10 muscular contraction

8/10/2019 10 Muscular Contraction

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10 -Muscular

Contraction

Taft College

HumanPhysiology


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Muscular Contraction Sliding filament theory (Hanson

and Huxley, 1954)

These 2 investigators proposedthat skeletal muscle shortensduring contraction because the

thick (myosin) and thin (actin)fi laments slide past one another.

The previous idea was that the

filaments change in length.

The myosin heads pull the thinfilaments toward the center ofthe sarcomere which shortens thesarcomere.

Remember, the I band and the Hzones disappear as the thinfilaments move to the center. The

A band stays the same length.

Only the length of the sarcomerechanges, not the length of thefilaments!

2 Sarcomeres

Sarcomere Sarcomere


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Closer Look at the Events During

Contraction We will now take a look at contraction in a

step-by-step fashion. We will discuss 17 steps during a muscle

contraction event. Figure 10.12, explains these events in 9

steps. It is not important that you can

name a step, but that you can explain how

muscle contraction works.


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Events During

Muscle Contraction

Diagram

In Text


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Events During Muscle Contraction

(Steps 1- 4 represent nerve impulse)

1. Nerve impulse arrives at neural muscular junction.

2. ACh release from axon terminals.

3. ACh binds to active sites (receptors) on motor endplate.

4a.ACh receptor protein channel opens and increasespermeability of Na+ into sarcoplasm.

4b. If there is enough ACh, an action potential (AP)willoccur.

4c.Acetylcholinesterase degrades ACh.


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(Steps 5-7 represent depolarization.)

5. Na+ enters muscle fiber, rapid depolarization ofsarcolemma occurs = action potential.

Voltage changes to a less negative charge.

6. The action potential spreads away from the end platein all directions and depolarizes the T tubules.

7. The action potential continues down the T tubules

into the sarcoplasm where it depolarizes thesarcoplasmic reticulum (SR) membranes.


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8. The SR responds to the action potential byopening Ca++ release channels which floods thesurrounding sarcoplasm located between thethick and thin filaments with Ca++.

9. Ca++

combines with regulatory proteintroponin, associated with actin filaments.

10. Troponin changes shape, and

exposes the myosin binding sites on actin. Steps 5-10 are all a part of the latent period =

lag time between stimulation and contraction.


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The Role of Ca++ in Contraction


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11. Myosin heads (cross bridges) attach to actin bindingsites on thin filament.

12. Myosin head flexes (tilts, shifts), drawing actinfilaments of sarcomere toward each other.

13. Once myosin head is flexed,ATP binding site isexposed andATP binds to the head.

14. Myosin head detaches from actin binding site under

the influence of ATP binding. Energy from ATP returnsthe myosin head to the cocked forward position. Myosinhead attaches to a new binding site on actin.

(Steps 11-14 = Contraction and are repeated overand over during a single contraction event as longas ATP and Ca++ are available.)

myosin

actin Z


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The Contraction Cycle

11

12

13

14


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Rigor Mortis = Stiff Death

Rigor mortis- Notice thatATP is responsible for myosinheads detaching from actin, which leads to muscle

relaxation. This is illustrated by rigor mortis = stiff death. When a

person dies, no more ATP is synthesized as no more 02and glucose are supplied to the tissues.

The myosin heads cannot detach themselves from actinresulting in a condition in which muscles are in a state ofrigidity called rigor mortis. The muscles contract as Ca++diffuses out of sarcoplasmic reticulum (the Ca++ pump

energized by ATP has quit working). This state lasts about 24 hours and disappears as the

tissues undergo autolysis.


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Steps 15-17 = Relaxation

15. Ca++ is returned to the SR by Ca++ active transportpump (requires ATP). Sarcoplasm is now Ca++ poor.

16. Troponin again covers actin binding sites. Therefore

no myosin actin interaction can occur. 17. Muscle fiber relaxes. Movement of relaxation is due

to:

A. "Elastic effect" of coiled elastic fiber (titan)molecules. And/or,

B. Due to pull of C.T. within muscle.

1 N i l


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1. Nerve impulse

2. Ach released

3. Ach binds to motor end plate

4. Increased permeability of Na+

into sarcolemma5. Depolarization of sarcolemma,

action potential

6. Depolarization of T-tubule

7. Depolization of SR membranes

8. SR releases Ca++ between thin& thick filaments

9. Ca++ combines w/ troponin

10. Troponin changes shape and

exposes myosin binding site

11. Myosin heads attach to actinbinding site

12. Myosin heads tilts/shifts

drawing actins of sarcomere

toward each other

13. Til ting of myosin head exposesATP binding site- ATP Binds

14. Myosin head detaches, ATP

repositions myosin head,

myosin bind to new site

15. Ca++

is returned to S-R16. Troponin again covers actin-

myosin binding sites

17. Muscle relaxes

1

17

16

15

9-10

11-14 = Contraction

2

3-56-8


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ATP and Contraction We see thatATP is required for 3 major roles

in contraction:

1. Repositions (cocks) the myosin heads.

2. Detachment of myosin heads from actin

once the power stroke is complete.

3. Powers the Ca++ active transport pumps

that rapidly remove Ca++ from the sarcoplasm

back into the sarcoplasmic reticulum (reservoir). The concentration of Ca++ is 10,000 times lower

in the sarcoplasm of a relaxed muscle fiber than

inside the SR.


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ATP Produced in 3 Ways ATP is very important but muscle only stores enough for about

4-6 seconds of activity ATP is produced in 3 ways

1. Phosphagen System = ATP Creatine Phosphate System

Product = 1 ATP + 1 creatine phosphate + 1 creatine Duration of energy = 15 seconds

Function = Quick Power , 100 meter sprint


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ATP Produced in 3 Ways

2.Anaerobic System =

Glycogen Lactic Acid System

Product = 2 ATP/ Glucose

Duration = 30- 40 Seconds

Function = 300 meter sprint

Lactic acid is produced as a

waste product that causeburning sensation and pain.

Together creatine phosphate (1)

and anaerobic system (2) can

provide enough ATP for a 400

meter sprint.

With out Oxygen


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ATP Produced in 3 Ways3.Aerobic System = Aerobic Respiration With Oxygen

Product = 36 ATP / Glucose

Duration = Hours

Function =Aerobic work , long distance running or

swimming

36Occurs in Mitochondria


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Oxygen Consumption after

Exercise oxygen debt = recovery oxygen uptake

(Older term) (New term)

= the amount of oxygen that must be paid backto the body following exercise

Oxygen does 3 things:

1. Converts the lactic acid back into glycogen(fuel) stores in the liver

2. Allows production of creatinine phosphateandATP.

3. Replaces oxygen removed from storage inmuscle tissue (myoglobin).

Ph i l i l P ti f M l


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Physiological Properties of Muscles Stimulus = an impulse.

An impulse may travel along a motor neuron that is not strongenough to cause a contraction.

A stimulus that does not cause a response by the muscle is calledsubliminal or subthreshold stimulus. (Ex. -70 mv to -60 mv)

By increasing the stimulus, a barely perceptible response may be

obtained = liminal or threshold stimulus. (Ex -70 to -55 mv). A liminal stimulus is just strong enough to cause a depolarization

and production of an action potential.

All or noneif threshold is reached all muscle cells of a motorunit will contract maximally, if not reached, none will contract.

= Polarized at Rest =-70 mV

When threshold is reached,

a rapid depolarization

occurs called an action

potential that leads to a

muscle contraction.

1st Domino


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Grading of the Strength of a

Muscle Contraction How can we control how much strength a muscle (like

the biceps or triceps brachii) produces?

An individual motor unit fires all muscle fibers in that unitin an all or none fashion. All fibers contract to theirfullest extent or not at all.

However, the tension or force produced by an entiremuscle can be adjusted.

There are 2 ways to control strength of a musclecontraction:

1. Recruitment of motor units.

2. Altering the contractil ity of individual musclefibers.


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Muscle Contraction 1. Recruitment of motor units.

An individual neuron branches to many different muscle fibers (cells).

The neuron and the muscle fibers it innervates are called = motor unit.

Motor units vary in size- A small motor unit may consist of as few as 10fibers, while a large one may consist of several 100 (or even 2000).

Example: Fingers contain very small motor units so they can carry our finemovement.

Simply speaking: If a muscle needs more force, it will recruit (activate) moremotor units. The strength of the electrical stimulus determines the number ofmotor units recruited.

If less force is necessary, less motor units are recruited.

Experience is important to in knowing how many motor units to recruit.

More motor units

= greater force

G di f th St th f


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Muscle Contraction 2. Altering the contractility of individual

muscle fibers (cells).

This means changing the properties of musclefibers irrespective of how many fibers areinvolved.

There are 2 ways to change the contractilityof fibers.

a. Increase the frequency of stimulation to

individual fibers. b. Vary the length of the fiber(length-tension

relationships).

G di f th St th f


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Muscle Contraction2. Altering the contractility of individual muscle fibersby a. Increasing frequency of stimulation.

If we were to stimulate a muscle with a single liminal

stimulus S1, the muscle will exhibit a single quick

contraction of minimal force called a twitch.

If we follow 1 stimulation S1 quickly by another S2,

before the muscle has a chance to relax, we see whatis called the summation effect or wave summation =

the tension produced by the second stimulation will

be added to the first:

The increased tension is due to increased Ca++ inthe sarcoplasm produced by additional stimuli.

It takes a little more time for the Ca++ to leave and for

the muscle to relax.

The increased tension of summation is not an infiniteeffect.

S1 S1 S2

2. Altering the contractility of individual muscle fibers by :


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a. Increasing frequency of stimulation.

If there is repeated st imulation, tension will reach a certain plateau and stay there.

The sustained contraction of a muscle is known as tetanus.

Unfused (incomplete) tetanus is observed at 20-30 stimuli/sec, the muscle shows

some relaxation between stimuli.

Fused (complete) tetanus is observed at 80+ stimuli per second. Note, there is no

sign of relaxation in force between stimuli. The tension (strength) produced in tetanus is 2-4 times the tension of a single twitch.

Tetanus represents a normal muscle contraction!!

If you continue to stimulate the muscle, it wi ll run out of ATP and will fatigue.

Fatigue

Tetanus =2-4 x force

of twitch

Stimuli

2. Altering the contractility of individual muscle fibers by :


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b. Vary the length of the fiber(length-tension relationship)

Using the same device as above, we can vary the length of the muscle and

measure the amount of tension each length could produce we would get the

following kind of plot see below.

Maximum tension occurs at 2.2 um. This is the sweet spot for f iber overlap and

strength.

What is the reason for this? Let's look at a sarcomere at the different lengths. We can see that, the more contracted, the greater the interaction between thick and

thin filaments (as long as the actin does not overlap and interfere with interaction).

The more they overlap (without interference), the more cross bridges which can

connect and hence, more tension can be produced.

L th T i R l ti hi f


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Length - Tension Relationship of

Skeletal MuscleHere, greatest number of myosin

heads can pull on actin.


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Summary

How do you get more tension (strength)

out of a muscle? 2 ways 1. recruit more motor units

2. alter the contractility of each musclefiber or muscle cell by :

2A.Altering frequency of stimulation.

2B.Altering the length of the cells.

10 muscular contraction

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