Ch9 Ppt Mod8e

PowerPoint® Lecture Slides prepared by Janice Meeking, Mount Royal College

C H A P T E R

Copyright © 2010 Pearson Education, Inc.

9

Muscles and Muscle Tissue:


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



2. Cardiac muscle tissue:

• Only in the heart

• Striated

• Involuntary

• More details in Chapter 18



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

Copyright © 2010 Pearson Education, Inc. 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

Copyright © 2010 Pearson Education, Inc. Figure 9.1

Bone

Perimysium

Endomysium(between individualmuscle fibers)

Muscle fiber

Fascicle(wrapped by perimysium)

Epimysium

Tendon

Epimysium

Muscle fiberin middle ofa fascicle

Blood vessel

Perimysium

Endomysium

Fascicle(a)

(b)


Skeletal Muscle: Attachments

• Muscles attach:

• Directly—epimysium of muscle is fused to the periosteum of bone or perichondrium of cartilage

• Indirectly—connective tissue wrappings extend beyond the muscle

• tendon = ropelike

• aponeurosis = sheetlike



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


NucleusLight I bandDark A band

Sarcolemma

Mitochondrion

(b) Diagram of part of a muscle fiber showing the myofibrils. Onemyofibril is extended afrom the cut end of the fiber.

Myofibril


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

Copyright © 2010 Pearson Education, Inc. Figure 9.2c, d

I band I bandA bandSarcomere

H zoneThin (actin)filament

Thick (myosin)filament

Z disc Z disc

M line

(c) Small part of one myofibril enlarged to show the myofilamentsresponsible for the banding pattern. Each sarcomere extends fromone Z disc to the next.

Z disc Z discM line

Sarcomere

Thin (actin)filament

Thick(myosin)filament

Elastic (titin)filaments

(d) Enlargement of one sarcomere (sectioned lengthwise). Notice the myosin heads on the thick filaments.


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


Flexible hinge region

Tail

Tropomyosin Troponin Actin

Myosin head

ATP-bindingsite

Heads Active sitesfor myosinattachment

Actinsubunits

Actin-binding sites

Thick filamentEach thick filament consists of manymyosin molecules whose heads protrude at opposite ends of the filament.

Thin filamentA thin filament consists of two strandsof actin subunits twisted into a helix plus two types of regulatory proteins(troponin and tropomyosin).

Thin filamentThick filament

In the center of the sarcomere, the thickfilaments lack myosin heads. Myosin heads are present only in areas of myosin-actin overlap.

Longitudinal section of filamentswithin one sarcomere of a myofibril

Portion of a thick filamentPortion of a thin filament

Myosin molecule Actin subunits


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 cell’s interior

• Associate with the paired terminal cisternae to form triads that encircle each sarcomere

• conduct impulses deep into muscle fiber


Myofibril

Myofibrils

Triad:

Tubules ofthe SR

Sarcolemma

Sarcolemma

Mitochondria

I band I bandA band

H zone Z discZ disc

Part of a skeletalmuscle fiber (cell)

• T tubule• Terminal

cisternaeof the SR (2)

M line


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


I

Fully relaxed sarcomere of a muscle fiber

Fully contracted sarcomere of a muscle fiber

IA

Z ZH

I IA

Z Z

1

2


Requirements for Skeletal Muscle Contraction

1. Activation: neural stimulation at aneuromuscular 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


Nucleus

Actionpotential (AP)

Myelinated axonof motor neuron

Axon terminal ofneuromuscular junction

Sarcolemma ofthe muscle fiber

Ca2+Ca2+

Axon terminalof motor neuron

Synaptic vesiclecontaining ACh

MitochondrionSynapticcleft

Fusing synaptic vesicles

1 Action potential arrives ataxon terminal of motor neuron.

2 Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal.

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

PLAYPLAY A&P Flix™: Events at the Neuromuscular Junction


Nucleus

Actionpotential (AP)

Myelinated axonof motor neuron

Axon terminal ofneuromuscular junction

Sarcolemma ofthe muscle fiber

Ca2+Ca2+


Synaptic vesiclecontaining AChMitochondrionSynapticcleft

Junctionalfolds ofsarcolemma

Fusing synaptic vesicles

ACh

Sarcoplasm ofmuscle fiber

Postsynaptic membraneion channel opens;ions pass.

Na+ K+

Ach–

Na+

K+

Degraded ACh

Acetyl-cholinesterase

Postsynaptic membraneion channel closed;ions cannot pass.

1 Action potential arrives ataxon terminal of motor neuron.

2 Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal.

3 Ca2+ entry causes some synaptic vesicles to release their contents (acetylcholine)by exocytosis.

4 Acetylcholine, aneurotransmitter, diffuses across the synaptic cleft and binds to receptors in the sarcolemma.

5 ACh binding opens ionchannels that allow simultaneous passage of Na+ into the musclefiber and K+ out of the muscle fiber.

6 ACh effects are terminated by its enzymatic breakdown in the synaptic cleft by acetylcholinesterase.


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


Na+

Na+

Open Na+

Channel

Closed Na+

Channel

Closed K+

Channel

Open K+

Channel

Action potential++++++

+++++

+

Axon terminal

Synapticcleft

ACh

ACh

Sarcoplasm of muscle fiber

K+

2 Generation and propagation ofthe action potential (AP)

3 Repolarization

1 Local depolarization: generation of the end plate potential on the sarcolemma

K+

K+Na+

K+Na+

Wave ofde

po

lari

zatio

n


Na+ channelsclose, K+ channelsopen

K+ channelsclose

Repolarizationdue to K+ exit

Threshold

Na+

channelsopen

Depolarizationdue to Na+ entry


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

Copyright © 2010 Pearson Education, Inc. Figure 9.11, step 1


Muscle fiberTriad

One sarcomere

Synaptic cleft

Setting the stage

Sarcolemma

Action potentialis generated

Terminal cisterna of SR ACh

Ca2+


Steps inE-C Coupling:

Terminal cisterna of SR

Voltage-sensitivetubule protein

T tubule

Ca2+

releasechannel

Ca2+

Sarcolemma

Action potential ispropagated along thesarcolemma and downthe T tubules.

1


Steps inE-C Coupling:



T tubule

Ca2+

releasechannel

Ca2+

Sarcolemma

Action potential ispropagated along thesarcolemma and downthe T tubules.

Calciumions arereleased.

1

2


Troponin Tropomyosinblocking active sitesMyosin

Actin

Ca2+

The aftermath



Actin

Active sites exposed and ready for myosin binding

Ca2+

Calcium binds totroponin and removesthe blocking action oftropomyosin.

The aftermath

3



Actin


Ca2+

Myosincross bridge

Calcium binds totroponin and removesthe blocking action oftropomyosin.

Contraction begins

The aftermath

3

4


Action potential is propagated alongthe sarcolemma and down the T tubules.

Steps in E-C Coupling:

Troponin Tropomyosinblocking active sites

Myosin

Actin


Ca2+



T tubule

Ca2+

releasechannel

Myosincross bridge

Ca2+

Sarcolemma

Calcium ions are released.

Calcium binds to troponin andremoves the blocking action oftropomyosin.

Contraction begins

The aftermath

1

2

3

4


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 formation—high-energy myosin head attaches to thin filament

• Working (power) stroke—myosin head pivots and pulls thin filament toward M line

• Cross bridge detachment—ATP attaches to myosin head and the cross bridge detaches

• “Cocking” of the myosin head—energy from hydrolysis of ATP cocks the myosin head into the high-energy state


1

Actin

Cross bridge formation.

Cocking of myosin head. The power (working) stroke.

Cross bridge detachment.

Ca2+

Myosincross bridge

Thick filament

Thin filament

ADP

Myosin

Pi

ATPhydrolysis

ATP

ATP

24

3

ADP

Pi

ADPPi


Actin


Ca2+

Myosincross bridge

Thick filament

Thin filament

ADP

Myosin

Pi

1


The power (working) stroke.

ADP

Pi

2



ATP

3


Cocking of myosin head.

ATPhydrolysis

ADPPi

4


1

Actin


Cocking of myosin head. The power (working) stroke.


Ca2+

Myosincross bridge

Thick filament

Thin filament

ADP

Myosin

Pi

ATPhydrolysis

ATP

ATP

24

3

ADP

Pi

ADPPi


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

Copyright © 2010 Pearson Education, Inc. Figure 9.13a

Spinal cord

Motor neuroncell body

Muscle

Nerve

Motorunit 1

Motorunit 2

Musclefibers

Motorneuronaxon

Axon terminals atneuromuscular junctions

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.


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 response—a muscle twitch


Contraction

Relaxation

Stimulus

Single stimulus single twitch

A single stimulus is delivered. The muscle contracts and relaxes



• 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

Copyright © 2010 Pearson Education, Inc. Figure 9.15b

Stimuli

Partial relaxation

Low stimulation frequencyunfused (incomplete) tetanus

(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.



• If stimuli are given quickly enough, fused (complete) tetany results

Copyright © 2010 Pearson Education, Inc. Figure 9.15c

Stimuli

High stimulation frequencyfused (complete) tetanus

(c) At higher stimulus frequencies, there is no relaxation at all between stimuli. This is fused (complete) tetanus.


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

Proportion of motor units excited

Strength of muscle contraction

Maximal contraction

Maximalstimulus

Thresholdstimulus


Response to Change in Stimulus Strength

• Size principle: motor units with larger and larger fibers are recruited as stimulus intensity increases


Motorunit 1Recruited(smallfibers)

Motorunit 2recruited(mediumfibers)

Motorunit 3recruited(largefibers)


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 muscle’s capacity, but the muscle neither shortens nor lengthens



Muscle Metabolism: Energy for Contraction

• ATP is the only source used directly for contractile activities

• Available stores of ATP are depleted in 4–6 seconds

• ATP is regenerated by:

• Direct phosphorylation of ADP by creatine phosphate (CP)

• Anaerobic pathway (glycolysis)

• Aerobic respiration


Coupled reaction of creatinephosphate (CP) and ADP

Energy source: CP

(a) Direct phosphorylation

Oxygen use: NoneProducts: 1 ATP per CP, creatineDuration of energy provision:15 seconds

Creatinekinase

ADPCP

Creatine ATP


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


Energy source: glucose

Glycolysis and lactic acid formation

(b) Anaerobic pathway

Oxygen use: NoneProducts: 2 ATP per glucose, lactic acidDuration of energy provision:60 seconds, or slightly more

Glucose (fromglycogen breakdown ordelivered from blood)

Glycolysisin cytosol

Pyruvic acid

Releasedto blood

net gain

2

Lactic acid

O2

O2ATP


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

Copyright © 2010 Pearson Education, Inc. Figure 9.19c

Energy source: glucose; pyruvic acid;free fatty acids from adipose tissue;amino acids from protein catabolism

(c) Aerobic pathway

Aerobic cellular respiration

Oxygen use: RequiredProducts: 32 ATP per glucose, CO2, H2ODuration of energy provision: Hours

Glucose (fromglycogen breakdown ordelivered from blood)

32

O2

O2

H2O

CO2

Pyruvic acidFattyacids

Aminoacids

Aerobic respirationin mitochondriaAerobic respirationin mitochondria

ATP

net gain perglucose


Short-duration exerciseProlonged-durationexercise

ATP stored inmuscles isused first.

ATP is formedfrom creatinePhosphateand ADP.

Glycogen stored in muscles is brokendown to glucose, which is oxidized togenerate ATP.

ATP is generated bybreakdown of severalnutrient energy fuels byaerobic pathway. Thispathway uses oxygenreleased from myoglobinor delivered in the bloodby hemoglobin. When itends, the oxygen deficit ispaid back.


Muscle Fatigue

• Physiological inability to contract

• Occurs when:

• Ionic imbalances (K+, Ca2+, Pi) interfere with E-C 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 fibers—hypertrophy 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 relationship—muscles contract most strongly when muscle fibers are 80–120% of their normal resting length


Largenumber of

musclefibers

activated

Contractile force

Highfrequency ofstimulation

Largemusclefibers

Muscle andsarcomere

stretched to slightly over 100%of resting length


Sarcomeresgreatly

shortened

Sarcomeres atresting length

Sarcomeres excessivelystretched

170%

Optimal sarcomereoperating length(80%–120% ofresting length)

100%75%


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 fibers—use aerobic pathways

• Glycolytic fibers—use anaerobic glycolysis


Muscle Fiber Type

Three types:

• Slow oxidative fibers

• Fast oxidative fibers

• Fast glycolytic fibers



Predominanceof fast glycolytic(fatigable) fibers

Predominanceof slow oxidative(fatigue-resistant)

fibers

Small load

Contractilevelocity

Contractileduration


FO

FG

SO


Influence of Load

load latent period, contraction, and duration of contraction


Stimulus

Intermediate load

Light load

Heavy load

(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


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)


Smallintestine

(a) (b) Cross section of theintestine showing thesmooth muscle layers(one circular and theother longitudinal)running at rightangles to each other.

Mucosa

Longitudinal layerof smooth muscle (shows smooth muscle fibers in cross section)

Circular layer ofsmooth muscle (shows longitudinalviews of smooth muscle fibers)


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




Innervation of Smooth Muscle

• Autonomic nerve fibers innervate smooth muscle at diffuse junctions

• Varicosities (bulbous swellings) of nerve fibers store and release neurotransmitters


Smoothmusclecell

Varicosities releasetheir neurotransmittersinto a wide synaptic cleft (a diffuse junction).

Synapticvesicles

Mitochondrion

Autonomicnerve fibersinnervatemost smoothmuscle fibers.

Varicosities


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




Special Features of Smooth Muscle ContractionStress-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



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



• 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



• 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



• 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



•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

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