10 - Muscular Contraction - Taft College Home Page

10 -Muscular

Contraction

Taft College Human

Physiology

Muscular Contraction• Sliding filament theory (Hanson

and Huxley, 1954)• These 2 investigators proposed

that skeletal muscle shortens during contraction because the thick (myosin) and thin (actin) filaments slide past one another.

• The previous idea was that the filaments change in length.

• The myosin heads pull the thin filaments toward the center of the sarcomere which shortens the sarcomere.

• Remember, the I band and the H zones disappear as the thin filaments move to the center. The A band stays the same length.

• Only the length of the sarcomerechanges, not the length of the filaments!

2 Sarcomeres

Sarcomere Sarcomere

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.

Events During Muscle Contraction

DiagramIn Text


• (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 end

plate.• 4a. ACh receptor protein channel opens and increases

permeability of Na+ into sarcoplasm.• 4b. If there is enough ACh, an action potential (AP)will

occur. • 4c. Acetylcholinesterase degrades ACh.


• (Steps 5-7 represent depolarization.)

• 5. Na+ enters muscle fiber, rapid depolarization of sarcolemma occurs = action potential.

• Voltage changes to a less negative charge.• 6. The action potential spreads away from the end plate

in all directions and depolarizes the T tubules.• 7. The action potential continues down the T tubules

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


• 8. The SR responds to the action potential by opening Ca++ release channels which floods the surrounding sarcoplasm located between the thick and thin filaments with Ca++.

• 9. Ca++ combines with regulatory protein troponin, 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.

The Role of Ca++ in Contraction

Events During Muscle Contraction• 11. Myosin heads (cross bridges) attach to actin binding

sites on thin filament.• 12. Myosin head flexes (tilts, shifts), drawing actin

filaments of sarcomere toward each other.• 13. Once myosin head is flexed, ATP binding site is

exposed and ATP binds to the head.• 14. Myosin head detaches from actin binding site under

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

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

myosin

actin Z

The Contraction Cycle

11

12

13

14

Rigor Mortis = Stiff Death• Rigor mortis- Notice that ATP is responsible for myosin

heads 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 of rigidity 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.


• Steps 15-17 = Relaxation

• 15. Ca++ is returned to the SR by Ca++ active transport pump (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. Nerve impulse2. Ach released3. Ach binds to motor end plate4. Increased permeability of Na+

into sarcolemma5. Depolarization of sarcolemma,

action potential6. Depolarization of T-tubule7. Depolization of SR membranes8. SR releases Ca++ between thin

& thick filaments9. Ca++ combines w/ troponin10. Troponin changes shape and

exposes myosin binding site11. Myosin heads attach to actin

binding site12. Myosin heads tilts/shifts

drawing actins of sarcomeretoward each other

13. Tilting of myosin head exposes ATP 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 sites17. Muscle relaxes

1

17

16

15

9-10

11-14 = Contraction

2

3-56-8

ATP and Contraction• We see that ATP 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 sarcoplasmback 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.

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

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 cause burning sensation and pain.•Together creatine phosphate (1) and anaerobic system (2) can provide enough ATP for a 400 meter sprint.

With out Oxygen

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

Oxygen Consumption after Exercise

• oxygen debt = recovery oxygen uptake(Older term) (New term)

• = the amount of oxygen that must be paid back to 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 phosphate

and ATP.• 3. Replaces oxygen removed from storage in

muscle tissue (myoglobin).

Physiological Properties of Muscles• Stimulus = an impulse. • An impulse may travel along a motor neuron that is not strong

enough to cause a contraction.• A stimulus that does not cause a response by the muscle is called

subliminal 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 none –if threshold is reached all muscle cells of a motor

unit will contract maximally, if not reached, none will contract.

= Polarized at Rest =-70 mV

When threshold is reached, a rapid depolarizationoccurs called an action potential that leads to a muscle contraction.

“1st Domino”

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 unit in an ‘all or none’ fashion. All fibers contract to their fullest extent or not at all.

• However, the tension or force produced by an entire muscle can be adjusted.

• There are 2 ways to control strength of a muscle contraction:

• 1. Recruitment of motor units.• 2. Altering the contractility of individual muscle

fibers.


• 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 10

fibers, while a large one may consist of several 100 (or even 2000).• Example: Fingers contain very small motor units so they can carry our fine

movement.• Simply speaking: If a muscle needs more force, it will recruit (activate) more

motor units. The strength of the electrical stimulus determines the number of motor 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


• 2. Altering the contractility of individual muscle fibers (cells).

• This means changing the properties of muscle fibers irrespective of how many fibers are involved.

• There are 2 ways to change the contractility of fibers.

• a. Increase the frequency of stimulation to individual fibers.

• b. Vary the length of the fiber (length-tension relationships).


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

• If we were to stimulate a muscle with a single liminalstimulus 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 what is 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++ in the 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 infinite effect.

S1 S1 S2

2. Altering the contractility of individual muscle fibers by :

a. Increasing frequency of stimulation.

• If there is repeated stimulation, 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 will 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 :

• 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 fiber 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.

Length - Tension Relationship of Skeletal Muscle

Here, greatest number of myosin heads can pull on actin.

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 muscle

fiber or muscle cell by :• 2A. Altering frequency of stimulation.• 2B. Altering the length of the cells.

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