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.

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

© 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

© 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

© 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

© 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

© 2013 Pearson Education, Inc. Special Characteristics of Muscle Tissue Excitability (responsiveness): 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. 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. 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

© 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

© 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

© 2013 Pearson Education, Inc. Microscopic Anatomy of a Skeletal Muscle Fiber Long, cylindrical cell Multiple peripheral nuclei Sarcolemma = plasma membrane Sarcoplasm = cytoplasm – myoglobin for O 2 storage

© 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

© 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

© 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

© 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

© 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

© 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.

© 2013 Pearson Education, Inc. Sarcoplasmic Reticulum (SR) Network of smooth endoplasmic reticulum surrounding each myofibril –Most run longitudinally Functions in regulation of intracellular Ca 2+ levels –Stores and releases Ca 2+

© 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

© 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 4 3 2 1 5 6

© 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

© 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

© 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. 1 2 3

© 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. 1 2 3 4

© 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

© 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.

© 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 4 3 2 1 5 6

© 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 4 3 2 1 5 6

© 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. 1 2 3 Closed Na + channel Open K + channel Na + K+K+ – – – – – – – – – – – – + + – – + + + + + + + + + + + + + + + + + – – – – – – – – – – –

© 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

© 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 + + + + + + – – – – – – – – – – – – – –

© 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. 1 2 3 Closed Na + channel Open K + channel Na + K+K+ + + + + + + + + + + + + + + + + + – – – – – – – – – – – – – – – – – – – – – – – – –

© 2013 Pearson Education, Inc. Figure 9.10 Action potential tracing indicates changes in Na + and K + ion channels. Membrane potential (mV) +30 0 –90 0 5101520 Depolarization due to Na + entry Na + channels close, K + channels open Repolarization due to K + exit K + channels closed Na + channels open Time (ms)

© 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 1 2 3 4 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

© 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 potential is generated Muscle fiber T tubule Terminal cistern of SR Triad One sarcomere One myofibril Sarcolemma ACh

© 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 2 1 3 4

© 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

© 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

© 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

© 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

© 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

© 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. A&P Flix™: Excitation- contraction coupling. PLAY Slide 9 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 2 1 3 4

© 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 10 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 1 2 3 4 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

© 2013 Pearson Education, Inc. Figure 9.12 The cross bridge cycle is the series of events during which myosin heads pull thin filaments toward the center of the sarcomere. Slide 1 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. 1 2 3 4

© 2013 Pearson Education, Inc. Figure 9.12 The cross bridge cycle is the series of events during which myosin heads pull thin filaments toward the center of the sarcomere. Slide 2 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

© 2013 Pearson Education, Inc. Figure 9.12 The cross bridge cycle is the series of events during which myosin heads pull thin filaments toward the center of the sarcomere. Slide 3 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

© 2013 Pearson Education, Inc. Figure 9.12 The cross bridge cycle is the series of events during which myosin heads pull thin filaments toward the center of the sarcomere. Slide 4 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. Figure 9.12 The cross bridge cycle is the series of events during which myosin heads pull thin filaments toward the center of the sarcomere. Slide 5 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.

© 2013 Pearson Education, Inc. Figure 9.12 The cross bridge cycle is the series of events during which myosin heads pull thin filaments toward the center of the sarcomere. Slide 6 A&P Flix™: The Cross Bridge Cycle PLAY 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. 1 2 3 4

© 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

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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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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