Chapter 10 Muscle Tissue (Mostly Skeletal Muscle).

transcript

Chapter 10

Muscle Tissue(Mostly Skeletal Muscle)

skeletal

cardiac

smooth

“hollow organs”

Muscle tissue:

skeletal muscle functions

move skeletonmaintain balance/posturesupport soft tissuesguard entrances/exitsmaintain body tempstore nutrients

muscle cellsconnective tissuenerves (axons)blood vessels

Muscle tissue:

muscle contains

surrounded by epimysium subdivided into fascicles

surrounded by perimysium fascicles contain myofibers

surrounded by endomysium

muscle (and connective tissue)

fig. 10-1

three connective tissues:

epimysiumperimysiumendomysiyum

blend into each other,and the end of the muscle

blend into the tendon

three connective tissues:

contain: blood vesselsand nerves

that supply the muscle

skeletal muscle

voluntary muscle

although many are also controlled subconsciously too

skeletal muscle

formation and structure

fig. 10-2

myoblast fuse

forming

largemultinucleated

cells(myofibers)

myofibers

cell membrane sarcolemmacytoplasm sarcoplasmfilaments organized into myofibrils

T-tubules (transverse)-extensions of the sarcolemma

to the interior of the cell-surround myofibrils

fig. 10-3

sarcoplasmic reticulum (SR)

•modified sER(smooth endoplasmic reticulum)

•also surrounds myofibrils•expanded ends called

terminal cisternae•gather and store Ca2+

fig. 10-3

myofibriltc tcT

myofibers:

contain myofibrils

myofibrils:

contain myofilaments

thin filamentsthick filaments

actinmyosin

G actin (globular)

Factin

(filamentous)Other components:Troponin (covers active site)TropomyosinNebulin

Thin filaments:

fig. 10-7b

Thin filaments:

fig. 10-7a, b

Thick filaments:

myosin

fig. 10-7d

Thick filaments:

binds to active site onthin filaments

fig. 10-7c, d

to hereMonday 2/5lec # 13

muscle

fascicles

myofibers

myofibrils

thick & thinfilaments

fig. 10-6

fig. 10-4

Z line Z line

I band I bandA bandA band A band

from Z line to Z linesarcomere

M line

H zone

A band

overlap

I band

where myosinmyosin is

center of A band

where actin isn’tcenter of A band

where myosinmyosin isn’tZ line in center

actin and myosinmyosinmusc

T tctctriad

fig. 10-5

when muscle contracts:

A band sameI band shrinksH zone shrinksZ lines closeroverlap increases

sliding filament theory

fig. 10-8

The contraction of skeletal m.

background physics:

tension pull towardscompression push away

overcome resistance

muscle cells only pull (produce tension)generate force by getting shorter

fig. 10-9

motorneuron APrelease ntAP in myofiberrelease Ca2+

thick/thin interactcontraction

tension

OVERVIEW

fig. 10-9

control of skeletal muscle

motorneurons in CNS

synapse with myofiber

neuromuscular junctionaka myoneural junctionaka motor end plate (mep)

each myofiber is innervated by a myelinated motorneuron

neuromuscular junction (nmj)

axon terminal with ACh

synaptic cleft

postsynaptic membrane(aka sarcolemma)

junctional foldsAChR and AChE

fig. 10-10

neuronal AP

myofiber AP

contraction ?

Excitation-Contraction Coupling

myofiber AP(depolarization of sarcolemma)

depolarizationof the T-tubules

release of Ca2+

from sacroplasmic reticulum

release of Ca2+

from sacroplasmic reticulum

Ca2+ interacts with troponin(on thin filaments)

exposing active site(myosin will now bind)

fig. 10-7b

remember structure:

fig. 10-5

fig. 10-11

myosinheads

Now we are ready forthe contraction cycle

(almost)

fig. 10-7

fig. 10-12

expose active site form cross-bridges

fig. 10-12

cross bridge detachmentre”energize” the myosin

“POWER STROKE”

fig. 10-12

re energize myosin

As long as Ca2+ is present…

power stroke

re-energize

power stroke

re-energize

sarcomere shortens ~1%/cycle

tug-of-war

reachgrab

energizecross-bridge

power strokereleaserelease

tug-of-war

reachgrab

pullrelease

repeat cycle

what if everybody released at the same time?

myosinactin

sarcomere

cross bridge formation

power stroke

release

energize

power stroke

release

energize

power stroke

release

energize

power stroke

to here 2/7lec # 14

…each myofiber is lots of sarcomeres end to end…

with contraction cycle…each sarcomere get

shorter…

…myofiber gets shorter……muscle gets shorter

As muscle gets shorter……it generates tension (pulls)

Skeletal muscles are attachedto bone at both ends

origin

insertion

action:flex at elbow

origininsertionactions

fig. 11-2

How long will muscle contract ?

continued stimulus at nmj+ free Ca2+ in sarcoplasm+ ATP to energize myosin…

…muscle will keep contracting

As long as:

If stimulus disappears:

ACh broken down by AChE

sarcolemma returns to RP

Ca2+ is reabsorbed by SR

active sites covered by troponin

What happens to the musclewhen contraction stops ?

muscle cannot lengthen on its own

muscles are “paired”

agonist muscle that does action

antagonist has opposite action(stretches agonist)

Muscle cannot lengthen on its own…

…it has to be stretched.

flex forearm

no nutrients to muscleATP gets used upCa2+ pumps quitmyosin binds to actin“freezes” muscle

rigor mortis

occurs after a few hourslast for 15-25 hrs

until lyzozymal enzymes start to break down muscle proteins

Muscle architectureMechanism of contraction

Have covered:

Tension ProductionEnergy UseMuscle Performance

cardiac musclesmooth muscle

Still to come:

Tension production

by myofibersby muscles

Tension production

by myofibers:

Amount of tension produceddepends on number of“power strokes” happening

Cannot vary the amount of tension produced by a myofiber by varying number of sacromeres being used.

Tension production

by myofibers:

A single myofiber is either

stimulated “on”

relaxed (off)

Tension production

by myofibers:

“tension production at the level of the individual cell does vary”

Tension production

by myofibers:

frequency of stimulation resting length of fiber

but…

Tension production

by myofibers:

resting length vs. tension in myofibers

Amount of tension produceddepends on number ofpower strokes happening

the number of cross-bridges forming will depend on the degree of overlap between the thin and thick filaments(zone of overlap)

only those myosin molecules that can form cross-bridges will produce tension

fig. 10-14

length of sarcomere

Tension production

by myofibers:

frequency of stimulationresting length of fiber

single stimulus (AP)

frequency of stimulation

single contraction (twitch)

7-100 msec

a single twitch has phases

frequency of stimulation

latent phasecontraction phaserelaxation phase

fig. 10-15

Stimul

fig. 10-15

myogram

What if we stimulated a muscle cell,

let it contract and relax,

and then stimulated it again?

fig. 10-16a

What if we stimulated a muscle cell,

let it contract and relax(but not all the way),

and then stimulated it again?

fig. 10-16b

wave summation

fig. 10-16c

incomplete tentanus

fig. 10-16d

complete tentanus

stimulationrate < twitch

stimulationrate > twitch

stimulationrate >twitch cycle

stimulationrate >

latent p+

contraction p

fig. 10-15

1st 2nd

treppe

an aside…

Don’t play around rusty nails !

Don’t run around barefoot outside!

Have you had your tetanus shot ?

What is tetanus ?

Tetanus

prolonged contraction of muscle

Why rusty nails ?

puncture wound

closes very quicklyvery little bleeding

Clostridium tetani

live is soil(low O2 levels)

If it gets into the body:

dividerelease tetanospasmin

(powerful neurotoxin)

carried to CNS byretrograde transport

disables GABA-releasingneurons (inhibitory nt)

overstimulation of motorneurons

If it gets into the body:

overstimulation of motorneurons

sustained, powerful contraction of skeletal muscle throughout body

“lockjaw”

Sir Charles Bell ,1809

Not much of a problem in developed nations…

immunizations&

booster shots

(diptheria, tetanus, pertussis)

return from aside

to here 2/9lec # 15

Tension production

by myofibers

by muscles

myofiber lengthstimulation rate

Tension production

by muscles

tension from myofibers# myofibers stimulated

“The amount of tension produced by a muscle as a whole is the sum of the tensions generated by the individual muscle fibers,” (pg 304)

Tension production

•each muscle - 1000’s of fibers

•muscle fibers - controlled by neurons•motorneurons - control many myofibers

all the fibers controlledby a single neuron…

…motor unit

size of motor unit…

…indication of how precisely

the muscle is controlled

(how many myofibers/unit)

for example

eye muscles

leg muscles

4-6 fibers/unit

1000-2000

within the muscle

myofibers are intermingled

fig. 10-17

think… …move muscle

activate smallest motor units

activate larger motor units…

keep thinking… …move muscle

smooth, steady increase in tension

recruitment

peak tension is produced when all motor units are in complete tetany

(can’t do it for long)

in sustained contractions:

(can’t do it at max. tension)

rotate which motor units are being activated

asynchronous motor unit summation

fig. 10-17

Key (pg 305)

“All voluntary muscle contractions and intentional movements involve sustained contractions of skeletal muscle fibers. The force exerted can be increased by increasing the frequency or motor neuron action potentials or the number of stimulated motor units (recruitment).”

muscle tone

resting muscle…

…always has some fibers contracting

don’t produce enough tension to cause movement, but they tense and firm the muscle

muscle tone

•holds bones in place•keeps body balanced(position)•prevent sudden movements•shock absorption•a muscle with good tone will

burn more Calories than one with poor muscle tone

contractions

isotonicisometric

contractions

isotonic (equal tension)

rise in tension leads to change in the muscle length

fig. 10-18

isotonic contractions

concentric

eccentric

muscle shortens(overcomes resistance)

muscle lengthens(control)

contractions

isometric (equal measure)

•muscle length does not change

•doesn’t produce enough tension

to overcome resistance

fig. 10-18

isometric

isometric contractions

although whole muscle does not shorten…

individual fibers do

isometric contractions

when would it be used?

…hold head up…carrying books…maintaining posture

Resistance and speed of contraction

lighter resistance…

…faster speed of contraction

inversely related

heavier resistance…

…slower speed of contraction

Returning a muscle to resting length

can’t actively lengthen muscle

can stretch it

opposing muscleelastic forcesgravity

Energy use and Muscle activity

single myofiber:

may have 15 billion thick filaments

each thick filament:

uses 2500 ATP molecules/sec

~ bazillion

muscle need lots of ATP

but ATP is for short-term storage

hot $ ?

ATP + creatine

ADP +creatine

phosphate(CP)

ATP ADP +

myosin (unenergized):

myosin (energized):

ATP ADP + P

ADP + creatinephosphate

ATP + creatine

(as muscle uses ATP it makes ADP)

TABLE 10-2

ATP ADP + P

ADP + creatinephosphate

ATP + creatine

(as muscle uses ATP it makes ADP)

CPK (or CK)

creatine phosphokinase

if muscle is damaged, CKleaks out of the cell into the blood ( high [CK] = muscle damage)

Aerobic metabolism(living with oxygen)

Most ATP demands (at rest) are met through TCA and ETS

organic molecules from cytoplasm

ETS ATP

ß oxidation

of fatty acids

during contraction

swtiches to pyruvate as entry point into TCA

Where does pyruvate come from?

glycolysis

during contraction

What do we need to do glycolysis?

glucose

What does glucose come from?

glycogen in myofibers

at rest

low demand for ATPuse fatty acids for C sourcelots of O2 availableextra ATP --->CPglycogen is stored

fig. 10-20

at rest

moderate activity

higher demand for ATPif enough of O2 availablemitochondria can supply ATPvia cellular respiration

fig. 10-20

high activity

enormous demand for ATPno enough O2 delivered

(ETS will not work fast enough)cells use ATP from glycolysismake pyruvateconverted to lactic acid

anaerobic

fig. 10-20

muscle fatigue

when the muscle can no longer perform at the required level

muscle fatigue

•depletion of energy reserves•damage to cell membrane, etc•decline in pH of myofibers

(decrease Ca2+ binding)

normal muscle function needs:

•intracellular energy reserves•normal blood supply•normal O2 levels•normal blood pH

interfere with any one of them…

…premature muscle fatigue

recovery period:

time needed for muscle to return to pre-exertion conditions

moderate activity hourspeak activity days-week

to here 2/12lec # 16

review 1

muscles cells contract… or ……don’t

vary tension by: ??

muscles have motor units:

vary tension by:

maximum tension is called

review 2

isotonic contraction: concentric?

isometric contraction:

Energy use by muscles

need ATP

stored as ??

review 3

Energy use by muscles

at rest fatty acidsmoderate work aerobic metab.heavy work anaerobic

(leads to build up of ?)

recovery period

removal of lactic acid (LA)

with O2, can be converted back to pyruvateliver can convert LA to glucose which goes back to the muscle

Cori cycle

Oxygen debt

supply O2 to tissues and allow for restoring pre-exertion levels of ATP, CP, glycogen,…

Heat production

~58 % of energy produced is lost as heatonly 42% goes to producing ATP

Hormones

GH and testosterone

stimulate synthesis of muscle tissue

stimulate energy consumption by muscle tissue

Hormones

epinephrine

stimulate muscle metabolism and contraction

Muscle Performance

How much force can be produced

tension produced by a muscle or group of muscles

How long can the muscle continue

endurance

Muscle Performance

Two factors influence performance

types of muscle fibersphysical conditioning

Muscle Performance

Two factors influence performance

types of muscle fibers

fast fibers

slow fibersintermediate fibers

Muscle Performance

fast fibers

contract very quickly after stimulationlarge diameterpacked with myofibrilslarge glycogen reservesfew mitochondriafatigue easilyaka “white muscle fibers”

Muscle Performance

slow fibers

slower rate of contraction1/2 diameter of fast fibersmore mitochondria (and what they need)good blood supplycontain abundant myoglobinmore for extended contractionsaka “red muscle fibers”

Muscle Performance

intermediate fibers

in betweenlook like fast fibers

little myoglobin (pale)but…

better blood supply than fastmore resistant to fatigue than fast

table 10-3

Muscle Performance

skeletal muscle

can have different percentages of the different fiber types

hand/eye fastback/calf slow

genetically determinedcan be altered with exercise

Muscle Performance

skeletal muscle growth

repeated, exhaustive stimulation

more mitochondriamore glycolytic enzymesmore myofibrilsmore filaments

cells get bigger

hypertrophy

Muscle Performance

non-stimulated muscles

get smallerloose muscle tonebecome weaker

atrophy

Muscle Performance

atrophy

temporary immobilization(leg in a cast)

initially reversiblein extreme cases: permanent

physical therapy

Muscle Performance

Physical conditioning

improve power (ability to generate tension)

improve endurance

Muscle Performance

anaerobic endurance

how long the muscle can work supported by glycolysis and stored ATP and CP

Muscle Performance

anaerobic endurance

limited by:

amount of ATP and CP stored[glycogen] availabletolerance to lactic acid

sprint work, pole vault, short events

Muscle Performance

anaerobic endurance

training:

frequent, brief,intense workouts

stimulate hypertrophy

Muscle Performance

aerobic endurance

how long the muscle can work supported by mitochondrial activity

Muscle Performance

aerobic endurance

limited by:

availability of substrates for aerobic respiration

dependent on blood supply

jogging, distance running, swimming, etc.,don’t require peak tension production

Muscle Performance

aerobic endurance improvement

changing characteristics of fibers

improving CV performance

fast fibers can take on intermediate characteristics

increased capillarityaccelerate blood flow

Muscle Performance

aerobic endurance improvement

does not promote hypertrophy

cross-trainingcombination aerobic and anaerobicexercise for benefits of both

Cardiac Muscle

like skeletal:striated (organized myofibrils)

unlike skeletal:smaller cellsno triadsSR lacks terminal cisternaedependent on aerobic metabolismspecial cell-cell junctions

Cardiac Muscle

junctions to hold the cells together(adhering junctions)

junctions allowing forcell-cell communication

(gap junctions)

functional syncytium (fused cells)

intercalated discs

Cardiac Muscle

•contract without neural stimulation

(beat is intrinsic)•nervous system can alter “pace”

and adjust tension produced•contractions are slower than

skeletal•wave summation and tetany don’t

functional specializations:

fig. 10-22

Smooth Muscle

forms sheets, bundles or sheaths

skin: blood vessels regulate blood

flow to surface (thermoregulation)

cardiovascular: blood distributionblood

pressure

respiratory: change airways / airflow

Smooth Muscle

forms sheets, bundles or sheaths

digestion: move material through

urinary: urine production, transport…

reproduction: gamete movementlabor

Smooth Muscle

structure

small, single cells, central nucleusno organized myofibrils

(no striations)have thick and thin filamentsconnected to neighbors

to here 2/14lec # 17

Smooth Muscle

functional differences:

1. excitation-contraction coupling

calcium enters cells at stimulationbinds to calmodulinactivates an enzyme to

permits cross-bridges to form

Smooth Muscle

2. length-tension relationship

ability to contract over a wide range of lengths

plasticity

Smooth Muscle

3. control of contractions

multiunit

visceral

similar to skeletaliris m., arrector pili m., ….

contraction spreads in waves(peristalsis in gut)

Smooth Muscle

4. smooth muscle tone

neural and hormonal control

table 10-4

fig. 10-23

Muscle strains(pulls, tears)

sprain

strain

injury to a ligament

injury to a muscle to tendon

There are two basic causes of cramping. One is inadequate oxygenation of muscle,

and the other is lack of water or salt.

Electrolyte disturbance may cause cramping and tetany of muscles,

particularly hypokalemia (a low level of potassium) and hypocalcemia (a low level

of calcium).

Muscle cramps(via wikipedia)

(postive feedback-next chapter)

Chapter 10 Muscle Tissue (Mostly Skeletal Muscle).

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