1. MUSCLES

2. 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. Skeletal Muscle

4. Types of Muscle Tissue Skeletal muscles Organs attached to bones and skin Elongated cells called muscle fibers Striated (striped) Voluntary (i.e., conscious control) Require nervous system stimulation

5. Cardiac Muscle

6. Types of Muscle Tissue Cardiac muscle Only in heart; bulk of heart walls Striated Can contract without nervous system stimulation Involuntary

7. Cardiac Muscle

8. Smooth Muscle

9. 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

10. 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. 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. 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

13. 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. Skeletal Muscle: Attachments Attach in at least two places Insertion – movable bone Origin – immovable (less movable) bone

15. © 2013 Pearson Education, Inc. 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

16. Microscopic Anatomy of A Skeletal Muscle Fiber Sarcolemma = plasma membrane Sarcoplasm = cytoplasm Glycosomes for glycogen storage, myoglobin for O 2 storage Modified structures: myofibrils, sarcoplasmic reticulum, and T tubules

17. Myofibrils Contain sarcomeres - contractile units Sarcomeres contain myofilaments Exhibit striations - perfectly aligned repeating series of dark A bands and light I bands

18. 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

19. © 2013 Pearson Education, Inc. 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

20. © 2013 Pearson Education, Inc. 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

21. © 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

22. Myofibril Banding Pattern Actin myofilaments = thin filaments Anchored to Z discs Myosin myofilaments = thick filaments Connected at M line

23. Myosin Thick Filament 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

24. Actin Thin Filament G (globular) actin bears active sites for myosin head attachment during contraction Tropomyosin and troponin - regulatory proteins bound to actin

25. © 2013 Pearson Education, Inc. 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

26. 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+

27. T Tubules Associate with paired terminal cisterns to form triads that encircle each sarcomere

28. © 2013 Pearson Education, Inc. 1 Fully relaxed sarcomere of a muscle fiber Z H Z I I A

29. © 2013 Pearson Education, Inc. 2 Fully contracted sarcomere of a muscle fiber ZZ II A

30. © 2013 Pearson Education, Inc. 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

31. 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

32. 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)

33. 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

34. © 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

35. 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

36. © 2013 Pearson Education, Inc. 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

37. © 2013 Pearson Education, Inc. 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

38. © 2013 Pearson Education, Inc. 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

39. © 2013 Pearson Education, Inc. 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

40. © 2013 Pearson Education, Inc. 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

41. © 2013 Pearson Education, Inc. 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.

42. © 2013 Pearson Education, Inc. 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

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

44. Events at the Neuromuscular Junction Nerve impulse arrives at axon terminal  ACh released into synaptic cleft ACh diffuses across cleft and binds with receptors on sarcolemma  Electrical events  generation of action potential

45. © 2013 Pearson Education, Inc. 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

46. 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

47. 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

48. 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

49. 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

50. 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

51. 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

52. © 2013 Pearson Education, Inc. 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

53. © 2013 Pearson Education, Inc. 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 −  −  −  −  −  −  −  − −  −  −  −  − −  −  −  −  −  −  −  −  −  −  

54. © 2013 Pearson Education, Inc. 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+ −  −  −  −  −  −  −  − −  −  −  −  − −  −  −  −  −  −  −  −  −  −     −  −  −  −  −  −  −  − −  −  −  −−  −  −  −  −  −  −  −

55. © 2013 Pearson Education, Inc. Membrane potential (mV) +30 0 –95 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)

56. 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

57. 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

58. © 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 poten- tial is generated Muscle fiber T tubule Terminal cistern of SR Triad One sarcomere One myofibril Sarcolemma ACh

59. © 2013 Pearson Education, Inc. 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

60. © 2013 Pearson Education, Inc. 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

61. © 2013 Pearson Education, Inc. Myosin Tropomyosin blocking active sites Actin Troponin The aftermath

62. © 2013 Pearson Education, Inc. 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

63. © 2013 Pearson Education, Inc. 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

64. © 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 2 1 3 4

65. © 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 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

66. 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

67. 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

68. 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

69. 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

70. 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

71. © 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

72. © 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

73. © 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

74. © 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.

75. © 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. 1 2 3 4

76. 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

77. © 2013 Pearson Education, Inc.