Ch9 PPT Mod8e

PowerPoint Lecture Slides prepared by Janice Meeking, Mount Royal College
CHAPTER
Muscles and Muscle Tissue:

Copyright 2010 Pearson Education, Inc.
Three Types of Muscle Tissue 1. Skeletal muscle tissue:

Attached to bones and skin Striated Voluntary (i.e., conscious control) Powerful Primary topic of this chapter
Three Types of Muscle Tissue 2. Cardiac muscle tissue:

Only in the heart Striated Involuntary More details in Chapter 18
Three Types of Muscle Tissue 3. Smooth muscle tissue:

In the walls of hollow organs, e.g., stomach, urinary bladder, and airways Not striated Involuntary More details later in this chapter
Table 9.3
Special Characteristics of Muscle Tissue Excitability (responsiveness or irritability): ability to receive and respond to stimuli Contractility: ability to shorten when stimulated Extensibility: ability to be stretched Elasticity: ability to recoil to resting length
Muscle Functions 1. Movement of bones or fluids (e.g., blood) 2. Maintaining posture and body position 3. Stabilizing joints 4. Heat generation (especially skeletal muscle)
Skeletal Muscle
Each muscle is served by one artery, one nerve, and one or more veins Connective tissue sheaths of skeletal muscle:
Epimysium: dense regular connective tissue surrounding entire muscle Perimysium: fibrous connective tissue surrounding fascicles (groups of muscle fibers) Endomysium: fine areolar connective tissue surrounding each muscle fiber
Epimysium Bone Epimysium Tendon Perimysium Endomysium Muscle fiber in middle of a fascicle Blood vessel Fascicle (wrapped by perimysium) Endomysium (between individual muscle fibers) Muscle fiber
(b)
Perimysium Fascicle (a)
Figure 9.1
Skeletal Muscle: Attachments Muscles attach:

Directlyepimysium of muscle is fused to the periosteum of bone or perichondrium of cartilage Indirectlyconnective tissue wrappings extend beyond the muscle tendon = ropelike aponeurosis = sheetlike
Table 9.1
Microscopic Anatomy of a Skeletal Muscle Fiber Cylindrical cell 10 to 100 m in diameter, up to 30 cm long Multiple peripheral nuclei Many mitochondria Glycosomes for glycogen storage, myoglobin for O2 storage Also contain myofibrils, sarcoplasmic reticulum, and T tubules
Myofibrils Densely packed, rodlike elements ~80% of cell volume Exhibit striations: perfectly aligned repeating series of dark A bands and light I bands
Sarcolemma
Mitochondrion
Myofibril Dark A band Light I band Nucleus (b) Diagram of part of a muscle fiber showing the myofibrils. One myofibril is extended afrom the cut end of the fiber.
Sarcomere Smallest contractile unit (functional unit) of a muscle fiber The region of a myofibril between two successive Z discs Composed of thick and thin myofilaments made of contractile proteins
Features of a Sarcomere
Thick filaments: run the entire length of an A band Thin filaments: run the length of the I band and partway into the A band Z disc: coin-shaped sheet of proteins that anchors the thin filaments and connects myofibrils to one another H zone: lighter midregion where filaments do not overlap M line: line of protein myomesin that holds adjacent thick filaments together
Thin (actin) filament
Z disc
H zone
Z disc
Thick (myosin) filament
I band
A band Sarcomere
I band
M line
(c) 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.
Sarcomere Z disc M line Z disc Thin (actin) filament Elastic (titin) filaments Thick (myosin) filament (d) Enlargement of one sarcomere (sectioned lengthwise). Notice the myosin heads on the thick filaments.
Figure 9.2c, d
Ultrastructure of Thick Filament Composed of the protein myosin

Myosin tails contain: 2 interwoven, heavy polypeptide chains Myosin heads contain: act as cross bridges during contraction Binding sites for actin of thin filaments Binding sites for ATP ATPase enzymes
Ultrastructure of Thin Filament Twisted double strand of fibrous protein F actin F actin consists of G (globular) actin subunits G actin bears active sites for myosin head attachment during contraction Tropomyosin and troponin: regulatory proteins bound to actin
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 A thin filament consists of two strands myosin molecules whose heads protrude of actin subunits twisted into a helix at opposite ends of the filament. 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 ATPbinding site Heads Tail Actin subunits Actin subunits
Figure 9.3
Flexible hinge region Myosin molecule
Active sites for myosin attachment
Sarcoplasmic Reticulum (SR) Network of smooth endoplasmic reticulum surrounding each myofibril Functions in the regulation of intracellular Ca2+ levels
T Tubules Continuous with the sarcolemma Penetrate the cells interior Associate with the paired terminal cisternae to form triads that encircle each sarcomere conduct impulses deep into muscle fiber
Part of a skeletal muscle fiber (cell) Myofibril
I band Z disc
A band H zone M line
I band Z disc
Sarcolemma Triad: T tubule Terminal cisternae of the SR (2) Tubules of the SR Myofibrils Mitochondria
Sarcolemma
Figure 9.5
Contraction The generation of force Does not necessarily cause shortening of the fiber Shortening occurs when tension generated by cross bridges on the thin filaments exceeds forces opposing shortening
Sliding Filament Model of Contraction In the relaxed state, thin and thick filaments overlap only slightly During contraction, myosin heads bind to actin, detach, and bind again, to propel the thin filaments toward the middle of the saarcomere (M line) As sarcomeres shorten, muscle cells shorten, and the whole muscle shortens
Z I
H A
Z I
1 Fully relaxed sarcomere of a muscle fiber
Z I A
Z I
2 Fully contracted sarcomere of a muscle fiber

Figure 9.6
Requirements for Skeletal Muscle Contraction 1. Activation: neural stimulation at a neuromuscular junction 2. Excitation-contraction coupling:
Generation and propagation of an action potential along the sarcolemma Final trigger: a brief rise in intracellular Ca2+ levels
Neuromuscular Junction Skeletal muscles are stimulated by somatic motor neurons Axons of motor neurons travel from the central nervous system via nerves to skeletal muscles Each axon forms several branches as it enters a muscle Each axon ending forms a neuromuscular junction with a single muscle fiber
Neuromuscular Junction Situated midway along the length of a muscle fiber Axon terminal and muscle fiber are separated by a gel-filled space called the synaptic cleft Synaptic vesicles of axon terminal contain the neurotransmitter acetylcholine (ACh) Junctional folds of the sarcolemma contain ACh receptors
Action potential (AP) Nucleus
Myelinated axon of motor neuron Axon terminal of neuromuscular junction Sarcolemma of the muscle fiber
1 Action potential arrives at axon terminal of motor neuron. 2 Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal. Ca2+
Ca2+
Synaptic vesicle containing ACh Mitochondrion Synaptic cleft
Axon terminal of motor neuron Fusing synaptic vesicles
Figure 9.8
Events at the Neuromuscular Junction Nerve impulse arrives at axon terminal ACh is released and binds with receptors on the sarcolemma Electrical events lead to the generation of an action potential
A&P Flix: Events at the Neuromuscular Junction
PLAY
Action potential (AP) Nucleus
Myelinated axon of motor neuron Axon terminal of neuromuscular junction Sarcolemma of the muscle fiber
1 Action potential arrives at axon terminal of motor neuron.

open and Ca2+ enters the axon terminal.
2 Voltage-gated Ca channels
2+
Ca2+
Axon terminal of motor neuron Fusing synaptic vesicles
Ca2+
3 Ca2+ entry causes some synaptic vesicles to release their contents (acetylcholine) by exocytosis. 4 Acetylcholine, a neurotransmitter, diffuses across the synaptic cleft and binds to receptors in the sarcolemma.
channels that allow simultaneous passage of Na+ into the muscle fiber and K+ out of the muscle fiber. by its enzymatic breakdown in the synaptic cleft by acetylcholinesterase.
Synaptic vesicle containing ACh Mitochondrion Synaptic cleft Junctional folds of sarcolemma
ACh
Sarcoplasm of muscle fiber

Na+ K+
5 ACh binding opens ion
Postsynaptic membrane ion channel opens; ions pass.
6 ACh effects are terminated
Ach
Degraded ACh Na+
Postsynaptic membrane ion channel closed; ions cannot pass.
Acetylcholinesterase
K+
Figure 9.8
Destruction of Acetylcholine ACh effects are quickly terminated by the enzyme acetylcholinesterase Prevents continued muscle fiber contraction in the absence of additional stimulation
Action Potential
Generation of Action Potential
Local depolarization wave continues to spread, changing the permeability of the sarcolemma: Na rushes in and K rushes out
Propagation of Action potential

Voltage-regulated Na+ channels open in the adjacent patch, causing it to depolarize to threshold
Repolarization of membrane
Na-K pump re-establishes the resting membrane state
Axon terminal Open Na+ Channel Na+ Closed K+ Channel
Synaptic cleft ACh ACh Na+ K+ Na+ K+

tio n
l a ri
++ ++ + +
K+
Action potential
2 Generation and propagation of

the action potential (AP) Closed Na+ Open K+ Channel Channel Na+
+ + +++ +
e Wa v
1 Local depolarization:
generation of the end plate potential on the sarcolemma
of
de po
za
Sarcoplasm of muscle fiber

3 Repolarization
Figure 9.9
K+
Depolarization due to Na+ entry
Na+ channels close, K+ channels open Repolarization due to K+ exit
Na+ channels open
Threshold K+ channels close
Figure 9.10
Excitation-Contraction (E-C) Coupling

Sequence of events by which transmission of an AP along the sarcolemma leads to sliding of the myofilaments AP is propagated along sarcomere to T tubules Voltage-sensitive proteins stimulate Ca2+ release from SR
Ca2+ is necessary for contraction
Latent period:
Time when E-C coupling events occur Time between AP initiation and the beginning of contraction
Setting the stage Axon terminal of motor neuron Action potential Synaptic cleft is generated ACh Sarcolemma Terminal cisterna of SR Muscle fiber Ca2+ Triad
One sarcomere
Figure 9.11, step 1
Steps in E-C Coupling:
propagated along the sarcolemma and down the T tubules. Sarcolemma T tubule
1 Action potential is
Voltage-sensitive tubule protein
Ca2+ release channel Terminal cisterna of SR
Ca2+
Figure 9.11, step 3
propagated along the sarcolemma and down the T tubules. Sarcolemma T tubule
1 Action potential is
Voltage-sensitive tubule protein
Ca2+ release channel Terminal cisterna of SR
ions are released.
2 Calcium
Ca2+
Figure 9.11, step 4
Actin Ca2+ Troponin Tropomyosin blocking active sites Myosin
The aftermath
Figure 9.11, step 5
Actin Ca2+ Troponin Tropomyosin blocking active sites Myosin troponin and removes the blocking action of tropomyosin. Active sites exposed and ready for myosin binding
3 Calcium binds to
The aftermath
Figure 9.11, step 6
Actin Ca2+ Troponin Tropomyosin blocking active sites Myosin troponin and removes the blocking action of tropomyosin. Active sites exposed and ready for myosin binding
3 Calcium binds to
Myosin cross bridge The aftermath

4 Contraction begins
Figure 9.11, step 7

Sarcolemma Voltage-sensitive tubule protein T tubule 1 Action potential is propagated along the sarcolemma and down the T tubules.
Ca2+ release channel 2 Calcium ions are released. Terminal cisterna of SR
Ca2+
Actin Troponin Tropomyosin blocking active sites Myosin 3 Calcium binds to troponin and removes the blocking action of tropomyosin.
Ca2+
Active sites exposed and ready for myosin binding
4 Contraction begins Myosin cross bridge
The aftermath
Figure 9.11, step 8
Role of Calcium (Ca2+) in Contraction

At low intracellular Ca2+ concentration:
Tropomyosin blocks the active sites on actin Myosin heads cannot attach to actin Muscle fiber relaxes
At higher intracellular Ca2+ concentrations:

Ca2+ binds to troponin Troponin changes shape and moves tropomyosin away from active sites Events of the cross bridge cycle occur When nervous stimulation ceases, Ca2+ is pumped back into the SR and contraction ends
Cross Bridge Cycle

Continues as long as the Ca2+ signal and adequate ATP are present Cross bridge formationhigh-energy myosin head attaches to thin filament Working (power) strokemyosin head pivots and pulls thin filament toward M line Cross bridge detachmentATP attaches to myosin head and the cross bridge detaches Cocking of the myosin headenergy from hydrolysis of ATP cocks the myosin head into the high-energy state
Thin filament Actin Ca

2+
Myosin cross bridge
ADP Pi
Myosin 1 Cross bridge formation.
Thick filament
ADP Pi
ADP Pi
ATP hydrolysis
4 Cocking of myosin head.
2 The power (working) stroke.
ATP ATP
3 Cross bridge detachment.
Figure 9.12
Actin
Ca2+
Thin filament
Myosin cross bridge
ADP Pi Thick filament

Figure 9.12, step 1
ADP Pi

Figure 9.12, step 3
ATP

Figure 9.12, step 4
ADP ATP Pi hydrolysis

Figure 9.12, step 5
Thin filament Actin Ca

2+
Myosin cross bridge
ADP Pi
Thick filament
ADP Pi
ADP Pi
ATP hydrolysis
ATP ATP
Figure 9.12
Basic Principles of Muscle Mechanics

1. Same principles apply to contraction of a single fiber and a whole muscle 2. Contraction produces tension, the force exerted on the load or object to be moved 3. Contraction does not always shorten a muscle:
Isometric contraction: no shortening; muscle tension increases but does not exceed the load Isotonic contraction: muscle shortens because muscle tension exceeds the load
4. Force and duration of contraction vary in response to stimuli of different frequencies and intensities
Motor Unit: The Nerve-Muscle Functional Unit
Motor unit = a motor neuron and all (four to several hundred) muscle fibers it supplies
Small motor units in muscles that control fine movements (fingers, eyes) Large motor units in large weight-bearing muscles (thighs, hips) Muscle fibers from a motor unit are spread throughout the muscle so that a single motor unit causes weak contraction of entire muscle Motor units in a muscle usually contract asynchronously; helps prevent fatigue
Spinal cord Motor Motor unit 1 unit 2
Axon terminals at neuromuscular junctions
Motor neuron cell body Motor Muscle
Nerve
neuron axon
Muscle fibers
Axons of motor neurons extend from the spinal cord to the muscle. There each axon divides into a number of axon terminals that form neuromuscular junctions with muscle fibers scattered throughout the muscle.
Figure 9.13a
Muscle Twitch Response of a muscle to a single, brief threshold stimulus Simplest contraction observable in the lab (recorded as a myogram)
Graded Muscle Responses Variations in the degree of muscle contraction Required for proper control of skeletal movement Responses are graded by:
1. Changing the frequency of stimulation 2. Changing the strength of the stimulus
Response to Change in Stimulus Frequency A single stimulus results in a single contractile responsea muscle twitch
Single stimulus
single twitch
Contraction Relaxation
Stimulus
A single stimulus is delivered. The muscle contracts and relaxes

Figure 9.15a
Response to Change in Stimulus Frequency Increase frequency of stimulus (muscle does not have time to completely relax between stimuli) Ca2+ release stimulates further contraction temporal (wave) summation Further increase in stimulus frequency unfused (incomplete) tetanus
Low stimulation frequency unfused (incomplete) tetanus
Partial relaxation
Stimuli
(b) If another stimulus is applied before the muscle relaxes completely, then more tension results. This is temporal (or wave) summation and results in unfused (or incomplete) tetanus.
Figure 9.15b
Response to Change in Stimulus Frequency If stimuli are given quickly enough, fused (complete) tetany results
High stimulation frequency fused (complete) tetanus
Stimuli
(c) At higher stimulus frequencies, there is no relaxation at all between stimuli. This is fused (complete) tetanus.
Figure 9.15c
Response to Change in Stimulus Strength Threshold stimulus: stimulus strength at which the first observable muscle contraction occurs Muscle contracts more vigorously as stimulus strength is increased above threshold Contraction force is precisely controlled by recruitment (multiple motor unit summation), which brings more and more muscle fibers into action
Stimulus strength Maximal stimulus Threshold stimulus
Proportion of motor units excited
Strength of muscle contraction Maximal contraction
Figure 9.16
Response to Change in Stimulus Strength Size principle: motor units with larger and larger fibers are recruited as stimulus intensity increases
Motor unit 1 Recruited (small fibers)

Motor unit 2 recruited (medium fibers)
Motor unit 3 recruited (large fibers)

Figure 9.17
Muscle Tone Constant, slightly contracted state of all muscles Due to spinal reflexes that activate groups of motor units alternately in response to input from stretch receptors in muscles Keeps muscles firm, healthy, and ready to respond
Types of Contractions Isotonic Contraction

Muscle changes in length and moves the load
Isometric Contraction
The load is greater than the tension the muscle is able to develop Tension increases to the muscles capacity, but the muscle neither shortens nor lengthens
Figure 9.18b
Muscle Metabolism: Energy for Contraction ATP is the only source used directly for contractile activities Available stores of ATP are depleted in 46 seconds ATP is regenerated by:
Direct phosphorylation of ADP by creatine phosphate (CP) Anaerobic pathway (glycolysis) Aerobic respiration
(a)
Direct phosphorylation
Coupled reaction of creatine phosphate (CP) and ADP Energy source: CP
CP
ADP Creatine kinase
Creatine
ATP
Oxygen use: None Products: 1 ATP per CP, creatine Duration of energy provision: 15 seconds
Figure 9.19a
Anaerobic Pathway: Glycolysis & Fermentation
At 70% of maximum contractile activity:

Bulging muscles compress blood vessels Oxygen delivery is impaired Pyruvic acid is converted into lactic acid
Lactic acid:
Diffuses into the bloodstream Used as fuel by the liver, kidneys, and heart Converted back into pyruvic acid by the liver
(b)
Anaerobic pathway
Glycolysis and lactic acid formation Energy source: glucose Glucose (from glycogen breakdown or delivered from blood) Glycolysis in cytosol O2 Pyruvic acid O2 Lactic acid
ATP net gain
Released to blood
Oxygen use: None Products: 2 ATP per glucose, lactic acid Duration of energy provision: 60 seconds, or slightly more
Figure 9.19b
Aerobic Pathway Produces 95% of ATP during rest and light to moderate exercise Fuels: stored glycogen, then bloodborne glucose, pyruvic acid from glycolysis, and free fatty acids
(c)
Aerobic pathway
Aerobic cellular respiration Energy source: glucose; pyruvic acid; free fatty acids from adipose tissue; amino acids from protein catabolism Glucose (from glycogen breakdown or delivered from blood) O2 Pyruvic acid Fatty acids Amino acids CO2 H2O Aerobicrespiration Aerobic respiration in mitochondria mitochondria 32 ATP O2
net gain per glucose
Oxygen use: Required Products: 32 ATP per glucose, CO2, H2O Duration of energy provision: Hours
Figure 9.19c
Short-duration exercise
Prolonged-duration exercise
ATP stored in muscles is used first.
ATP is formed from creatine Phosphate and ADP.
Glycogen stored in muscles is broken down to glucose, which is oxidized to generate ATP.
ATP is generated by breakdown of several nutrient energy fuels by aerobic pathway. This pathway uses oxygen released from myoglobin or delivered in the blood by hemoglobin. When it ends, the oxygen deficit is paid back.
Figure 9.20
Muscle Fatigue Physiological inability to contract Occurs when:

Ionic imbalances (K+, Ca2+, Pi) interfere with EC coupling Prolonged exercise damages the SR and interferes with Ca2+ regulation and release
Total lack of ATP occurs rarely, during states of continuous contraction, and causes contractures (continuous contractions)
Oxygen Deficit Extra O2 needed after exercise for: Replenishment of

Oxygen reserves Glycogen stores ATP and CP reserves
Conversion of lactic acid to pyruvic acid, glucose, and glycogen
Heat Production During Muscle Activity ~ 40% of the energy released in muscle activity is useful as work Remaining energy (60%) given off as heat Dangerous heat levels are prevented by radiation of heat from the skin and sweating
Force of Muscle Contraction

The force of contraction is affected by:
Number of muscle fibers stimulated (recruitment) Relative size of the fibershypertrophy of cells increases strength
The force of contraction is affected by:

Frequency of stimulation frequency allows time for more effective transfer of tension to noncontractile components Length-tension relationshipmuscles contract most strongly when muscle fibers are 80120% of their normal resting length
Large number of muscle fibers activated
Large muscle fibers
High frequency of stimulation
Muscle and sarcomere stretched to slightly over 100% of resting length
Contractile force
Figure 9.21
Sarcomeres greatly shortened 75%
Sarcomeres at resting length
Sarcomeres excessively stretched
100%
170%
Optimal sarcomere operating length (80%120% of resting length)
Figure 9.22
Velocity and Duration of Contraction Influenced by:

1. Muscle fiber type 2. Load 3. Recruitment
Muscle Fiber Type

Classified according to two characteristics: 1. Speed of contraction: slow or fast, according to:
Speed at which myosin ATPases split ATP Pattern of electrical activity of the motor neurons
2. Metabolic pathways for ATP synthesis:

Oxidative fibersuse aerobic pathways Glycolytic fibersuse anaerobic glycolysis
Muscle Fiber Type Three types:

Slow oxidative fibers Fast oxidative fibers Fast glycolytic fibers
Table 9.2
Predominance of fast glycolytic (fatigable) fibers
Small load
Predominance of slow oxidative (fatigue-resistant) fibers
Contractile velocity
Contractile duration
Figure 9.23
FO SO
FG
Figure 9.24
Influence of Load load latent period, contraction, and duration of contraction
Light load Intermediate load Heavy load
Stimulus (a) The greater the load, the less the muscle shortens and the shorter the duration of contraction
(b) The greater the load, the slower the contraction
Figure 9.25
Influence of Recruitment Recruitment faster contraction and duration of contraction
Effects of Exercise
Aerobic (endurance) exercise: Leads to increased:
Muscle capillaries Number of mitochondria Myoglobin synthesis
Results in greater endurance, strength, and resistance to fatigue May convert fast glycolytic fibers into fast oxidative fibers
Effects of Resistance Exercise Resistance exercise (typically anaerobic) results in:

Muscle hypertrophy (due to increase in fiber size) Increased mitochondria, myofilaments, glycogen stores, and connective tissue
The Overload Principle Forcing a muscle to work hard promotes increased muscle strength and endurance Muscles adapt to increased demands Muscles must be overloaded to produce further gains
Smooth Muscle Found in walls of most hollow organs (except heart) Usually in two layers (longitudinal and circular)
Longitudinal layer of smooth muscle (shows smooth muscle fibers in cross section) Small intestine (a)
Mucosa Circular layer of smooth muscle (shows longitudinal views of smooth muscle fibers)
(b) Cross section of the intestine showing the smooth muscle layers (one circular and the other longitudinal) running at right angles to each other.
Figure 9.26
Peristalsis Alternating contractions and relaxations of smooth muscle layers that mix and squeeze substances through the lumen of hollow organs
Longitudinal layer contracts; organ dilates and shortens Circular layer contracts; organ constricts and elongates
Microscopic Structure Spindle-shaped fibers: thin and short compared with skeletal muscle fibers Connective tissue: endomysium only SR: less developed than in skeletal muscle Pouchlike infoldings (caveolae) of sarcolemma sequester Ca2+ No sarcomeres, myofibrils, or T tubules
Table 9.3
Table 9.3
Innervation of Smooth Muscle Autonomic nerve fibers innervate smooth muscle at diffuse junctions Varicosities (bulbous swellings) of nerve fibers store and release neurotransmitters
Varicosities
Autonomic nerve fibers innervate most smooth muscle fibers.
Smooth muscle cell
Synaptic vesicles
Mitochondrion
Varicosities release their neurotransmitters into a wide synaptic cleft (a diffuse junction).
Figure 9.27
Contraction of Smooth Muscle Slow, synchronized contractions Cells are electrically coupled by gap junctions Some cells are self-excitatory (depolarize without external stimuli); act as pacemakers for sheets of muscle Rate and intensity of contraction may be modified by neural and chemical stimuli
Table 9.3
Table 9.3
Special Features of Smooth Muscle Contraction

Stress-relaxation response:
Responds to stretch only briefly, then adapts to new length Retains ability to contract on demand Enables organs such as the stomach and bladder to temporarily store contents
Length and tension changes:

Can contract when between half and twice its resting length
Hyperplasia:
Smooth muscle cells can divide and increase their numbers Example: estrogen effects on uterus at puberty and during pregnancy
Table 9.3
Developmental Aspects All muscle tissues develop from embryonic myoblasts Multinucleated skeletal muscle cells form by fusion Growth factor agrin stimulates clustering of ACh receptors at neuromuscular junctions Cardiac and smooth muscle myoblasts develop gap junctions
Developmental Aspects Cardiac and skeletal muscle become amitotic, but can lengthen and thicken Myoblast-like skeletal muscle satellite cells have limited regenerative ability Injured heart muscle is mostly replaced by connective tissue Smooth muscle regenerates throughout life
Developmental Aspects Muscular development reflects neuromuscular coordination Development occurs head to toe, and proximal to distal Peak natural neural control occurs by midadolescence Athletics and training can improve neuromuscular control
Developmental Aspects Female skeletal muscle makes up 36% of body mass Male skeletal muscle makes up 42% of body mass, primarily due to testosterone Body strength per unit muscle mass is the same in both sexes
Developmental Aspects With age, connective tissue increases and muscle fibers decrease By age 30, loss of muscle mass (sarcopenia) begins Regular exercise reverses sarcopenia Atherosclerosis may block distal arteries, leading to intermittent claudication and severe pain in leg muscles
Muscular Dystrophy Group of inherited muscle-destroying diseases Muscles enlarge due to fat and connective tissue deposits Muscle fibers atrophy
Muscular Dystrophy
Duchenne muscular dystrophy (DMD):
Most common and severe type Inherited, sex-linked, carried by females and expressed in males (1/3500) as lack of dystrophin Victims become clumsy and fall frequently; usually die of respiratory failure in their 20s No cure, but viral gene therapy or infusion of stem cells with correct dystrophin genes show promise

Ch9 PPT Mod8e

Caricato da

Informazioni sul documento

Descrizione originale:

Titolo originale

Copyright

Formati disponibili

Condividi questo documento

Condividi o incorpora il documento

Opzioni di condivisione

Hai trovato utile questo documento?

Questo contenuto è inappropriato?

Copyright:

Formati disponibili

Ch9 PPT Mod8e

Caricato da

Copyright:

Formati disponibili

PowerPoint Lecture Slides prepared by Janice Meeking, Mount Royal College

Muscles and Muscle Tissue:

Three Types of Muscle Tissue 1. Skeletal muscle tissue:

Copyright 2010 Pearson Education, Inc.

Three Types of Muscle Tissue 2. Cardiac muscle tissue:

Copyright 2010 Pearson Education, Inc.

Three Types of Muscle Tissue 3. Smooth muscle tissue:

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Perimysium Fascicle (a)

Copyright 2010 Pearson Education, Inc.

Skeletal Muscle: Attachments Muscles attach:

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Thin (actin) filament

Thick (myosin) filament

Copyright 2010 Pearson Education, Inc.

Ultrastructure of Thick Filament Composed of the protein myosin

Copyright 2010 Pearson Education, Inc.

Longitudinal section of filaments within one sarcomere of a myofibril

Flexible hinge region Myosin molecule

Active sites for myosin attachment

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Part of a skeletal muscle fiber (cell) Myofibril

A band H zone M line

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

1 Fully relaxed sarcomere of a muscle fiber

2 Fully contracted sarcomere of a muscle fiber

Copyright 2010 Pearson Education, Inc.

Action potential (AP) Nucleus

Synaptic vesicle containing ACh Mitochondrion Synaptic cleft

Axon terminal of motor neuron Fusing synaptic vesicles

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Action potential (AP) Nucleus

1 Action potential arrives at axon terminal of motor neuron.

Sarcoplasm of muscle fiber

5 ACh binding opens ion

Postsynaptic membrane ion channel opens; ions pass.

6 ACh effects are terminated

Degraded ACh Na+

Postsynaptic membrane ion channel closed; ions cannot pass.

Copyright 2010 Pearson Education, Inc.

Copyright 2010 Pearson Education, Inc.

Propagation of Action potential

Copyright 2010 Pearson Education, Inc.

Axon terminal Open Na+ Channel Na+ Closed K+ Channel

Synaptic cleft ACh ACh Na+ K+ Na+ K+

2 Generation and propagation of

Sarcoplasm of muscle fiber

Depolarization due to Na+ entry