Musculoskeletal System Flashcards

Lec 17, 18, 19, 20

1
Q

What are the characteristics of mm?

A
  1. excitable - respond to stimuli and produce aps. 2. contractile - can shorten, thicken 3. extensible - stretch when pulled 4. elastic - return to original shape after contraction or extension.
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2
Q

What are the functions of mm?

A
  1. mvmt - walking, breathing, etc. 2. posture, facial expressions 3. heat production - byproduct of producing atp 4. protection of viscera - body wall
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3
Q

What is the ratio of mm fibres and neurons?

A

1 mm fibre is innervated by 1 neuron. 1 neuron branches and innervates many mm fibres.

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4
Q

What is a motor unit?

A

a single motor neuron and all the mm fibres it innervates.

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5
Q

What is the structure of the neuromuscular jxn?

A

presynaptic cell (neuron) with axon terminal filled with vesicles containing ACh. postsynaptic cell membrane is a specialized region of the sarcolemma of a mm fibre called the motor end plate which has many receptors for ACh. pre and postsynaptic membranes separated by the synaptic cleft.

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6
Q

What is the mechanism for stimulating a skel mm fibre?

A
  1. AP reaches axon terminal and synaptic end bulb of neuron 2. ca voltage gated channels open3. ca enters the cell and causes exoctyosis by vesicles of ACh 4. ACh binds to receptors on the motor end plate 5. chemically gated channels open and Na enters the skel mm fibre creating an end plate potential (depol) 6. EPP causes opening of Na voltage gated channels on adjacent sarcolemma resulting in an ap on the sarcolemma. 7. the ap propagates along the sarcolemma and down the t-tubules.
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7
Q

Why is there always a critical stimulus/ why does an EPP always lead to an ap?

A
  1. lots of ach released at neuromuscular jxn 2. the motor end plate has many receptor for ach. so EPPs aer happening everytime, and theres so many that it always meets ap threshold. as a result, to inhibit contraction of a skel mm, the motor neuron must be inhibited.
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8
Q

What happens during myosin head activation?

A

atp on myosin head –> breaksdown into adp and pi (still on myosin head activated) and energy (stored in myosin head)

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9
Q

What are the 3 steps for skel mm contraction (list)?

A
  1. excitation of mm fibre (electrical event) 2. excitation-contraction coupling 3. contraction (mechanical event
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10
Q

What happens during excitation of a mm fibre?

A

sarcolemma is depolarized and the EPP triggers an ap. ap then propagates down t-tubules deep within fibre.

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11
Q

What happens during excitation-contraction coupling?

A

converts the electrical event of the ap into the mechanical event of contraction of the mm fibre. ap in t-tubules causes release of Ca (coupling agent) from terminal cisternae in the sarcoplasmic reticulum via mechanically gated channels. ca binds to troponin. troponin-tropomyosin complex moves exposing binding sites on actin.

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12
Q

What happens during Contraction (mechanical) the sliding filament mechanism (what are the steps)?

A
  1. activated myosin heads attach to the exposed actin binding sites (cross bridge formation) 2. nrg stored in the myosin heads are released (adp and Pi) - myosin head pivots ie the power stroke. actin slides over myosin towards the centre of the sarcomere (M line). 3. atp attaches to myosin head causing it to release from actin and unpivots - recovery stroke. 4. myosin head reactivates when atp is broken down into adp and Pi. 5. if ca cytosol remains high, these steps repeat.
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13
Q

How does the length of the parts of the mm fibre change or not change?

A

sarcomeres shorten; the H zone and I band shorten but the A band stays the same length. myofibrils (bunch of sarcomeres) shorten therefore the mm shortens. thin (actin) and thick (myosin) filaments remain the same length.

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14
Q

What are the steps to mm fibre relaxation?

A
  1. ACh is broken down by AChE on the motor end plate (postsynaptic membrane). becomes acetic acid which is converted into acetyl CoA to go into the Krebs cycle, and choline which is recycled. 2. Ca is taken back into the SR by the Ca ATPase pump which actively transports it back in 3. atp binds to myosin heads allowing them to release (crossbridge breaks) 4. tropomyosin moves back to cover the myosin binding sites on actin
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15
Q

What is ATP necessary for during mm fibre relaxation?

A
  1. cross bridge release - atp binging to myosin heads and them releasing from actin binding site. 2. Ca-ATPase pump into SR 3. activation of myosin heads - atp broken down into adp and Pi. 4. fibre Na/K- ATPase activity
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16
Q

What is botulism?

A

results from improper canning of food bc a bacteria called clostridium botulinum produces toxins which prevents exocytosis of ACh leading to flaccid paralysis (no EPP happens, no AP, no contraction)

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17
Q

What is botulism used for medically?

A

treat uncontrolled blinking, crossed eyes, so paralyzing specific mms. cosmetic - botox (wrinkles, sweating)

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18
Q

What is rigor mortis?

A

stiffness of death. Ca leaks from SR and ECF (outside cell) leading to actin sites being uncovered. myosin heads then bind but cant be released bc there’s no new atp being produced to release them. happens around 3-12 hrs after death. after a few days proteins and cells start to degrade and no longer see effect.

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19
Q

What is myasthenia gravis?

A

decreased number of ACh receptors as a result of an autoimmune condition (so ach doesnt have anything to bind onto). results in flaccid paralysis (no epp no ap no contraction). treatment - ACHe inhibitors so more ach can bind to remaining receptors.

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20
Q

What is curare poisoning?

A

prevents ACh from binding to receptors get flaccid paralysis. was used historically in surgery to prevent ppl from moving during a procedure.

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21
Q

How does nicotine affect mm fibre contraction?

A

mimics ACh effect (binds to receptors) and causes mm spasms.

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22
Q

How does black widow spider venom affect mm contraction?

A

triggers massive release of ACh so mms continuously contract and we stop breathing.

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23
Q

What is mm tension and what is it determined by?

A

force exerted by a mm or mm fibre. determined by number of cross bridges formed. (more = more tension).

24
Q

What is mm tension in a fibre affected by?

A

frequency of stimulation, fiber length, size of fibre, fatigue.

25
What are the different frequencies of stimulation of a mm fibre?
single stimulus, 2nd stimulus arrives before complete relaxation from 1st rapid sequence of stimulation, and high frequency of stimuli.
26
What happens when theres a single stimulus acting on a mm fibre? (list periods)
produces a twitch with 4 different periods. 1. single stim 2. latent period 3. contraction period 4. relaxation
27
What is a twitch?
a weak contraction and relaxation not normally occurring in skel mm only rlly in lab.
28
What happens during single stimulus period?
single stimulus leads to 1 AP that lasts 1-2 msec
29
What happens during the latent period?
around 2 msec, excitation-contraction coupling occuring.
30
What happens during the contraction period?
lasts 10-100 msec. get increased tension. cross bridge attachment and sliding filaments happen. a lot of Ca released from SR on stimulation, but taken back rapidly by SR Ca-atpase so not all myosin heads attach, and does not reach max possible tension.
31
What happens during the relaxation period ?
get decreased tension, Ca pumped into SR, atp releases myosin, binding sited covered.
32
What happens when the 2nd stimulus arrives before the complete relaxation of the 1st?
mm AP always completes bc of refractory period (so aps still dont summate but just complete as normal), but the uptake of Ca by the SR is not yet complete (fibre relaxing). this means that when the 2nd stimulus causes the release of more Ca, it adds to that which is already in the cytosol, therefore more myosin heads can attach. this produces a 2nd contraction with increased tension called wave summation. contraction does not have a refractory period.
33
What happens when there is a rapid sequence of stimuli?
tension increases further (increased Ca availability = wave summation). so get wave summation but more frequently, so partial relaxation btwn contractions produces quivering = incomplete tetanus.
34
What happens with a high frequency of stimuli?
no relaxation btwn contractions so sustained contraction = complete tetanus. all troponin saturated with Ca (regulating proteins out of the way) and fiber warm (atp synth - heat), so works faster. occurs normally in the body
35
What happens when the resting fiber length is optimum?
allows for a maximum number of cross bridges formed upon stimulation, so get max tension.
36
Why do we get decreased tension if the fiber length is shorter or longer?
Shorter: thin filaments overlap and interfere with cross bridge attachment (min length is 70% of optimal). Stretched: not all myosin heads near actin binding sites (max length is 170% of optimal)
37
How does the size of the fibre affect tension?
thickness= more myofibrils/fiber. thicker= more tension. gets thicker with testosterone and exercise.
38
how does fatigue of a fibre affect mm tension?
mm does not contract well, reduced max tension.
39
What are the different fibre types in a mm?
1. fast twitch - contract/relax rapidly, have little myoglobin so anaerobic, explosive power. 2. slow twitch - contract/relax slowly, have more myoglobin so aerobic, endurance, postural mms.
40
in a whole mm, what is tension affected by? (list)
1. number of fibers contracting 2. number of fibers per motor unit 3. mm size 4. fatigue
41
How do the number of fibers contracting affect whole mm tension?
more active motor units = more tension. small motor units recruited first then larger ones added when more tension is needed.
42
How do the number of fibers per motor unit affect whole mm tension?
more fibres per unit = increased tension. 1 neuron innervating 10 fibres is weak, whereas 1 neuron innervating 1000 fibres is strong.
43
How does mm size affect whole mm tension?
larger = more fibers
44
What is mm tone?
low lvls of tension in a few fibres that develops as diff groups of motor units are alternatively stimulated over time. gives firmness to mms.
45
What are the types of whole mm contraction?
1. isotonic 2. isometric
46
What is an isotonic contraction?
mm changes length, ie flexion at elbow - tension greater than weight of forearm. tension (relatively constant) exceeds the resistance of the load lifted. so able to pick smthn up, causing the mm to change shape. uses atp.
47
What is an isometric contraction?
mm length is constant. tension less than required to move load. so cant pick thing up and mm doesnt change shape. tension increases and crossbridges still from but no shortening. uses atp.
48
What are the different periods where nrg is used for contraction?
1. during resting conditions. 2. during short term exercise (less than 1 min) 3. during long term exercise (1 min - hrs)
49
During resting conditions how is mm metabolism done?
FAs used to produce atp (aerobic). storage of glycogen, creatine phosphate atp + creatine = adp + C˜P. little atp. wnat to build mols to use later on.
50
During short term exercise how is mm metabolism done?
primarily anaerobic. use available atp. creatine phosphate used to produce atp (lasts around 15 seconds) -> C˜P + adp = atp + creatine. mm glycogen -> glucose -> pyruvic acid -> anaerobic pathway -> lactic acid (lasts around 30 sec), produce atp as a byproduct of glycolysis
51
During long term exercise how is mm metabolism done?
atp - from aerobic pathway into mito, ie krebs cycle and etc. glucose from liver. FAs used more as exercise continues. o2 sources are bl hemoglobin and mm myoglobin. sometimes can be anaerobic under fatigue.
52
What are the types of mm fatigue? (list)
physiological fatigue and psychological fatigue.
53
What is physiological fatigue?
the inability to maintain mm tension. fatigue reduces atp use and is therefore protective bc if too little atp cross bridges cant release.
54
What is physiological fatigue due to?
1. depletion of nrg supplies (glucose). 2. build-up if end products. ie. H+ from lactic acid - mm contraction compresses bl vessels, decreases O2 to mms therefore atp production is anaerobic fro certain periods even in long term exercise. ie Pi binds to Ca, this causes; a. less Ca binding to troponin and therefore less cross bridges formed b. slows the release of Pi from the myosin - slows cross bridge release from actin 3. failure of aps. increased conc of K in small space of t-tubules during rapid stimuli disturbs the MP and stops Ca release from the SR. long term; neuron runs out of ACh (not usu in a healthy person).
55
What is psychological fatigue?
failure of the cns to send commands to the mms, prob due to lactic acid.
56
What is EPOC?
excess post-exercise O2 consumption. recovery O2 consumption, deep rapid breathing. need extra O2 after exercise to; 1. replenish stores of glycogen, creating phosphate, O2 on hemoglobin and myoglobin. 2. convert lactic acid to pyruvic acid to go into krebs cycle and glucose in liver. also increased body temp from ex increases the o2 demand.