 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 Myosin Tropomyosin blocking active sites Actin Troponin The aftermath

75 © 2013 Pearson Education, Inc. Figure 9.11 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 Calcium binds to troponin and removes the blocking action of tropomyosin. When Ca 2+ binds, troponin changes shape, exposing binding sites for myosin (active sites) on the thin filaments. Active sites exposed and ready for myosin binding Myosin Tropomyosin blocking active sites Actin Troponin The aftermath 3

76 © 2013 Pearson Education, Inc. Figure 9.11 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 Calcium binds to troponin and removes the blocking action of tropomyosin. When Ca 2+ binds, troponin changes shape, exposing binding sites for myosin (active sites) on the thin filaments. Contraction begins: Myosin binding to actin forms cross bridges and contraction (cross bridge cycling) begins. At this point, E-C coupling is over. Myosin cross bridge Active sites exposed and ready for myosin binding Myosin Tropomyosin blocking active sites Actin Troponin The aftermath 3 4

77 © 2013 Pearson Education, Inc. The action potential (AP) propagates along the sarcolemma and down the T tubules. 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. Steps in E-C Coupling: Terminal cistern of SR Ca 2+ release channel Voltage-sensitive tubule protein T tubule Sarcolemma Calcium binds to troponin and removes the blocking action of tropomyosin. When Ca 2+ binds, troponin changes shape, exposing binding sites for myosin (active sites) on the thin filaments. Contraction begins: Myosin binding to actin forms cross bridges and contraction (cross bridge cycling) begins. At this point, E-C coupling is over. The aftermath When the muscle AP ceases, the voltage-sensitive tubule proteins return to their original shape, closing the Ca 2+ release channels of the SR. Ca 2+ levels in the sarcoplasm fall as Ca 2+ is continually pumped back into the SR by active transport. Without Ca 2+, 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. Myosin cross bridge Active sites exposed and ready for myosin binding Myosin Tropomyosin blocking active sites Actin Troponin

78 © 2013 Pearson Education, Inc. 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. Synaptic cleft Axon terminal of motor neuron at NMJ Action potential is generated ACh Muscle fiber T tubule Terminal cistern of SR Triad One sarcomere One myofibril Sarcolemma The action potential (AP) propagates along the sarcolemma and down the T tubules. 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. Steps in E-C Coupling: Terminal cistern of SR Ca 2+ release channel Voltage-sensitive tubule protein T tubule Sarcolemma Calcium binds to troponin and removes the blocking action of tropomyosin. When Ca 2+ binds, troponin changes shape, exposing binding sites for myosin (active sites) on the thin filaments. Contraction begins: Myosin binding to actin forms cross bridges and contraction (cross bridge cycling) begins. At this point, E-C coupling is over. The aftermath When the muscle AP ceases, the voltage-sensitive tubule proteins return to their original shape, closing the Ca 2+ release channels of the SR. Ca 2+ levels in the sarcoplasm fall as Ca 2+ is continually pumped back into the SR by active transport. Without Ca 2+, 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. Myosin cross bridge Active sites exposed and ready for myosin binding Myosin Tropomyosin blocking active sites Actin Troponin

79 © 2013 Pearson Education, Inc. Channels Involved in Initiating Muscle Contraction Nerve impulse reaches axon terminal  voltage- gated calcium channels open  ACh released to synaptic cleft ACh binds to its receptors on sarcolemma  opens ligand-gated Na + and K + channels  end plate potential  Opens voltage-gated Na + channels  AP propagation  Voltage-sensitive proteins in T tubules change shape  SR releases Ca 2+ to cytosol

80 © 2013 Pearson Education, Inc. Role of Calcium (Ca 2+ ) in Contraction At low intracellular Ca 2+ concentration –Tropomyosin blocks active sites on actin –Myosin heads cannot attach to actin –Muscle fiber relaxed

81 © 2013 Pearson Education, Inc. Role of Calcium (Ca 2+ ) in Contraction At higher intracellular Ca 2+ concentrations –Ca 2+ 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, Ca 2+ pumped back into SR and contraction ends

82 © 2013 Pearson Education, Inc. Cross Bridge Cycle Continues as long as Ca 2+ 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

83 © 2013 Pearson Education, Inc. 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

84 © 2013 Pearson Education, Inc. Actin Ca 2+ Thin filament Myosin cross bridge Thick filament Myosin ATP hydrolysis In the absence of ATP, myosin heads will not detach, causing rigor mortis. *This cycle will continue as long as ATP is available and Ca 2+ is bound to troponin. Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming a cross bridge. 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. * Cross bridge detachment. After ATP attaches to myosin, the link between myosin and actin weakens, and the myosin head detaches (the cross bridge “breaks”). The power (working) stroke. ADP and P i 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

85 © 2013 Pearson Education, Inc. Actin Thin filament Myosin cross bridge Thick filament Myosin Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming a cross bridge. 1

86 © 2013 Pearson Education, Inc. The power (working) stroke. ADP and P i 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

87 © 2013 Pearson Education, Inc. 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

88 © 2013 Pearson Education, Inc. 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 ATP hydrolysis *This cycle will continue as long as ATP is available and Ca 2+ is bound to troponin.

89 © 2013 Pearson Education, Inc. Actin Ca 2+ Thin filament Myosin cross bridge Thick filament Myosin ATP hydrolysis In the absence of ATP, myosin heads will not detach, causing rigor mortis. *This cycle will continue as long as ATP is available and Ca 2+ is bound to troponin. Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming a cross bridge. 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. * Cross bridge detachment. After ATP attaches to myosin, the link between myosin and actin weakens, and the myosin head detaches (the cross bridge “breaks”). The power (working) stroke. ADP and P i 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

90 © 2013 Pearson Education, Inc. 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


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