Lecture 7 Muscular Physiology Flashcards
Each muscle fibre is innervated by only one neuron but one motor neuron may go on to
Innervate many muscle fibres
Each muscle fibre is innervated by how many neurons ?
Just one
1 neuron innervates _____ fibres within the same whole muscle
150 ave
Presynaptic neuron contains vesicles with nT (acetylcholine) and on the post synaptic membrane of the muscle fibre (sarcolemma), it is a region with _____ and is referred to as ______
ACH receptors
Motor end plate
After acetylcholine binds to the ACH receptors on the motor end plate of the sarcolemma what happens?
Chemical gates open and Na+ floods into the cell. Creating a end plate potential which is a graded potential. This EPP is always sufficient enough to cause an action potential.
Why is the transmission of action potential always propagated from the lower motor neuron to the muscle fibre?
Because a lot of ACH is released in the synaptic cleft.
And there are many ACH receptors on the motor end plate
One action potential from a neuron to an end plate will cause how many APs in the muscle?
Just one
When a muscle fiber is in a relaxed state what covers the myosin binding sites on actin ?
Tropomyosin
When the muscle fibre is in a state of rest is the myosin head activated ?
If so, how is it?
It is activated only it’s biding site is covered
The ATP on the myosin has become
ADP + Pi and NRG (stored in the myosin head) so now it is ready to bind as soon as the binding sites on actin are exposed
When a muscle fiber is excited
The sarcolemma is depolarized; the EPP produces an AP
When the AP propagates, where does it go and how ?
It propagates down the t tubules to deep within the fibre
The excitation of the muscle fibre sets the stage for the excitation - contraction coupling. This is going from an electrical to________ event
Mechanical
What is the next step after AP has been propagated down to the t-tubules ?
Calcium ions are released into cytosol (coupling agent) from terminal cisternae sarcoplasmic reticulum
This happens because the voltage sensitive tubule proteins change shape. (Voltage gates)
After the calcium has been released from the terminal cisternae during the EC coupling what happens
The calcium binds to troponin (go signal) which removes the blocking action of tropomyosin
Now the binding sites are exposed on the thin filaments
After the calcium has bound to troponin… Changing the shape of the tropomyosin … Exposing the binding sites on the thin filament what then will happen ?
Now contraction can occur
Activated myosin can attach to binding sites on actin
This is called cross bridge attachment
When actin and myosin form cross bridges, the energy in the myosin head is released, how does this happen
Myosin head pivots ( power stroke )
The ADP and organic phosphate are released
The power stroke causes actin to slide over myosin toward the center of the sarcomere
What action of myosin is responsible for causing the actin to slide over myosin toward the center of the sarcomere?
Power stroke
At which point is E-C coupling over ?
When contraction
Cross bridge cycling begins
The mechanical event of contraction is also called
Sliding filament mechanism
After the power stroke occurs and actin moves toward middle of sarcomere what happens to he myosin head ?
ATP attaches to the myosin head which releases the myosin head from actin and un-pivot occurs
When the myosin head is released from actin it’s called unpivot
What’s another name for this action ?
Recovery stroke
After a recovery stroke the myosin head becomes activated once again. Which means…
It converts the ATP to ADP and Pi and NRG
If after a contraction occurs via action potential in the muscle and myosin head has become activated once again (ADP Pi) if there is sufficient _______ in the ________ it can continue to bind to _________
Calcium
Sarcoplasm
Troponin
Then the cycle may continue to repeat many times to shorten a muscle
If there is sufficient enough calcium in the sarcoplasm after a contraction occurs what will happen
Calcium will bind to troponin
Tropomyosin will change shape and actin binding site will be exposed
Then activated myosin head will undergo powerstroke to pivot up to actin
Actin will then slide over myosin toward the middle of the sarcomere
Then an ATP will bind to myosin and release it from actin
Repeat until no more calcium to shorten muscle
In the sliding filament mechanism what shortens and what stays the same length
Myofibrils shorten / H zone and I band shortens / sarcomere shortens
Actin / myosin stay same length / A band stays same length
Acetylcholine broken down by what on the motor end plate
Acetylcholinesterase
During relaxation ACh is broken down by ache and the sarcoplasmic reticulum takes up Ca2+ occurs via
Ca2+ - ATPase
During relaxation of muscle cell ____ binds to myosin heads causing
ATP binds to myosin heads causing them to activate and release from actin and tropomyosin covers actin once again
Thick filaments bind to what and what
Actin and ATP
Thin filaments bind to what and what
Myosin and calcium
What Are All the things ATP is used for in muscle contraction
Na+ K+ ATPase pump for maintaining gradient
Activation of myosin and powerstroke
Release of cross bridge
Pump calcium into SR
What is rigor Mortis
Stiffness of body after death
Why do the muscles of the body remain in a contracted state shortly after death
Before death : myosin heads are activated and able to bind to actin
After death: no O2 in and no ATP being produced. Calcium comes from ECF to ICF –> SR
Since there is no ATP, myosin can not be released from actin and muscles remain in contracted state
When does rigor mortis begin and peak?
3 hours AD
12 hrs AD
If extra cellular Ca2+ is low
Pregnancy or lactation
What happens
Na+ enters the cell and cramps happen
If intracellular ca2 is low
Contractions not initiated
What is myasthenia gravis
What is it caused by
Treatment ?
It is an autoimmune disease
Caused by decrease in # of acetylcholine receptors
Treatment: acetylchonesterase inhibitors. Increases binding of remaining acetylcholine receptors
What is curare poisoning ?
What can it be used for
Prevents acetylcholine from binding to receptors (no connection from lower motor neuron to skeletal muscle)
Causes flaccid paralysis
Used in surgeries
What is botulism
How is it caused
What does it do to acetylcholine
How is it used clinically
Caused by improper canning resulting in an infection with bacterium clostridium botulinum
Prevents exocytosis of acetylcholine
Flaccid paralysis
Used to treat crossed eyes and uncontrolled blinking
Botox: cosmetic - wrinkles / sweating
What are the effects of nicotine in acetylcholine
Binds to receptors and mimics effect of acetylcholine
Causes muscle spasms
Black widow spider venom does what to acetylcholine
What is the result
Causes mass release of acetylcholine
As a result muscles contract so much breathing stops
Leads to initial stimulation of acetylcholine receptors
Long term can cause receptor desensitization
Firing of muscle can become depressed
What is tension
The amount of force exerted by a muscle
Determined by a total number of cross bridge attachments
There’s different degrees of frequency of stimulation of muscle fibers: single stimulus, 2nd stimulus, rapid sequence and
High frequency
Single stimulus frequency in muscle fiber is not normally not seen in _________muscles
Produces ____________
Skeletal muscles
Produces twitch
Weak contraction followed by relaxation
For the single stimulus the action potential lasts 1-2 seconds
In muscle there’s 3 phases : latent, contraction and relaxation
Describe latent/ lag phase
~2 milliseconds
Period between application of stimulus and muscle contraction
Processes associated with exciting and coupling
***Movement of AP down T-tubule release of calcium which binds to troponin exposing myosin binding sites
Describe the contraction phase of the single stimulus frequency
How long
~10-100 milliseconds
Mechanical (time when head groups contract)
Cross bridge attachment and sliding filaments
Increased tension
Relaxation phase of the single stimulus frequency
Ca2+ pumped back kno sarcoplasmic reticulum by Ca2+ ATPase
ATP attaches to myosin heads and recovery stroke
Decrease in tension
Describe a 2nd stimulus frequency on a muscle –> tension
2nd stimulus arrives before muscle has completely relaxed
Produces contraction with increased tension / no refractory period with contraction (due to Ca2+ availability)
Much Ca2+ released on first stimulus but taken back into SR before all myosin heads are able to attach
Second stimulus releases more Ca2+ so cytosolic concentration rises and more myosin heads able to attach
What is wave summation ?
The increase of tension aquired by more than 1 stimulus due to increasing calcium levels
Rapid sequence of stimuli on muscle —> tension
Allows partial relaxation between contractions
Tension increases (wave summation) (increased Ca2+ availability)
Incomplete tension results
What is tetanus
Smooth sustained muscle contraction resulting from high frequency stimulation
High frequency of stimulation
No relaxation between contractions
Sustained
Highest tension results (3-4x that of a twitch)
All troponin saturated with Ca2+
Fiber is warm because ATP synthesis releases heat
Everything working faster , this occurs normally in the boy
Complete tetanus
Describe fast fibers
Contract / reflex rapidly
Appear white because lack of myoglobin
Describe slow fibers
Contract and relax slowly
Appear red because of more myoglobin
- postural muscles
Muscle length has a lot to do with how much tension it can produce resting fiber length is is optimal, why
Max number of + bridges can be attached therefore stimulate maximum tension
Fiber length that is shorter than resting when stimulated …
Thin filaments overlap and interfere with cross bridge attachment
Fewer cross bridges attack and a decrease in tension results
Minimum length for tension to occur is 70 % of resting
Sometimes when a fiber is stretched it becomes more difficult for it to accomplish tension why
Not all myosin heads are near active binding sites
Fewer cross bridges attach
Decreased tension
The maximum length is 130% of optimal
The size of the fiber affects the tension
How does it
When it’s
Thicker / larger
Thickness. More Myofibrils
Larger. More tension
What are factors that affect tension in a whole muscle
-Number of fibres contracting (#of active motor units)
-Number of fibres per motor unit (one neuron > 10 fibers - delicate contractions. One neuron : 1000- strong)
Fatigue
A large muscle will have ____ number of fibers contracting and _____ # of fibers per motor unit
High
Muscle tone
Few fibers in low tension
Different motor units stimulated over tjme but tone relatively constant
Gives firmness to muscle
There are 2 types of muscle contractions isotonic and isometric
Describe isotonic
Muscle changes length
Tension relatively constant during contraction
Tension exceeds resistance of load lifted
Used for body movement and moving objects
Flexion of elbow - tension greater than weight of forearm
Isometric contraction
Muscle length is constant
Tension increases : cross bridges attached but no shortening
Tension is less than required to move load
Used for standing - holding a book in place
In the example of lifting a book to read
Where would isotonic and isometric contraction take place
Isotonic lifting
Isometric holding
Muscle metabolism during resting conditions (aerobic)
Fatty acids used to produce ATP
Storage: of glycogen creatine phosphate and little ATP
When ATP and creatine together
P is cleaved off of ATP to produce ADP and creatine phosphate (c~p)
During short term exercise (less than a minute) –> primarily anabolic
A) creatine phosphate is used to make ATP
C~P + ADP –> ATP + Creatine (via creatine kinase)
C~P lasts 15 seconds
b) muscle glycogen –> glucose –> pyruvic acid
(Pyruvic acid then takes the anarobic pathway to create lactic acid)
Lasts 30 seconds
During long term exercise
One minute to hours
Glucose from liver is used
Fatty acids used more as exercise continues
ATP; from aerobic pathway
Oxygen sources include hemoglobin in blood and myoglobin in muscle
Muscle fatigue
What is it
What does it do
How does it protect
Not fully understood
Inability to maintain tension
Decreases ATP use
Protective exhausting ATP would be detrimental for vital function
ATO only decreases 70% of Resting if too little cross bridges can’t release and contraction continues
What is fatigue potentially caused by
-depletion of NRG supply ( glycogen) lack of ATP normally not a problem
- built up end products
Failure of action potentials
What are the built of end products potentially causing fatigue
- -H+ from lactic acid (muscle contraction compresses blood vessels –> decrease O2 to muscle. Muscle needs to be anarobic for periods of time (potentially during long term exercise)
- -phosphate (from conversion of ATP - ADP and Pi– will bind to Ca2+ therefore less Ca2+ available to troponin
- this slows the release of Pi from myosin which slows release of myosin from actin
Explain how failure of action potential could lead to fatigue
Concentration of K increases jn the small space of the t-tubules during rapid stimuli
Disturbs membrane potential and stops ca2+ release from sarcoplasmic reticulum
Long term; neurons run out of ACh –> usually not seen in a healthy person
Post exercise the body is in oxygen debt
The increase of body temperature increases need for O2
Deep rapid breathing is happening until body returns to resting state
What else is 02 used for post exercise
Replenish glycogen stores C~P
O2 on hemoglobin and myoglobin
To convert lactic acid to pyruvic acid permitting into Krebs cycle and to glucose in liver
