MUSCULOSKELETAL SYSTEM II Flashcards

1
Q

Most energy required for muscle contraction is used for?

A

Walk along/ sliding filament mechanism.

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2
Q

Small amount of energy is required for muscle contraction is used for what?

A

A. Calcium reuptake (from sarcoplasm to SR stores)
B. Na+/K+ ATPase pump located along muscle fibers for maintenance of appropriate environment for AP propagation along the muscle fibers.

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3
Q

The ATP concentration in muscle fibers is equal to what?

A

= TO 4 millimolar which is enough to maintain full contraction for 1-2 secs.

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4
Q

ATP split to ?

A

ADP to produce energy for contracting muscle fibers

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5
Q

ADP is phosphorylated to what?

A

To form new ATP, happens within secs to allow the continuation of the muscle contraction

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6
Q

List 3 sources of energy for muscle contraction

A

A. Phosphocreatine (creatine + phosphate- CP) a high energy molecule
B. Glycolysis of Glycogen: Previously stored in muscle cells.
C. Oxidative metabolism: aerobic process

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7
Q

When ATP react with Creatine what are 2 products

A
  1. ADP
  2. Phosphocreatine
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8
Q

Phosphocreatine get cleaved to produce what?

A

Free energy

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9
Q

The reaction of CP+ ADP produces which products and uses which enzyme

A

ATP
Creatine
The creatine kinase is the enzyme used.

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10
Q

Rapidly breakdown of glycogen produces which three products

A
  1. ATP
  2. LATIC ACID
    3.PYRUVIC ACID
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11
Q

Muscle contraction can be sustained up to how long?

A

1 minute

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12
Q

ATP can be used to re-inform which compound?

A

Phosphocreatine

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13
Q

Over 95% of ATP utilized by muscles for sustained, long-term contraction
is derived from?

A

Oxidative metabolism

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14
Q

The single skeletal muscle twitch lasts for how long?

A

25 to 200 ms depending on a type of a muslce.

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15
Q

Each twitch is elicited by a single what?

A

AP

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16
Q

Duration of a single twitch is long compared to the?

A

Duration of exciting AP

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17
Q

The muscle twitch occurs in 3 phase name those phases and explain them.

A

A. Latent phase
Begin of stimulation (excitation) (2ms)
B. Contraction phase
Ca2+ binds with troponin C
Cross bridges form
Increase in tension.
exposure of active site
last for about 15ms
C. Relaxation Phase
Ca2+ decreases
Decreases in tension to rest.
Cross bridges detach.
last for about 25ms

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18
Q

Due to difference in duration of twitch and AP it is possible to initiates what?

A

Initiates a 2nd AP before 1st muscle contraction ends.

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19
Q

2nd AP stimulates what? explain

A

A twitch over the residual tension of the 1st twitch. Greater isometric tension than the 1st twitch= summation

20
Q

When multiple AP occurs close enough in time, what will summate?
Increases what?

A

Multiple twitches will summate
Increased in tension

21
Q

The higher the frequency of AP the higher?

A

Tension- frequency summation

22
Q

What is tetanus?

A

State at which individual twitches are not distinguishable from each other

23
Q

What happen when a stimulation is greatly increased?

A

Individual twitches occur close together in time.
Become fused
causes muscle tension remain at a steady plateau

24
Q

Each motor neurons leaving the spinal cord innervates a single muscle.
True or FALSE

A

False because Each motoneuron leaving spinal cord innervates multiple muscle
fibres

25
Q

What is the motor unit

A

all muscle fibers innervated by a single nerve fiber

26
Q

What is a Motor unit recruitment?

A

sequential activation of the motor unit to perform a designated task.

27
Q

What leads to muscle fatigue

A

prolonged and strong contraction of muscle

28
Q

Muscle fatigue is an inability of what?

A

The inability of contractile and metabolic process of muscle fibers to continue supply the work output.

29
Q

During muscle fatigue, there is a low blood supply. explain how?

A

Interruption of blood flow through a contracting muscle→ almost complete
muscle fatigue within 1 or 2 minutes due to lack nutrient and oxygen supply

30
Q

In marathon runners the muscle fatigue occurs when?

A

occurs with a rate of muscle glycogen depletion.

31
Q

In sprinters what is the primary source of energy?

A

Glycolysis

32
Q

what happen in sprinters after few minutes or seconds of intense activity muscle

A

Lactic acid and its dissociation increases
PH decreases
Muscle activity decreases
Rapid fatigue

33
Q

Analysis of lever system in the body depends on the knowledge of?

A

A. The point of muscle insertion
2. The distance between fulcrum and lever
3. The length of the lever
4. The position of the lever

34
Q

Explain the following terns
Motor-end-plate
Synaptic gutter/trough
Synaptic cleft/space
Subneural clelft

A
  • A specialized region of the sarcolemma that invaginate closest to the presynaptic nerve
    terminal = motor-end-plate.
  • Synaptic gutter/trough= invagination membrane
  • Synaptic space/cleft= space between the terminal and the fibre membrane.
  • Subneural clefts= numerous smaller folds greatly increase the surface area at which
    neurotransmitter can act.
  • In axon terminal, there are many mitochondria which produce ATP used for excitatory
    neurotransmitter, ACh.
35
Q

Explain the secretion of acetylcholine by the nerve terminals

A
  • Upon the arrival of AP at the NMJ, ACh are released from the synaptic terminal vesicles
    into synaptic cleft.
  • On the membrane of the motor neuron, are voltage-gated calcium channels, activated by
    the change in electrical potential in the neuronal membrane (presynaptic membrane)→
    Ca2+ influx.
  • Ca2+ is believed to activate Ca2+ -calmodulin dependent protein kinase, which
    phosphorylates synapsin proteins which anchor ACh vesicles from the cytoskeleton and
    allow them to move to active zone of the presynaptic neural membrane adjacent to the
    voltage-gated Ca2+ channels.
  • Synaptic vesicles dock at release sites, fuse with the neural membrane, and empty their
    ACh into the synaptic space by the process of exocytosis.
36
Q

Acetylcholine Opens Ion Channels on Postsynaptic Membranes, explain.

A

ACh bind to ACh-gated Na+ channels (nicotinic receptors) located on postsynaptic
membrane (at subneural clefts) → allow influx of Na+ ions → cause graded,
depolarized end-plate potential (50 to 75 mV).
* End-plate potential great enough to increase membrane potential to threshold → lead
to activation of voltage-gated Na+ channels located near the end-plate → trigger an
AP → propagates along the sarcolemma.
* AP propagates along sarcolemma into the interior of the muscle fibres through Ttubules

37
Q

explain the Destruction of the Released Acetylcholine by Acetylcholinesterase:

A
  • ACh in the synaptic cleft continues activating nicotinic receptors as long as it still persist in
    the synaptic space.
  • Acetylcholinesterase (ACh-E) rapidly deactivate ACh→ decline ACh levels in the synaptic
    cleft
  • Some ACh molecules diffuse out of the synaptic cleft.
38
Q

Action Potential in Skeletal Muscle
1. Resting membrane potential =
2. Duration of an AP =
3. Velocity of conduction =

A
  1. -80 to -90 mV
  2. 1 to 5 ms
  3. 3 to 5 m/s
39
Q

Action Potential Spread to the Interior of the Muscle Fibre, explain

A
  • AP generated from NMJ, propagates along the sarcolemma into transverse-tubule (Ttubule).
  • AP in T-tubule activates Ca2+ release from the SR.
  • Release of Ca2+ → muscle contraction = excitation-contraction coupling
40
Q

T tubules runs transvers to ?

A

Myofibrils

41
Q

Along the length of t tubules at terminals what are found

A

2 terminal cisternae

42
Q

Inside the SR, is a protein that can bind more Ca2+, name of the protein

A

Calsequestrin.

43
Q

Combination of T-tubule and 2 terminal cisternae is called?

A

= triad/triad junction.

44
Q

L type Ca2+ channel is also known as ?

A

DHP receptor

45
Q

explain what happen when the AP arrives in T- Tubules until contraction of a muscle

A

AP arrives in T-tubules & activates L-type Ca2+ channels (also know as DHP
receptors) to open.
* L-type Ca2+ channels are physically coupled with SR Ca2+-release channels
(RYR1) → lead to Ca2+ release from the SR into the sarcoplasm.
* Ca2+ binds to troponin-C → gets activated, conformational change, displaces
tropomyosin→ troponin-tropomyosin complex inhibition→ exposure of active
sites on F-actin (actin filament activation) → initiate muscle contraction.