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9 Muscles and Muscle Tissue: Part A.

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1 9 Muscles and Muscle Tissue: Part A

2 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.

3 Types of Muscle Tissue Skeletal muscles
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.

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

5 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.

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

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

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

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

10 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.

11 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.

12 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.

13 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.

14 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.

15 Microscopic Anatomy of a Skeletal Muscle Fiber
Long, cylindrical cell Multiple peripheral nuclei Sarcolemma = plasma membrane Sarcoplasm = cytoplasm Glycosomes for glycogen storage, myoglobin for O2 storage © 2013 Pearson Education, Inc.

16 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.

17 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.

18 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.

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 Myosin myofilaments = thick filaments Extend length of A band © 2013 Pearson Education, Inc.

20 Ultrastructure of Thin Filament
Tropomyosin and troponin - regulatory proteins bound to actin © 2013 Pearson Education, Inc.

21 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.

22 Sarcoplasmic Reticulum (SR)
Network of smooth endoplasmic reticulum surrounding each myofibril Functions in regulation of intracellular Ca2+ levels Stores and releases Ca2+ © 2013 Pearson Education, Inc.

23 Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released.
Slide 1 Myelinated axon of motor neuron Action potential (AP) Axon terminal of neuromuscular junction Sarcolemma of the muscle fiber Action potential arrives at axon terminal of motor neuron. 1 Voltage-gated Ca2+ channels open. Ca2+ enters the axon terminal moving down its electochemical gradient. Synaptic vesicle containing ACh 2 Axon terminal of motor neuron Synaptic cleft Fusing synaptic vesicles 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 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. Degraded ACh ACh Ion channel closes; ions cannot pass. ACh effects are terminated by its breakdown in the synaptic cleft by acetylcholinesterase and diffusion away from the junction. 6 Acetylcho- linesterase © 2013 Pearson Education, Inc.

24 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) © 2013 Pearson Education, Inc.

25 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.

26 Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released.
Myelinated axon of motor neuron Action potential (AP) Axon terminal of neuromuscular junction Sarcolemma of the muscle fiber Action potential arrives at axon terminal of motor neuron. 1 Voltage-gated Ca2+ channels open. Ca2+ enters the axon terminal moving down its electochemical gradient. Synaptic vesicle containing ACh 2 Axon terminal of motor neuron Synaptic cleft Fusing synaptic vesicles 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 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. Degraded ACh ACh Ion channel closes; ions cannot pass. ACh effects are terminated by its breakdown in the synaptic cleft by acetylcholinesterase and diffusion away from the junction. 6 Acetylcho- linesterase © 2013 Pearson Education, Inc.

27 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 1 Steps in E-C Coupling: Sarcolemma Voltage-sensitive tubule protein T tubule The action potential (AP) propagates along the sarcolemma and down the T tubules. 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. 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 Synaptic cleft Axon terminal of motor neuron at NMJ Action potential is generated ACh Sarcolemma Actin T tubule Troponin Tropomyosin blocking active sites Terminal cistern of SR 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 Muscle fiber Triad Active sites exposed and ready for myosin binding One sarcomere 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 One myofibril 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.

28 The events at the neuromuscular junction (NMJ)
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 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 ACh Sarcolemma T tubule Terminal cistern of SR Muscle fiber Triad One sarcomere One myofibril © 2013 Pearson Education, Inc.

29 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 3 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 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 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.

30 The action potential (AP) propagates along the sarcolemma and down the
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 4 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 Ca2+ release channel Terminal cistern of SR © 2013 Pearson Education, Inc.

31 The action potential (AP) propagates along the sarcolemma and down the
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 5 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 Ca2+ release channel 2 Calcium ions are released. Terminal cistern of SR © 2013 Pearson Education, Inc. 31

32 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.

33 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.

34 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.

35 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.

36 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 10 Steps in E-C Coupling: Sarcolemma Voltage-sensitive tubule protein T tubule The action potential (AP) propagates along the sarcolemma and down the T tubules. 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. 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 Synaptic cleft Axon terminal of motor neuron at NMJ Action potential is generated ACh Sarcolemma Actin T tubule Troponin Tropomyosin blocking active sites Terminal cistern of SR 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 Muscle fiber Triad Active sites exposed and ready for myosin binding One sarcomere 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 One myofibril 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. 36

37 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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