1a1-chapter 11 muscle tissue Flashcards Preview

Keiser A&P 1 > 1a1-chapter 11 muscle tissue > Flashcards

Flashcards in 1a1-chapter 11 muscle tissue Deck (220):
1

Characteristics of Muscle

responsiveness (excitability)
conductivity
contractility
extensibility
elasticity

2

responsiveness (excitability)

to chemical signals, stretch and electrical changes across the plasma membrane

3

conductivity

local electrical change triggers a wave of excitation that travels along the muscle fiber

4

contractility

shortens when stimulated

5

extensibility

capable of being stretched between contractions

6

elasticity

returns to its original resting length after being stretched

7

skeletal muscle

voluntary, striated muscle attached to one or more bones

8

striations

alternating light and dark transverse bands
–results from an overlapping of internal contractile proteins

9

voluntary

usually subject to conscious control

10

myofiber

muscle cell, muscle fiber, (myofiber) as long as 30 cm

11

tendons are attachments between muscle and bone matrix

–endomysium–connective tissue around muscle cells
–perimysium–connective tissue around muscle fascicles
–epimysium–connective tissue surrounding entire muscle
–continuous with collagen fibers of tendons
–in turn, with connective tissue of bone matrix

12

endomysium

connective tissue around muscle cells

13

perimysium

connective tissue around muscle fascicles

14

epimysium

connective tissue surrounding entire muscle

15

collagenis 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
•contribute to power output and muscle efficiency

16

sarcolemma

plasma membrane of a muscle fiber

17

sarcoplasm

cytoplasm of a muscle fiber

18

myofibrils

long protein bundles that occupies the main portion of the sarcoplasm

19

glycogen

stored in abundance to provide energy with heightened exercise

20

myoglobin

red pigment –stores oxygen needed for muscle activity

21

multiple nuclei

flattened nuclei pressed against the inside of the sarcolemma

22

myoblasts

stem cells that fuse to form each muscle fiber

23

satellite cells

unspecialized myoblasts remaining between the muscle fiber and endomysium
•may multiply and produce new muscle fibers to some degree

24

repair by fibrosis

rather than regeneration of functional muscle

25

mitochondria

packed in spaces between myofibrils

26

sarcoplasmic reticulum

(SR) -smooth ER that forms a network around each myofibril –calcium reservoir
–calcium activates the muscle contraction process

27

terminal cisternae

dilated end-sacs of SR which cross muscle fiber from one side to the other

28

T tubules

tubular infoldings of the sarcolemma which penetrate through the cell and emerge on the other side

29

triad

a T tubule and two terminal cisterns

30

Thick Myofilaments

made of several hundred myosin molecules
–shaped like a golf club
–heads directed outward in a helical array around the bundle

31

Thin Myofilaments

fibrous (F) actin
tropomyosin
troponin

32

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

33

tropomyosin molecule

each blocking 6 or 7 active sites on G actin subunits

34

troponin molecule

small, calcium-binding protein on each tropomyosin molecule

35

Elastic Myofilaments

titin (connectin) –huge springy protein
–flank each thick filament and anchor it to the Z disc
–helps stabilize the thick filament
–center it between the thin filaments
–prevents over stretching

36

contractile proteins

myosin and actin
–do the work

37

regulatory proteins

tropomyosin and troponin
–like a switch that determine when the fiber can contract and when it cannot
–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

38

Overlap of Thick and Thin Filaments

bare zone

zone with no heads in the middle

39

Accessory Proteins

at least seven other accessory proteins in or associated with thick or thin filaments
–anchor the myofilaments, regulate length of myofilaments, alignment of myofilaments for maximum effectiveness

40

dystrophin

most clinically important
–links actin in outermost myofilaments to transmembrane proteins and eventually to fibrous endomysium surrounding the entire muscle cell
–transfers forces of muscle contraction to connective tissue around muscle cell
–genetic defects in dystrophin produce disabling disease muscular dystrophy

41

Striations

myosinand actin are proteins that occur in all cells
–function in cellular motility, mitosis, transport of intracellular material
•organized in a precise way in skeletal and cardiac muscle

42

A band

dark –A stands for anisotropic
•part of A band where thick and thin filaments overlap is especially dark

43

H band

in the middle of A band –just thick filaments

44

M line

is in the middle of the H band

45

I band

alternating lighter band –I stands for isotropic
•the way the bands reflect polarized light

46

z disc

provides anchorage for thin filaments and elastic filaments
•bisects I band

47

sarcomere

segment from Z disc to Z disc
–functional contractile unit of muscle fiber

48

functional contractile unit of the muscle fiber

sarcomere

49

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

50

Nerve-Muscle Relationship

skeletal muscle never contracts unless stimulated by a nerve
•if nerve connections are severed or poisoned, a muscle is paralyzed

51

denervation atrophy

shrinkage of paralyzed muscle when connection not restored

52

somatic motor neurons

nerve cells whose cell bodies are in the brainstem and spinal cord that serve skeletal muscles

53

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

54

motor unit

one nerve fiber and all the muscle fibers innervated by it

55

muscle fibers of one motor unit

–dispersed throughout the muscle
–contract in unison
–produce weak contraction over wide area
–provides ability to sustain long-term contraction as motor units take turns contracting (postural control)
–effective contraction usually requires the contraction of several motor units at once

56

average motor unit

200 muscle fibers for each motor unit

57

small motor units

-fine degree of control
–3-6 muscle fibers per neuron
–eye and hand muscles

58

large motor units

more strength than control
–powerful contractions supplied by large motor units –gastrocnemius –1000 muscle fibers per neuron
–many muscle fibers per motor unit

59

synapse

point where a nerve fiber meets its target cell

60

neuromuscular junction (NMJ)

when target cell is a muscle fiber
•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

61

Components of Neuromuscular Junction

synaptic knob
synaptic cleft
Schwann cell
basal lamina

62

synaptic knob

swollen end of nerve fiber
–contains synaptic vesicles filled with acetylcholine(ACh)

63

synaptic cleft

tiny gap between synaptic knob and muscle sarcolemma

64

Schwann cell

envelops & isolates all of the NMJ from surrounding tissue fluid

65

basal lamina

thin layer of collagen and glycoprotein separates Schwann cell and entire muscle cell from surrounding tissues
–contains acetylcholinesterase( AChE) that breaks down ACh after contraction causing relaxation

66

acetylcholinesterase( AChE)

that breaks down ACh after contraction causing relaxation

67

junctional folds

of sarcolemma beneath synaptic knob
•increases surface area holding ACh receptors
–lack of receptors leads to paralysis in disease myasthenia gravis

68

Neuromuscular Toxins

toxins that interfere with synaptic function can paralyze the muscles
•some pesticidescontain cholinesterase inhibitors
–bind to acetylcholinesterase and prevent it from degrading ACh
–spastic paralysis -a state of continual contraction of the muscles
–possible suffocation

69

tetanus

tetanus(lockjaw) is a form of spastic paralysis caused by toxin of Clostridiumtetani
–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

70

flaccid paralysis

a state in which the muscles are limp and cannot contract
–curare –compete with ACh for receptor sites, but do not stimulate the muscles
–plant poison used by South American natives to poison blowgun darts

71

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 for wrinkle removal

72

Electrically Excitable Cells

muscle fibers and neurons are electrically excitable cells
–their plasma membrane exhibits voltage changes in response to stimulation

73

electrophysiology

the study of the electrical activity of cells

74

in an unstimulated (resting) cell

–there are more anions (negative ions) on the inside of the plasma membrane than on the outside
–the plasma membrane is electrically polarized(charged)
–there are excess sodium ions (Na+) in the extracellular fluid (ECF)
–there are excess potassium ions (K+) in the intracellular fluid (ICF)

75

voltage (electrical potential)

a difference in electrical charge from one point to another

76

resting membrane potential

about -90mV
–maintained by sodium-potassium pump

77

stimulated (active) muscle fiber or nerve cell

–ion gates open in the plasma membrane
–Na+ instantly diffuses down its concentration gradient into the cell
–these cations override the negative charges in the ICF
–depolarization-inside of the plasma membrane becomes briefly positive
–immediately, Na+ gates close and K+ gates open
–K+ rushes out of cell
–repelled by the positive sodium charge and partly because of its concentration gradient
–loss of positive potassium ions turns the membrane negative again (repolarization

78

repolarization

loss of positive potassium ions turns the membrane negative again

79

action potential

quickly fluctuating voltage seen in an active stimulated cell
quick up-and-down voltage shift from the negative RMP to a positive value, and back to the negative value again.

80

four major phases of contraction and relaxation

excitation
excitation-contraction coupling
contraction
relaxation

81

excitation

the process in which nerve action potentials lead to muscle action potentials

82

excitation-contraction coupling

events that link the action potentials on the sarcolemma to activation of the myofilaments, thereby preparing them to contract

83

contraction

step in which the muscle fiber develops tension and may shorten

84

relaxation

when its work is done, a muscle fiber relaxes and returns to its resting length

85

Excitation step 1

Arrival of nerve signal
nerve signal opens voltage-gated calcium channels in synaptic knob

86

Excitation step 2

Acetylcholine (ACh) release
calcium stimulates exocytosis of ACh from synaptic vesicles
•ACh released into synaptic cleft

87

Excitation step 3

Binding of ACh to receptor
two ACh molecules bind to each receptor protein, opening Na+ and K+ channels.

88

Excitation step 4

Opening of ligand-regulated ion gate; creation of end–plate potential
Na+ enters shifting RMP goes from -90mV to +75mV, then K+ exits and RMP returns to -90mV -quick voltage shift is called an end-plate potential (EPP).

89

Excitation step 5

Opening of voltage-regulated ion gates; creation of action potentials
voltage change (EPP) in end-plate region opens nearby voltage-gated channels producing an action potential that spreads over muscle surface.

90

Excitation-Contraction Coupling 6

Action potentials propagated down T tubules
action potential spreads down into T tubules
•opens voltage-gated ion channels in T tubules and Ca2+channels in SR

91

Excitation-Contraction Coupling 7

Calcium released from terminal cisternae
Ca2+enters the cytosolAction

92

Excitation-Contraction Coupling 8

Binding of calcium to troponin
calcium binds to troponin in thin filaments

93

Excitation-Contraction Coupling 9

Shifting of tropomyosin; exposure of active sites on actin
troponin-tropomyosin complex changes shape and exposes active sites on actin

94

Contraction 10

Hydrolysis of ATP to ADP + Pi; activation and cocking of myosin head
•myosin ATPase enzyme in myosin head hydrolyzes an ATP molecule
•activates the head “cocking” it in an extended position
–ADP + Pi remain attached

95

Contraction 11

formation of myosin–actin cross-bridge
•head binds to actin active site forming a myosin -actin cross-bridge

96

Contraction 12

Binding of new ATP; breaking of cross-bridge

97

Contraction 13

ATP Power stroke; sliding of thin filament over thick filament
myosin head releases ADP and Pi, flexes pulling thin filament past thick -power stroke
•upon binding more ATP, myosin releases actin and process is repeated
–each head performs 5 power strokes per second
–each stroke utilizes one molecule of ATP

98

Relaxation 14

Cessation of nervous stimulation and ACh release
nerve stimulation & ACh release stop

99

Relaxation 15

ACh breakdown by acetylcholinesterase (AChE)
AChE breaks down ACh & fragments reabsorbed into synaptic knob
•stimulation by ACh stopsAChECessation

100

Relaxation 16

Reabsorption of calcium ions by sarcoplasmic reticulum
Ca2+pumped back into SR by active transport. Ca2+binds to calsequestrin while in storage in SR
•ATP is needed for muscle relaxation as well as muscle contraction

101

Relaxation 17

Loss of calcium ions from troponin
Ca2+removed from troponin is pumped back into SR

102

Relaxation 18

Return of tropomyosin to position blocking active sites of actin
tropomyosin reblocks the active sites
•muscle fiber ceases to produce or maintain tension
•muscle fiber returns to its resting length
–due to recoil of elastic components & contraction of antagonistic muscles

103

rigor mortis

hardening of muscles and stiffening of body beginning 3 to 4 hours after death

104

rigor mortis

Timeline

muscle relaxation requires ATP, and ATP production is no longer produced after death
–fibers remain contracted until myofilaments begins to decay
•rigor mortis peaks about 12 hours after death, then diminishes over the next 48 to 60 hours

105

Length –Tension Relationship

the amount of tension generated by a muscle and the force of contraction depends on how stretched or contracted it was before it was stimulated

106

if overly contracted at rest,

a weak contraction results
–thick filaments too close to Z discs and can‟t slide

107

if too stretched before stimulated

a weak contraction results
–little overlap of thin and thick does not allow for very many cross bridges to form

108

optimum resting length produces

greatest force when muscle contracts

109

muscle tone

central nervous system continually monitors and adjusts the length of the resting muscle, and maintains a state of partial contraction called muscle tone
–maintains optimum length and makes the muscles ideally ready for action

110

myogram

a chart of the timing and strength of a muscle‟s contraction

111

threshold

the minimum voltage necessary to generate an action potential in the muscle fiber and produce a contraction

112

twitch

a quick cycle of contraction when stimulus is at threshold or higher

113

Phases of a Twitch Contraction

latent period
contraction phase
relaxation phase

114

latent period

2 msec delay between the onset of stimulus and onset of twitch response
–time required for excitation, excitation-contraction coupling and tensing of elastic components of the muscle

115

internal tension

force generated during latent period and no shortening of the muscle occurs

116

contraction phase

phase in which filaments slide and the muscle shortens
–once elastic components are taut, muscle begins to produce external tension –in muscle that moves a load
–short-lived phase

117

external tension

once elastic components are taut, muscle begins to produce external tension –in muscle that moves a load

118

relaxation phase

SR quickly reabsorbs Ca2+, myosin releases the thin filaments and tension declines
–muscle returns to resting length
–entire twitch lasts from 7 to 100 msec

119

Contraction Strength of Twitches

at subthreshold stimulus

no contraction at all

120

Contraction Strength of Twitches

at threshold intensity and above

a twitch is produced
–twitches caused by increased voltage are no stronger than those at threshold

121

not exactly true that muscle fiber obeys an all-or-none law-

contracting to its maximum or not at all
–electrical excitation of a muscle follows all-or-none law
–not true that muscle fibers follow the all or none law

122

twitches vary in strength depending upon:

stimulus frequency
concentration of Ca2+
how stretched muscle was
temperature of the muscles
lower than normal pH
state of hydration

123

stimulus frequency

stimuli arriving closer together produce stronger twitches

124

concentration of Ca2+

in sarcoplasm can vary the frequency

125

how stretched muscle was

how stretched muscle was before it was stimulated

126

temperature of the muscles

warmed-up muscle contracts more strongly –enzymes work more quickly

127

lower than normal pH

lower than normal pH of sarcoplasm weakens the contraction -fatigue

128

state of hydration

of muscle affects overlap of thick & thin filaments

129

recruitment or multiple motor unit (MMU) summation

the process of bringing more motor units into play

130

Stimulus Intensity

stimulating the nerve with higher and higher voltages produces stronger contractions
–higher voltages excite more and more nerve fibers in the motor nerve which stimulates more and more motor units to contract

131

when stimulus intensity (voltage) remains constant twitch strength can vary with the stimulus frequency
•up to 10 stimuli per second

each stimulus produces identical twitches and full recovery between twitches

132

when stimulus intensity (voltage) remains constant twitch strength can vary with the stimulus frequency

10-20 stimuli per second

produces treppe (staircase) phenomenon
–muscle still recovers fully between twitches, but each twitch develops more tension than the one before

133

when stimulus intensity (voltage) remains constant twitch strength can vary with the stimulus frequency

20-40 stimuli per second

produces incomplete tetanus
–each new stimulus arrives before the previous twitch is over
–new twitch “rides piggy-back” on the previous one generating higher tension

134

temporal summation

results from two stimuli arriving close together

135

wave summation

results from one wave of contraction added to another
–each twitch reaches a higher level of tension than the one before
–muscle relaxes only partially between stimuli

136

incomplete tetanus

produces a state of sustained fluttering contraction

137

when stimulus intensity (voltage) remains constant twitch strength can vary with the stimulus frequency

40-50 stimuli per second

produces complete tetanus
–muscle has no time to relax at all between stimuli
–twitches fuse to a smooth, prolonged contraction called complete tetanus

138

complete tetanus

twitches fuse to a smooth, prolonged contraction

139

Normal stimuli per second peak

rarely exceeds 25 stimuli per second

140

isometric muscle contraction

muscle is producing internal tension while an external resistance causes it to stay the same length or become longer

141

isotonic muscle contraction

muscle changes in length with no change in tension

142

concentric contraction

muscle shortens while maintains tension

143

eccentric contraction

muscle lengthens as it maintains tension

144

isometric phase

at the beginning of contraction –isometric phase
–muscle tension rises but muscle does not shorten
•when tension overcomes resistance of the load
–tension levels off

145

isotonic phase

muscle begins to shorten and move the load

146

Muscle Metabolism

all muscle contraction depends on ATP
•ATP supply depends on availability of:
–oxygen
–organic energy sources such as glucose and fatty acids

147

organic energy sources

glucose and fatty acids

148

two main pathways of ATP synthesis

anaerobic fermentation
aerobic respiration

149

anaerobic fermentation

enables cells to produce ATP in the absence of oxygen
•yields little ATP and toxic lactic acid, a major factor in muscle fatigue

150

aerobic respiration

•produces far more ATP
•less toxic end products (CO2and water)
•requires a continual supply of oxygen

151

Immediate Energy Needs

short, intense exercise (100 m dash)

–oxygen need is briefly supplied by myoglobin for a limited amount of aerobic respiration at onset –rapidly depleted
–muscles meet most of ATP demand by borrowing phosphate groups (Pi) from other molecules and transferring them to ADP

152

Immediate Energy Needs

phosphate transfers

two enzyme systems control these phosphate transfers
myokinase –transfers Pi from one ADP to another converting the latter to ATP
–creatine kinase –obtains Pi from a phosphate-storage molecule creatine phosphate (CP)

153

Immediate Energy Needs

phosphagen system

ATP and CP collectively
–provides nearly all energy used for short bursts of intense activity

154

Short-Term Energy Needs

as the phosphagen system is exhausted
•muscles shift to anaerobic fermentation

155

anaerobic fermentation

muscles obtain glucose from blood and their own stored glycogen
–in the absence of oxygen, glycolysis can generate a net gain of 2 ATP for every glucose molecule consumed
–converts glucose to lactic acid

156

glycogen-lactic acid system

the pathway from glycogen to lactic acid
•produces enough ATP for 30 –40 seconds of maximum activity

157

Long-Term Energy Needs

after 40 seconds or so, the respiratory and cardiovascular systems “catch up” and deliver oxygen to the muscles fast enough for aerobic respiration to meet most of the ATP demands

158

aerobic respiration produces

36 ATP per glucose

159

aerobic respiration

efficient means of meeting the ATP demands of prolonged exercise
–one‟s rate of oxygen consumption rises for 3 to 4 minutes and levels off to a steady state in which aerobic ATP production keeps pace with demand

160

muscle fatigue

progressive weakness and loss of contractility from prolonged use of the muscles

161

muscle fatigue

causes

-ATP synthesis declines as glycogen is consumed
–ATP shortage slows down the Na+-K+ pumps
-lactic acid lowers pH of sarcoplasm
–release of K+with each action potential causes the accumulation of extracellular K+
–motor nerve fibers use up their ACh

162

junctional fatigue

motor nerve fibers use up their ACh
•less capable of stimulating muscle fibers

163

endurance

the ability to maintain high-intensity exercise for more than 4 to 5 minutes
–determined in large part by one‟s maximum oxygen uptake (VO2max)

164

maximum oxygen uptake

the point at which the rate of oxygen consumption reaches a plateau and does not increase further with an added workload

165

Oxygen Debt

heavy breathing continues after strenuous exercise

166

excess post-exercise oxygen consumption (EPOC)

the difference between the resting rate of oxygen consumption and the elevated rate following exercise.
–typically about 11 liters extra is needed after strenuous exercise
–repaying the oxygen debt

167

11 liters extra is needed for

replace oxygen reserves
replenishing the phosphagen system
oxidizing lactic acid
serving the elevated metabolic rate

168

replace oxygen reserves

depleted in the first minute of exercise
•oxygen bound to myoglobin and blood hemoglobin, oxygen dissolved in blood plasma and other extracellular fluid, and oxygen in the air in the lungs

169

replenishing the phosphagen system

synthesizing ATP and using some of it to donate the phosphate groups back to creatine until resting levels of ATP and CP are restored

170

oxidizing lactic acid

•80% of lactic acid produced by muscles enter bloodstream
•reconverted to pyruvic acid in the kidneys, cardiac muscle, and especially the liver
•liver converts most of the pyruvic acid back to glucose to replenish the glycogen stores of the muscle

171

serving the elevated metabolic rate

occurs while the body temperature remains elevated by exercise and consumes more oxygen

172

66Beating Muscle Fatigue

-Taking oral creatine increases level of creatine phosphate in muscle tissue and increases speed of ATP regeneration
-carbohydrate loading –dietary regimen

173

Physiological Classes of Muscle Fibers

slow oxidative (SO), slow-twitch, red, or type I fibers

174

slow oxidative (SO), slow-twitch, red, or type I fibers

abundant mitochondria, myoglobin and capillaries -deep red color
•adapted for aerobic respiration and fatigue resistance
–relative long twitch lasting about 100 msec
–soleus of calf and postural muscles of the back

175

fast glycolytic (FG), fast-twitch, white, or type II fibers

fibers are well adapted for quick responses, but not for fatigue resistance
–rich in enzymes of phosphagen and glycogen-lactic acid systems generate lactic acid causing fatigue
–poor in mitochondria, myoglobin, and blood capillaries which gives pale appearance
•SR releases & reabsorbs Ca2+quickly so contractions are quicker
(7.5 msec/twitch)
–extrinsic eye muscles, gastrocnemius and biceps brachii

176

ratio of different fiber types have

genetic predisposition –born sprinter
–muscles differ in fiber types -gastrocnemius is predominantly FG for quick movements (jumping)
–soleus is predominantly SO used for endurance (jogging)

177

Strength and Conditioning

muscles can generate more tension than the bones and tendons can withstand

178

muscular strength depends primarily on

primarily on muscle size
•a muscle can exert a tension of 3 or 4 kg / cm2of cross-sectional area

179

muscular strength depends

other factors

fascicle arrangement
size of motor units
multiple motor unit summation –recruitment
temporal summation
length –tension relationship
fatigue

180

fascicle arrangement

pennate are stronger than parallel, and parallel stronger than circular

181

size of motor units

•larger the motor unit the stronger the contraction

182

multiple motor unit summation –recruitment

•when stronger contraction is required, the nervous system activates more motor units

183

temporal summation

•nerve impulses usually arrive at a muscle in a series of closely spaced action potentials
•the greater the frequency of stimulation, the more strongly a muscle contracts

184

length –tension relationship

a muscle resting at optimal length is prepared to contract more forcefully than a muscle that is excessively contracted or stretched

185

length –tension relationship

fatigued muscles contract more weakly than rested muscles

186

resistance training (weight lifting)

–contraction of a muscles against a load that resist movement
–a few minutes of resistance exercise a few times a week is enough to stimulate muscle growth
–growth is from cellular enlargement
–muscle fibers synthesize more myofilaments and myofibrils and grow thicker

187

endurance training (aerobic exercise)

–improves fatigue resistant muscles
–slow twitch fibers produce more mitochondria, glycogen, and acquire a greater density of blood capillaries
–improves skeletal strength
–increases the red blood cell count and oxygen transport capacity of the blood
–enhances the function of the cardiovascular, respiratory, and nervous systems

188

Cardiac Muscle

limited to the heart where it functions to pump blood

189

required properties of cardiac muscle

–contraction with regular rhythm
–muscle cells of each chamber must contract in unison
–contractions must last long enough to expel blood
–must work in sleep or wakefulness, with out fail, and without conscious attention
–must be highly resistant to fatigue

190

characteristics of cardiac muscle cells

striated like skeletal muscle, but myocytes (cardiocytes) are shorter and thicker

191

intercalated discs

each myocyte is joined to several others at the uneven, notched linkages –intercalated discs
•appear as thick dark lines in stained tissue sections
•electrical gap junctions allow each myocyte to directly stimulate its neighbors
•mechanical junctions that keep the myocytes from pulling apart

192

damaged cardiac muscle cells repair by

fibrosis
•a little mitosis observed following heart attacks
•not in significant amounts to regenerate functional muscle

193

can contract without need for

nervous stimulation
•contains a built-in pacemaker that rhythmically sets off a wave of electrical excitation
•wave travels through the muscle and triggers contraction of heart chambers

194

autorhythmic

because of its ability to contract rhythmically and independently

195

autonomic nervous system

does send nerve fibers to the heart
•can increase or decrease heart rate and contraction strength

196

very slow twitches

does not exhibit quick twitches like skeletal muscle
•maintains tension for about 200 to 250 msec
•gives the heart time to expel blood

197

uses aerobic respiration

almost exclusively
•rich in myoglobin and glycogen
•has especially large mitochondria
–25% of volume of cardiac muscle cell
–2% of skeletal muscle cell with smaller mitochondria

198

Smooth Muscle

•composed of myocytes that have a fusiform shape
•there is only one nucleus, located near the middle of the cell

199

Smooth Muscle

Differences from Skeletal Muscle

•no visible striations
•z discs are absent and replaced by dense bodies
•cytoplasm contains extensive cytoskeleton of intermediate filament
•sarcoplasmic reticulum is scanty and there are no T tubules

200

2 Types of Smooth Muscle

multiunit smooth muscle
single-unit smooth muscle

201

multiunit smooth muscle

–occurs in some of the largest arteries and pulmonary air passages, in piloerector muscles of hair follicle, and in the iris of the eye
–autonomic innervation similar to skeletal muscle
•terminal branches of a nerve fiber synapse with individual myocytes and form a motor unit
•each motor unit contracts independently of the others

202

single-unit smooth muscle

–more widespread
–occurs in most blood vessels, in the digestive, respiratory, urinary, and reproductive tracts –also called visceral muscle
•often in two layers
–inner circular
–outer longitudinal
–myocytes of this cell type are electrically coupled to each other by gap junctions
–they directly stimulate each other and a large number of cells contract as a single unit

202

Stimulation of Smooth Muscle

contraction

smooth muscle is involuntary and can contract without nervous stimulation
–can contract in response to chemical stimuli

203

most smooth muscle is innervated by

autonomic nerve fibers
–can trigger and modify contractions
–stimulate smooth muscle with either acetylcholine or norepinephrine
–can have contrasting effects
•relax the smooth muscle of arteries
•contract smooth muscles of the bronchioles

204

varicosities

in single unit smooth muscle, each autonomic nerve fibers has up to 20,000 beadlike swelling

205

diffuse junctions

no motor end plates, but receptors scattered throughout the surface –diffuse junctions –no one-to-one relationship between nerve fiber and myocyte

206

Contraction and Relaxation

contraction is triggered by Ca2+, energized by ATP, and achieved by sliding thin past thick filaments
•contraction begins in response to Ca2+that enters the cell from ECF, a little internally from sarcoplasmic reticulum
Ca2+channels open to allow Ca2+to enter cell
•calcium binds to calmodulin on thick filaments

207

contraction and relaxation very slow in comparison to skeletal muscle

–latent period in skeletal 2 msec, smooth muscle 50 -100 msec
–tension peaks at about 500 msec (0.5 sec)
–declines over a period of 1 –2 seconds
–slows myosin ATPase enzyme and slow pumps that remove Ca2+
–Ca2+binds to calmodulin instead of troponin
•activates kinases and ATPases that hydrolyze ATP

208

latch-bridge mechanism

is resistant to fatigue
–heads of myosin molecules do not detach from actin immediately
–do not consume any more ATP
–maintains tetanus tonic contraction (smooth muscle tone)
•arteries –vasomotor tone intestinal tone
–makes most of its ATP aerobically

209

Stretching Smooth Muscle

Stretch

stretch can open mechanically-gated calcium channels in the sarcolemma causing contraction

210

peristalsis

waves of contraction brought about by food distending the esophagus or feces distending the colon
•propels contents along the organ

211

stress-relaxation response

(receptive relaxation) -helps hollow organs gradually fill (urinary bladder)
–when stretched, tissue briefly contracts then relaxes –helps prevent emptying while filling

212

Contraction and Stretching

skeletal muscle cannot contract forcefully if overstretched
•smooth muscle contracts forcefully even when greatly stretched
•smooth muscle can be anywhere from half to twice its resting length and still contract powerfully

213

smooth muscle can be anywhere from half to twice its resting length and still contract powerfully

three reasons:

–there are no z discs, so thick filaments cannot butt against them and stop contraction
–since the thick and thin filaments are not arranged in orderly sarcomeres, stretching does not cause a situation where there is too little overlap for cross-bridges to form
–the thick filaments of smooth muscle have myosin heads along their entire length, so cross-bridges can form anywhere

214

plasticity

the ability to adjust its tension to the degree of stretch
–a hollow organ such as the bladder can be greatly stretched yet not become flabby when it is empty

215

muscular dystrophy

group of hereditary diseases in which skeletal muscles degenerate and weaken, and are replaced with fat and fibrous scar tissue

216

Duchenne muscular dystrophy

is caused by a sex-linked recessive trait (1 of 3500 live-born boys)
–most common form
–disease of males –diagnosed between 2 and 10 years of age
–mutation in gene for muscle protein dystrophin
•actin not linked to sarcolemma and cell membranes damaged during contraction, necrosis and scar tissue results
–rarely live past 20 years of age due to effects on respiratory and cardiac muscle –incurable

217

Myasthenia Gravis

autoimmune disease in which antibodies attack neuromuscular junctions and bind ACh receptors together in clusters
–disease of women between 20 and 40
–muscle fibers then removes the clusters of receptors from the sarcolemma by endocytosis
–fiber becomes less and less sensitive to ACh
–effects usually first appear in facial muscles
•drooping eyelids and double vision, difficulty swallowing, and weakness of the limbs

218

strabismus

inability to fixate on the same point with both eyes

219

Myasthenia Gravis

treatments

–cholinesterase inhibitors retard breakdown of ACh allowing it to stimulate the muscle longer
–immunosuppressive agents suppress the production of antibodies that destroy ACh receptors
–thymus removal (thymectomy) –helps to dampen the overactive immune response that causes myasthenia gravis
–plasmapheresis–technique to remove harmful antibodies from blood plasma