1. Chapter 11 Lecture Outline 1
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2. Introduction
Movement is a fundamental characteristic of all living organisms
Three types of muscular tissue—skeletal, cardiac, and smooth muscle
- all muscle types will respond to an electrical
stimulus, all muscle cells are excitable
Important to understand muscle at the molecular, cellular, and tissue levels of organization

3. Types and Characteristics of Muscular Tissue
Expected Learning Outcomes
Describe the physiological properties that all muscle types have in common.
List the defining characteristics of skeletal muscle.
Discuss the possible elastic functions of the connective tissue components of a muscle.

4. Universal Characteristics of Muscle
Excitability (responsiveness)
To chemical signals, stretch, and electrical changes across the plasma membrane
Conductivity
Local electrical change triggers a wave of excitation that travels along the muscle fiber
Contractility
Shortens when stimulated
Extensibility
Capable of being stretched between contractions
Elasticity
- Returns to its original rest length after being stretched
Irritability
Muscle tissue refers to the ability to respond to stimulation

5. Skeletal Muscle
Skeletal muscle—voluntary, striated muscle usually attached to bones
Striations—alternating light and dark transverse bands
Results from arrangement of internal contractile proteins
Voluntary—usually subject to conscious control
Muscle cell is a muscle fiber (myofiber)—as long as 30 cm
Figure 11.1

6. Skeletal Muscle Connective tissue wrappings
Endomysium: connective tissue around muscle cell
Perimysium: connective tissue around muscle fascicle
Epimysium: connective tissue surrounding entire muscle
Tendons are attachments between muscle and bone matrix
Continuous with collagen fibers of tendons
In turn, with connective tissue of bone matrix
Collagen is somewhat extensible and elastic
Stretches slightly under tension and recoils when released
Resists excessive stretching and protects muscle from injury
Returns muscle to its resting length
Contributes to power output and muscle efficiency

7. Microscopic Anatomy of Skeletal Muscle
Expected Learning Outcomes
Describe the structural components of a muscle fiber.
Relate the striations of a muscle fiber to the overlapping arrangement of its protein filaments.
Name the major proteins of a muscle fiber and state the function of each.

8. The Muscle Fiber Sarcolemma—plasma membrane of a muscle fiber
Sarcoplasm—cytoplasm of a muscle fiber
Myofibrils: long protein cords occupying most of sarcoplasm
Glycogen: carbohydrate stored to provide energy for exercise
Myoglobin: red pigment; provides some oxygen needed for muscle activity

9. The Muscle Fiber
Multiple nuclei—flattened nuclei pressed against the inside of the sarcolemma
Myoblasts: stem cells that fused to form each muscle fiber early in development
Satellite cells: unspecialized myoblasts remaining between the muscle fiber and endomysium
Play a role in regeneration of damaged skeletal muscle tissue
Mitochondria—packed into spaces between myofibrils

10. The Muscle Fiber
Sarcoplasmic reticulum (SR)—smooth ER that forms a network around each myofibril:
Terminal cisternae—dilated end-sacs of SR which cross the muscle fiber from one side to the other
Acts as a calcium reservoir; it releases calcium through channels to activate contraction
T tubules—tubular infoldings of the sarcolemma which penetrate through the cell and emerge on the other side
Triad—a T tubule and two terminal cisternae associated with it

11. The Muscle Fiber Figure 11.2 Muscle fiber Nucleus A band I band Z disc
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Muscle fiber
Nucleus
A band
I band
Z disc
Mitochondria
Openings into transverse tubules
Sarcoplasmic reticulum T
riad: T
erminal cisternae T
ransverse tubule
Sarcolemma
Myofibrils
Sarcoplasm
Figure 11.2
Myofilaments

12. Myofilaments Thick filaments—made of several hundred myosin molecules
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Head
Tail
(a) Myosin molecule
Myosin head
(b) Thick filament
Figure 11.3a, b, d
Thick filaments—made of several hundred myosin molecules
Each molecule shaped like a golf club
Two chains intertwined to form a shaft-like tail
Double globular head
Heads directed outward in a helical array around the bundle
Heads on one half of the thick filament angle to the left, while heads on other half angle to the right
Bare zone with no heads in the middle

13. Myofilaments Thin filaments Fibrous (F) actin: two intertwined strands
String of globular (G) actin subunits each with an active site that can bind to head of myosin molecule
Tropomyosin molecules
Each blocking six or seven active sites on G actin subunits
Troponin molecule: small, calcium-binding protein (calcium receptors) on each tropomyosin molecule in skeletal muscle
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Tropomyosin
Troponin complex
G actin
(c) Thin filament
Figure 11.3c

14. Myofilaments Elastic filaments Titin: huge, springy protein
Run through core of thin filament and anchor it to Z disc and M line
Help stabilize and position the thick filament
Prevent overstretching and provide recoil
Figure 11.5

15. Myofilaments
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Myosin head
(b) Thick filament
Tropomyosin
Troponin complex
G actin
Figure 11.3b,c
(c) Thin filament
Contractile proteins—myosin and actin do the work of contraction
Regulatory proteins—tropomyosin and troponin
Act like a switch that determines when fiber can (and cannot) contract
Contraction activated by release of calcium into sarcoplasm and its binding to troponin
Troponin changes shape and moves tropomyosin off the active sites on actin

16. Myofilaments Figure 11.3d Thick filament Thin filament Bare zone
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Thick filament
Thin filament
Bare zone
Portion of a sarcomere showing the overlap
of thick and thin filaments
Figure 11.3d

17. Myofilaments
Several other proteins associate with myofilaments to anchor, align, and regulate them
Dystrophin—clinically important protein
Links actin in outermost myofilaments to membrane proteins that link to endomysium
Transfers forces of muscle contraction to connective tissue ultimately leading to tendon
Genetic defects in dystrophin produce disabling disease muscular dystrophy

18. Striations
Striations result from the precise organization of myosin and actin in cardiac and skeletal muscle cells
Striations are alternating A-bands (dark) and I-bands (light)
Figure 11.5b

19. Striations A band: dark; “A” stands for anisotropic
Darkest part is where thick filaments overlap a hexagonal array of thin filaments
H band: not as dark; middle of A band; thick filaments only
M line: middle of H band
I band: light; “I” stands for isotropic
The way the bands reflect polarized light
Z disc: provides anchorage for thin filaments and elastic filaments
Bisects I band
Figure 11.5b

20. Striations
Figure 11.5a

21. Striations
Sarcomere—segment from Z disc to Z disc marks the boundaries of a sarcomere
Functional contractile unit of muscle fiber
Muscle cells shorten because their individual sarcomeres shorten
Z disc (Z lines) are pulled closer together as thick and thin filaments slide past each other
Neither thick nor thin filaments change length during shortening
Only the amount of overlap changes
During shortening, dystrophin and linking proteins also pull on extracellular proteins
Transfers pull to extracellular tissue

22. Structural Hierarchy of Skeletal Muscle

23. Structural Hierarchy of Skeletal Muscle

24. The Nerve—Muscle Relationship
Expected Learning Outcomes
Explain what a motor unit is and how it relates to muscle contraction.
Describe the structure of the junction where a nerve fiber meets a muscle fiber.
Explain why a cell has an electrical charge difference across its plasma membrane and, in general terms, how this relates to muscle contraction.

25. The Nerve—Muscle Relationship
Skeletal muscle never contracts unless stimulated by a nerve
- Muscle type depends solely on the sarcoplasmic reticulum as its calcium source
If nerve connections are severed or poisoned, a muscle is paralyzed
Denervation atrophy: shrinkage of paralyzed muscle when nerve remains disconnected

26. Motor Neurons and Motor Units
Somatic motor neurons
Nerve cells whose cell bodies are in the brainstem and spinal cord that serve skeletal muscles
Somatic motor fibers—their axons that lead to the skeletal muscle
Each nerve fiber branches out to a number of muscle fibers
Each muscle fiber is supplied by only one motor neuron

27. Motor Neurons and Motor Units
Motor unit—one nerve fiber and all the muscle fibers innervated by it
Muscle fibers of one motor unit
Dispersed throughout muscle
Contract in unison
Produce weak contraction over wide area
Provide ability to sustain long-term contraction as motor units take turns contracting
Effective contraction usually requires contraction of several motor units at once
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Spinal cord
Motor
neuron 1
Motor
neuron 2
Neuromuscular
junction
Skeletal
muscle
fibers
Figure 11.6

28. Motor Neurons and Motor Units
Average motor unit contains 200 muscle fibers
Small motor units—fine degree of control
Three to six muscle fibers per neuron
Eye and hand muscles
Large motor units—more strength than control
Powerful contractions supplied by large motor units with hundreds of fibers
Gastrocnemius of calf has 1,000 muscle fibers per neuron

29. The Neuromuscular Junction
Synapse—point where a nerve fiber meets its target cell
Neuromuscular junction (NMJ)—when target cell is a muscle fiber, where the muscle fiber and the nerve ending meet
Each terminal branch of the nerve fiber within the NMJ forms separate synapse with the muscle fiber
One nerve fiber stimulates the muscle fiber at several points within the NMJ

30. The Neuromuscular Junction
Synaptic knob—swollen end of nerve fiber
Contains synaptic vesicles with acetylcholine (ACh)
Synaptic cleft—gap between synaptic knob and sarcolemma
Schwann cell envelops and isolates NMJ
Figure 11.7b

31. The Neuromuscular Junction
To stimulate muscle contraction, Nerve impulse causes synaptic vesicles to undergo exocytosis releasing Acetylcholine (Ach) into synaptic cleft
Muscle cell has millions of ACh receptors—proteins incorporated into its membrane
- Chemical release to stimulate muscle contraction

32. The Neuromuscular Junction
Junctional folds of sarcolemma beneath synaptic knob increase surface area holding ACh receptors
Lack of receptors causes muscle weakness especially in face and throat and an autoimmune muscle disease is called Myasthenia gravis
Basal lamina—thin layer of collagen and glycoprotein separating Schwann cell and muscle cell from surrounding tissues
Contains acetylcholinesterase (AChE) that breaks down Ach, allowing for relaxation

33. The Neuromuscular Junction
Figure 11.7a

34. Electrically Excitable Cells
Muscle fibers and neurons are electrically excitable
Their membranes exhibit voltage changes in response to stimulation
Electrophysiology—the study of the electrical activity of cells
Voltage (electrical potential)—a difference in electrical charge from one point to another
Resting membrane potential—about −90 mV in skeletal muscle cells
Maintained by sodium–potassium pump

35. Electrically Excitable Cells
In an unstimulated (resting) cell
There are more anions (negatively charged particles) on the inside of the membrane than on the outside
These anions make the inside of the plasma membrane negatively charged by comparison to its outer surface
The plasma membrane is electrically polarized (charged) with a negative resting membrane potential (RMP)
There are excess sodium ions (Na+) in the extracellular fluid (ECF)
There are excess potassium ions (K+) in the intracellular fluid (ICF)

36. Electrically Excitable Cells
Stimulated (active) muscle fiber or nerve cell
Na + ion gates open in the plasma membrane
Na+ flows into cell down its electrochemical gradient
These cations override the negative charges in the ICF
Depolarization: inside of plasma membrane becomes positive
Immediately, Na+ gates close and K+ gates open
K+ rushes out of cell partly repelled by positive sodium charge and partly because of its concentration gradient
Loss of positive potassium ions turns the membrane negative again (repolarization)
This quick up-and-down voltage shift (depolarization and repolarization) is called an action potential

37. Electrically Excitable Cells
Resting membrane potential (RMP) is seen in a waiting excitable cell, whereas action potential is a quick event seen in a stimulated excitable cell
An action potential perpetuates itself down the length of a cell’s membrane
An action potential at one point causes another one to happen immediately in front of it, which triggers another one a little farther along and so forth
This wave of excitation is called an impulse

38. Neuromuscular Toxins and Paralysis
Toxins interfering with synaptic function can paralyze muscles
Some pesticides contain cholinesterase inhibitors
Bind to acetylcholinesterase and prevent it from degrading Ach
Spastic paralysis: a state of continual contraction of the muscles; possible suffocation
Tetanus (lockjaw) is a form of spastic paralysis caused by toxin Clostridium tetani, absence or inhibition of acetylcholinesterase at a synapse lead to tetanus
Glycine in the spinal cord normally stops motor neurons from producing unwanted muscle contractions
Tetanus toxin blocks glycine release in the spinal cord and causes overstimulation and spastic paralysis of the muscles, Tetany - types of muscle contraction is abnormal

39. Neuromuscular Toxins and Paralysis
Flaccid paralysis—a state in which the muscles are limp and cannot contract
Curare: competes with ACh for receptor sites, but does not stimulate the muscles
Plant poison used by South American natives to poison blowgun darts
Botulism—type of food poisoning caused by a neuromuscular toxin secreted by the bacterium Clostridium botulinum
Blocks release of ACh causing flaccid paralysis
Botox cosmetic injections used for wrinkle removal

40. Behavior of Skeletal Muscle Fibers
Expected Learning Outcomes
Explain how a nerve fiber stimulates a skeletal muscle fiber.
Explain how stimulation of a muscle fiber activates its contractile mechanism.
Explain the mechanism of muscle contraction.
Explain how a muscle fiber relaxes.
Explain why the force of a muscle contraction depends on sarcomere length prior to stimulation.

41. Behavior of Skeletal Muscle Fibers
Four major phases of contraction and relaxation
Excitation
Process in which nerve action potentials lead to muscle action potentials
Excitation–contraction coupling
Events that link the action potentials on the sarcolemma to activation of the myofilaments, thereby preparing them to contract
Contraction
Step in which the muscle fiber develops tension and may shorten
Relaxation
When stimulation ends, a muscle fiber relaxes and returns to its resting length

42. Excitation
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Nerve signal
Motor
nerve
fiber
Ca2+ enters
synaptic knob
Sarcolemma
Synaptic
knob
Synaptic
vesicles
ACh
Synaptic
cleft
ACh
receptors 1
Arrival of nerve signal 2
Acetylcholine (ACh) release
Figure 11.8 (1, 2)
Nerve signal opens voltage-gated calcium channels in synaptic knob
Calcium enters knob and stimulates release of ACh from synaptic vesicles into synaptic cleft
Ach diffuses across cleft

43. Excitation
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Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
ACh
ACh K+
ACh receptor
Sarcolemma
Na+ 3
Binding of ACh to receptor 4
Opening of ligand-regulated ion gate;
creation of end-plate potential
Figure 11.8 (3, 4)
Two ACh molecules bind to each receptor and open its channel
Na+ enters; shifting membrane potential from −90 mV to +75 mV
Then K+ exits and potential returns to −90 mV
The quick voltage shift is called an end-plate potential (EPP)

44. Excitation
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Plasma
membrane
of synaptic
knob
Na+
Voltage-regulated
ion gates
Sarcolemma
Figure 11.8 (5) 5
Opening of voltage-regulated ion gates;
creation of action potentials
Voltage change in end-plate region (EPP) opens nearby voltage-gated channels producing an action potential that spreads over muscle surface

45. Excitation–Contraction Coupling
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Figure 11.9 (6, 7)
Terminal
cisterna
of SR
T tubule
T tubule
Sarcoplasmic
reticulum
Ca2+
Ca2+ 6
Action potentials propagated
down T tubules 7
Calcium released from
terminal cisternae
Action potential spreads down T tubules
Opens voltage-gated ion channels in T tubules and Ca+2 channels in SR
Ca+2 leaves SR and enters cytosol

46. Excitation–Contraction Coupling
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Active sites
Troponin
Ca2+
Tropomyosin
Actin
Thin filament
Myosin
Ca2+ 8
Binding of calcium
to troponin 9
Shifting of tropomyosin;
exposure of active sites
on actin
Figure 11.9 (8, 9)
Calcium binds to troponin in thin filaments
Troponin–tropomyosin complex changes shape and exposes active sites on actin

47. Contraction - ATPase in myosin head hydrolyzes an ATP molecule
Skeletal muscles require energy to move, and they receive this energy from ATP
During muscle contraction a single myosin head consumes ATP at a rate of about 5 ATP per second
Figure (10, 11)

48. Contraction Activates the head “cocking” it in an extended position
ADP + Pi remain attached
Head binds to actin active site forming a myosin–actin cross-bridge
Figure (10, 11)

49. Contraction
Myosin releases ADP and Pi, and flexes pulling thin filament with it—power stroke
Upon binding more ATP, myosin releases actin and process can be repeated
Recovery stroke recocks head
Each head performs five power strokes per second
Each stroke utilizes one molecule of ATP
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ATP 13
Binding of new ATP;
breaking of cross-bridge
ADP
ADP Pi Pi 12
Power stroke; sliding of thin
filament over thick filament
Figure (12, 13)

50. Relaxation Nerve stimulation and ACh release stop
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Figure (14, 15)
AChE
ACh 14
Cessation of nervous stimulation
and ACh release 15
ACh breakdown by
acetylcholinesterase (AChE)
Nerve stimulation and ACh release stop
AChE breaks down ACh and fragments are reabsorbed into knob
Stimulation by ACh stops

51. Relaxation Ca+2 pumped back into SR by active transport
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Terminal cisterna
of SR
Ca2+
Ca2+
Figure (16) 16
Reabsorption of calcium ions by
sarcoplasmic reticulum
Ca+2 pumped back into SR by active transport
Ca+2 binds to calsequestrin while in storage in SR

52. Relaxation Ca+2 removed from troponin is pumped back into SR
Tropomyosin reblocks the active sites of actin
Muscle fiber ceases to produce or maintain tension
Muscle fiber returns to its resting length
Due to recoil of elastic components and contraction of antagonistic muscles
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Ca2+
ADP Pi
Ca2+ 17
Loss of calcium ions from troponin
Tropomyosin
ATP 18
Return of tropomyosin to position
blocking active sites of actin
Figure (17, 18)

53. The Length–Tension Relationship and Muscle Tone
Length–tension relationship—the amount of tension generated by a muscle depends on how stretched or shortened it was before it was stimulated
If overly shortened before stimulated, a weak contraction results, as thick filaments just butt against Z discs
If too stretched before stimulated, a weak contraction results, as minimal overlap between thick and thin filaments results in minimal cross-bridge formation
Optimum resting length produces greatest force when muscle contracts
The nervous system maintains muscle tone (partial contraction) to ensure that resting muscles are near this length

54. Length–Tension Relationship
Figure 11.12

55. Summary of Muscle Contraction
Nerve impulse arrives at axon end of the neuromuscular junction
Acetylcholine is released
Acetylcholine binds with receptor sites on sarcolemma
Muscle impulse travels through T- tubules and ends at sarcoplasmic reticulum
Calcium ions released from sarcoplasmic reticulum
Calcium binds with troponin
Shift of tropomysin, makes actin binding sites available for myosin
Myosin attaches to binding site on actin
ATP burned to release energy and bend myosin heads (power stroke)
Actin slides over myosin
New ATP binds to myosin heads
Myosin detaches from actin
Ach degrade: calcium ions rapidly return to sarcoplasmic reticulum
Tropomysin returns over binding sites on actin and contraction ceases

56. Rigor Mortis
Rigor mortis—hardening of muscles and stiffening of body beginning 3 to 4 hours after death
Deteriorating sarcoplasmic reticulum releases Ca+2
Deteriorating sarcolemma allows Ca+2 to enter cytosol
Ca+2 activates myosin-actin cross-bridging
Muscle contracts, but cannot relax
Muscle relaxation requires ATP, and ATP production is no longer produced after death
Fibers remain contracted until myofilaments begin to decay
Rigor mortis peaks about 12 hours after death, then diminishes over the next 48 to 60 hours