ch 09 lecture outline c

8/8/2019 Ch 09 Lecture Outline c

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PowerPoint Lecture Slidesprepared byJanice Meeking,

Mount Royal College

C H A P T E R

Copyright 2010 Pearson Education, Inc.

9Muscles andMuscleTissue: Part C


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Force of Mus cle Contraction

The force of contraction is affected by:

Number of muscle fibers stimulated(recruitment)

Relative size of the fibershypertrophy of cells increases strength


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Copyright 2010 Pearson Education, Inc. Fig u re 9.21

Largen umb er of

mus clefib er s

activated

Contractile force

Highfreq u ency of s timu lation

Largemus clefib er s

Mus cle ands arco m ere

s tretched to s lightly over 100%of re s ting length


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S arcomeresgreatly

shortened

S arcomeres atresting length

S arcomeres excessivelystretched

170%

Op tim al s arco m ereo p erating length(80%120% of re s ting length)

100%75%


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V elocity and Du ration of Contraction

Influenced by:

1. Muscle fiber type

2. Load3. Recruitment


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Mus cle Fib er Typ e

2. Metabolic pathways for ATP synthesis:

Ox idative fibersuse aerobic pathways

Glycolytic fibersuse anaerobic glycolysis


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Mus cle Fib er Typ e

Three types:

Slow o x idative fibers

Fast ox

idative fibersFast glycolytic fibers


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Copyright 2010 Pearson Education, Inc. Ta b le 9.2


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P redo m inanceof fa s t glycolytic(fatiga b le) fib er s

P redo m inanceof s low oxidative(fatig u e-re s is tant)

fib er s

Sm all load

Contractilevelocity

Contractileduration


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FO

FG

SO


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Effect s of Exerci s e

Aerobic (endurance) e x ercise:

Leads to increased:

Muscle capillaries

Number of mitochondria

Myoglobin synthesis

Results in greater endurance, strength, andresistance to fatigue

May convert fast glycolytic fibers into fast o x idativefibers


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Effect s of Re s is tance Exerci s e

Resistance e x ercise (typically anaerobic)results in:

Muscle hypertrophy (due to increase in fiber size)

Increased mitochondria, myofilaments,glycogen stores, and connective tissue


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The Overload P rinci p le

Forcing a muscle to work hard promotesincreased muscle strength and endurance

Muscles adapt to increased demands

Muscles must be overloaded to producefurther gains


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Sm ooth Mus cle

Found in walls of most hollow organs(e x cept heart)

Usually in two layers (longitudinal andcircular)


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Sm allinte s tine

(a) (b ) Cross section of the

intestine showing thesmooth muscle layers(one circular and theother longitudinal)running at rightangles to each other.

Mu co s a

Longitudinal layer of smooth muscle(s how s sm ooth mus cle fib er s in cro ss s ection)

Circular layer of

smooth muscle(s how s longit u dinalview s of sm ooth mus cle fib er s )


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Innervation of Sm ooth Mus cle

Autonomic nerve fibers innervate smoothmuscle at diffuse junctions

Varicosities (bulbous swellings) of nerve fibersstore and release neurotransmitters


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Sm oothmus clecell

V aricosities relea s etheir ne u rotran sm itter sinto a wide s yna p tic cleft (a diff us e ju nction) .

S yna p ticve s icle s

Mitochondrion

Autonomicnerve fi b ersinnervatem o s t sm ooth

mus cle fib er s.

Varico s itie s


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Myofila m ent s in Sm ooth Mus cle

Ratio of thick to thin filaments (1:13) is muchlower than in skeletal muscle (1:2)

Thick filaments have heads along their entirelength

No troponin comple x ; protein calmodulin bindsCa 2+


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Myofila m ent s in Sm ooth Mus cle

Myofilaments are spirally arranged, causingsmooth muscle to contract in a corkscrewmanner

Dense bodies: proteins that anchor noncontractile intermediate filaments tosarcolemma at regular intervals


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Copyright 2010 Pearson Education, Inc. Fig u re 9.2 8a


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Copyright 2010 Pearson Education, Inc. Fig u re 9.2 8b


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Contraction of Sm ooth Mus cle

Slow, synchronized contractions

Cells are electrically coupled by gap junctions

Some cells are self-e x citatory (depolarizewithout e x ternal stimuli); act as pacemakersfor sheets of muscle

Rate and intensity of contraction may bemodified by neural and chemical stimuli


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Sliding filament mechanism

Final trigger is o intracellular Ca 2+

Ca2+

is obtained from the SR and e x tracellular space


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Calci um ion s (Ca 2+ )enter the cyto s ol fro mthe EC F via voltage-de p endent or voltage-inde p endent Ca 2+channel s, or fro mthe s cant SR.

ATP

P i P i

Extracell u lar flu id (EC F)

ADP

Ca 2+

Ca 2+

Ca 2+

P la sm a m emb rane

Sarco p la sm icretic u lum

Inactive cal m od u lin

Inactive kina s e

Inactivem yo s in m olec u le

Activated (p ho sp horylated)m yo s in m olec u le

Activated kina s e

Activated cal m od u lin

Cyto p la sm

Ca 2+ b ind s to andactivate s cal m od u lin .

Activated cal m od u linactivate s the m yo s inlight chain kina s eenzy m e s.

The activated kina s e enzy m escatalyze tran s fer of p ho sp hateto m yo s in , activating the m yo s inATP as es.

Activated m yo s in for ms cro ssb ridge s with actin of the thinfila m ent s and s hortening b egin s.

Thinfila m ent

Thic kfila m ent

1

2

3

4

5


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Copyright 2010 Pearson Education, Inc. Fig u re 9.29, s te p 1

Calci um ion s (Ca 2+)enter the cyto s ol fro mthe EC F via voltage-de p endent or voltage-inde p endent Ca 2+channel s, or fro mthe s cant SR.

Extracellular fluid (ECF)

Ca 2+

Ca 2+

P la sm a m e mb rane

S arco p la sm icretic u lum

Cytoplasm

1


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Ca 2+

Inactive cal m od u lin Activated cal m od u lin


2


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Inactive kina s e Activated kina s e

Activated cal m od u linactivate s the m yo s inlight chain kina s eenzy m e s.

3


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ATP

P i

P i

ADP



The activated kina s e enzy m e scatalyze tran s fer of p ho sp hateto m yo s in , activating the m yo s inATP a s e s.

4


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Thinfila m ent

Thic kfila m ent

5


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Calci um ion s (Ca 2+ )enter the cyto s ol fro mthe EC F via voltage-de p endent or voltage-inde pendent Ca 2+channel s, or fro mthe s cant SR.

ATP

P i P i

Extracell u lar flu id (EC F)

ADP

Ca 2+

Ca 2+

Ca 2+

P la sm a m e mb rane

Sarco p la sm icretic u lum

Inactive cal m od u lin

Inactive kina s e



Activated kina s e


Cyto p la sm



activate s the m yo s inlight chain kina s eenzy m es.

The activated kina s e enzy m escatalyze tran s fer of p ho sp hateto m yo s in , activating the m yo s inATP as es.


Thinfila m ent

Thic kfila m ent

1

2

3

4

5


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Very energy efficient (slow ATPases)

Myofilaments may maintain a latch state for prolonged contractions

Rela x ation requires:

Ca 2+ detachment from calmodulin

Active transport of Ca 2+ into SR and ECF

Dephosphorylation of myosin to reducemyosin ATPase activity


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Reg u lation of Contraction

Neural regulation:

Neurotransmitter binding p o [Ca 2+] insarcoplasm; either graded (local) potential or action potential

Response depends on neurotransmitter released and type of receptor molecules


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Reg u lation of Contraction

Hormones and local chemicals:

May bind to G proteinlinked receptors

May either enhance or inhibit Ca 2+ entry


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Sp ecial Feat u re s of Sm ooth Mus cle Contraction

Stress-rela x ation response:

Responds to stretch only briefly, then adaptsto new length

Retains ability to contract on demandEnables organs such as the stomach andbladder to temporarily store contents

Length and tension changes:Can contract when between half and twice itsresting length


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Sp ecial Feat u re s of Sm ooth Mus cle Contraction

Hyperplasia:

Smooth muscle cells can divide and increasetheir numbers

Ex ample:

estrogen effects on uterus at puberty andduring pregnancy


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Typ e s of Sm ooth Mus cle

Single-unit (visceral) smooth muscle:

Sheets contract rhythmically as a unit (gap junctions)

O ften e x hibit spontaneous action potentials

Arranged in opposing sheets and e x hibitstress-rela x ation response


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Typ e s of Sm ooth Mus cle: Mu ltiu nit

Multiunit smooth muscle:

Located in large airways, large arteries,arrector pili muscles, and iris of eye

Gap junctions are rare

Arranged in motor units

Graded contractions occur in response toneural stimuli


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Develo pm ental Asp ect s

Female skeletal muscle makes up 36% of body mass

Male skeletal muscle makes up 42% of bodymass, primarily due to testosterone

Body strength per unit muscle mass is thesame in both se x es


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Mus c u lar Dys tro p hy

Group of inherited muscle-destroyingdiseases

Muscles enlarge due to fat and connectivetissue deposits

Muscle fibers atrophy


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Mus c u lar Dys tro p hy

Duchenne muscular dystrophy (DMD):

Most common and severe type

Inherited, se x -linked, carried by females and

e x pressed in males (1/3500) as lack of dystrophinVictims become clumsy and fall frequently; usually dieof respiratory failure in their 20s

No cure, but viral gene therapy or infusion of stemcells with correct dystrophin genes show promise

ch 09 lecture outline c

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