Chpt. 49 Muscles & Motor Locomotion Why Do We Need All That ATP?

Chpt. 49Chpt. 49Muscles &

Motor Locomotion

Why Do We Why Do We Need All Need All

That ATP?That ATP?

Function of Muscles:• To convert chemical energy of

ATP into mechanical work,• To get around… • To get your food• To digest your food• To pump your heart

so that oxygen canget to that

mitochondria

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• 1) Cardiacrapid contraction

• 2) Skeletalrapid contraction

• 3) Smoothslow sustained contraction

Types of Muscle Tissue:



voluntary, striated

involuntary, striated

auto-rhythmic

involuntary,

non-striated

evolved first

multi-nucleated

digestive systemarteries, veins

heartmoves bone

As a side …

• Insect flight muscles contract more rapidly than ANY OTHER

• 1,000 contractions/second

• Highest metabolic rate

• Contain more mitochondria than any other tissue

• HOW get oxygen???





HOW DO WE MOVE THESE 206 BONES?

SKELETAL MUSCLE

skeletal muscles move bones by pulling…not pushing, therefore they come in antagonistic pairs:

So in other words, in order to flex, you must contract your flexor muscles… and in order to, relax, you must contract the

antagonistic muscle

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flexorflexor vs. extensorextensor

Extensor

(quadracep)

Notice the TENDON connects the muscle to the bone.

One bone is pulled towards another bone upon contraction.

Vertebrate Skeletal Muscle

Structure:

tendon

skeletal muscle

muscle fiber (cell)

myofilamentsmyofibrils

plasma membrane

nuclei

composed of smaller & smaller & smaller units


each muscle fiber = one long, cylindrical, multinucleated cell




Muscle fiber cells composed of: bundles of myofibrils (threadlike

structures)

Bundle of fibers

Myofibrils are basically parallel “contractile units”



Myofibrils consist of even smaller structures:

thick filaments

thin filaments

myofibrils have a regular arrangement

regular arrangement

regular arrangement

regular arrangement

regular arrangement

sarcomere = basic unit of a myofibril - hundreds are connected end to end & make up the myofibril

sarcomeres are made of these proteins:

thick filaments

thin filaments

Thin filaments: actin•Complex (bunch) of proteins:

–braid of actin molecules & tropomyosin fibers•tropomyosin fibers secured with troponin complex•these are proteins

Thick filaments: myosin•Single protein

–myosin molecule•long protein with globular head

bundle of myosin proteins:globular heads aligned

Thick & thin filaments• MyosinMyosin tails aligned together & heads

pointed away from center of sarcomere

sarcomere = basic unit of a myofibril - hundreds are connected end to end & make up the myofibril

SARCOMERESARCOMERE

making up the sarcomere…

Z-lines = the borders

of the sarcomere (actin)

at rest, the thick myosin &

thin actin filaments in the sarcomere do not overlap completely:

area inwhich only thick myosin filaments = H zone

Area inwhich only

thin actin filaments =

I band

Area in which

both: thin actin filaments & thick myosin

filaments = A band



More muscle anatomy: SARCOLEMMA = plasma membrane



More muscle anatomy: T tubule = inward extension of the plasma membrane



More muscle anatomy: mitochondrion = ohh, there are plenty!



More muscle anatomy: sarcoplasmic reticulum = another name for endoplasmic reticulum

How does the Muscle Contract?

Sliding Filament Model

Motor Unit



(Usually hundreds of muscle fibers)

NEUROMUSCULAR JUNCTION



NEUROTRANSMITTOR ~ ACETYLCHOLINE released as action potential moves to synaptic terminal



of muscle fiber

The acetylcholine causes the action potential to continue in the muscle

fiber



The action potential spreads into T-Tubules (invaginations in the membrane of the muscle fibers)



The a.p. opens Ca+2 channels in the

sarcoplasmic reticulum (e.r.)



The special type of smooth endoplasmic reticulum found in smooth and striated muscle fibers whose function is to store and release calcium ions.

Ca+2 flows & binds to a protein in the actin

filament



Sliding Sliding Filament Filament ModelModel

At rest myosin binding sites are blocked (with trypomyosin)

Thin actin filament has myosin binding sites…

Sliding Sliding Filament Filament ModelModel

Thin actin filament has myosin binding sites…

myosin binding sites are opened when Ca+2 binds to the troponin.

(Ca+2 is released as a result of acetylcholein rushing through the T-tubules)


At rest, myosin head is bound to an ATP --

ATP


when Ca+2 floods into the cell, Myosin head hydrolyzes (breaks) ATP to ADP and P --.


Myosin binds to Actin --

this forms a cross-bridge

When this occurs, the myosin head changes shape and releases the ADP + P


the myosin head changes shape and releases the ADP + P


The thin actin filament is pulled toward the center of the sarcomere…



cross-bridge broken when ATP binds back to the myosin head

ATP

3

2

Cleaving ATP ADP + P allows myosin head to bind to actin filament

ATP

formcrossbridge

ADP

releasecrossbridge

shortensarcomere

1

4

ADP expelled

What is the Stimulus that causes muscle to

contract?

Synapse with Neuron & MuscleSynaptic Terminal

of neuron releases acetylcholine

Synapse with Neuron & Muscle

Ca++ released

Binding sites on actin are now exposed.

Myosin head now binds to the actin

Synapse with Neuron & Muscle

ATP

Muscles do not relax until the Ca+

+ is pumped back into the sarcoplasmic reticulum

Put it all together…1

ATP

2

3

4

5

7

6

ATP

Action potential travels

a.p, travels through T-Tubules

Ca+2 released & binds to troponin complex

Cross bridge formed

Ca+2 depleates; cross bridge broken/ ATP back on myosin head

Ca+2 pumped back into s.r. / ATP required

Acetylcholine released

Put it all together…1

ATP

2

3

4

5

7

6

ATP

Muscle limits:

• Muscle fatigue– lack of sugar

• lack of ATP to restore Ca2+

gradient

– low O2

• lactic acidcauses pH drop which interferes with protein function

– synaptic fatigue• loss of acetylcholine

• Muscle cramps– build up of lactic acid – ATP depletion– ion imbalance

• massage or stretching increases circulation

Rigor mortisRigor mortis• So why are dead people “stiffs”?

– no life, no breathing– no breathing, no O2

– no O2, no aerobic respiration– no aerobic respiration, no ATP– no ATP, no Ca2+ pumps– Ca2+ stays in muscle cytoplasm– muscle fibers continually contract• tetany or rigor mortis

– eventually tissues breakdown& relax• measurement for time of death

Money for BeautyMoney for Beauty• What is Botox?–Toxin derived from Closteridium botulinum

–blocks the release of acetylcholine

–Muscles relax… whichtakes away the

wrinkle QuickTime™ and a decompressor

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*The transmission of an impulse from a nerve to the surface of a resting muscle initiates a contraction in that muscle. Biochemical and biophysical studies of muscle tissue have resulted in an explanation for muscle contraction known as the sliding-filament theory.

a. Describe the chemical changes that occur when a nerve impulse is transmitted to the surface of a resting muscle cell.

b. Describe the internal structure of a muscle fiber as revealed by electron microscopy.

c. On the basis of this structure, explain the sliding-filament theory.

*7. Discuss the mechanism by which a muscle cell contracts or a nerve cell transmits an impulse. Include in your discussion the relationship between cell structure and function.

• Action potential causes Ca2+ release from SR– Ca2+ binds to troponin

• Troponin moves tropomyosin uncovering myosin binding site on actin

• Myosin binds actin– uses ATP to "ratchet" each time– releases, "unratchets" & binds to next actin

• Myosin pulls actin chain along• Sarcomere shortens

– Z discs move closer together

• Whole fiber shortens contraction!• Ca2+ pumps restore Ca2+ to SR relaxation!– pumps use ATP

ATP

ATP

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Chpt. 49 Muscles & Motor Locomotion Why Do We Need All That ATP?

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