Excitable Tissue : Muscle Flashcards

1
Q

Tendons

A

Where most skeletal muscles begin and end.

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2
Q

Muscle Fibre Morphology

A
  • begin and end in tendons
  • each muscle fibre is a single multinucleated cell
  • no communication between muscle fibres ( it can’t take a signal and recruit other cells to participate)
  • each muscle fibre is conmprosed of multiple filaments which execute contraction
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3
Q

Sliding filament theory

A

still just a theory, best information we have to date about muscle contractions.
- has a handful of different proteins but MYOCIN generates contraction

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4
Q

all or nothing muscle contraction

A

we do not want this and our muscles are not designed for this. we don’t want to use max energy when we want to sharpen a pencil or do accupuncture. We have a graded muscle response.

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5
Q

Actin

A

Contractile Protein

Polymerizes to form a thin filament. (gives structure)

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6
Q

Tropomysosin

A

Contractile Protein
Binds to the thin filament.
Additional structural protein

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7
Q

Myosin 2

A

Contractile Protein
Globular motor protein that has the ability to create tension and allow for contraction.
- thought of as little elastics that stretch and snap back

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8
Q

Troponin

A

3 Subunits :

Troponin I :
Inhibitory
Binds actin and prevents actin/myosin association at rest.
Makes sure that they do not touch

Troponin T :
provides stability - allows binding to create an environment where contraction is possible
binds tropomyosin and helps position it on actin.

Troponin C:
calcium binding site
on/off switch. When Ca2+ is around , it binds to Troponin C and muscle wants to contact
If Ca2+ is not bound/present the relaxed strate is reinforced

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9
Q

Calcium (Storage in Muscle contractions)

A

Stored in the T-tubules. When the fibres need more Ca2+, it is released to create contraction.

Important to have storage for calcium b/c free calcium may cause harm.

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10
Q

Excitation Contraction Coupling

A

(Dihydropyridine DHPR receptor voltage gated) (red tube)
- physically or spatialling linked to the ryanodine receptor (RyR) in the sarcoplasmic reticulum (Pink tube)

Activation of DHPR causes conformational change in RyR causing Ca2+ release from the SR

Contrast to calcium induced / calicum release in cardiac muscle

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11
Q

T/F :

Is there a change in length of individual thin or thick filaments?

A

False : no change in length. Increased amount of overlap within the cell.

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12
Q

At rest, where are myocin heads?

A

Myocin heads bound to ADP and in relaxed position relative to the thin filament. No Ca2+ bound.

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13
Q

Where does Ca2+ bind when it gets into the cytoplasm?

A

Binds to troponin C which induces a confirmational change , and exposes myosin binding sites on actin.

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14
Q

Power stroke

A

Myosin heads move into position to bind actin and “flex” , which shortens the muscle fibre releasing ADP in the process.

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15
Q

How does ATP detach from actin?

A

ATP binds the empty site where ADP was released.

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16
Q

What does ATP hydrolization cause?

A

Causes myosin to return to the relaxed position.

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17
Q

When do muscle contractions repeat?

A

If there is sufficient calcium and ATP present, the process repeats.

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18
Q

Muscle Contaction Steps :

A

1) Myocin heads bound to ADP and in relaxed position relative to the thin filament. No Ca2+ bound.
2) Influx of calcium Binds to troponin C which induces a confirmational change , and exposes myosin binding sites on actin.
3) Powerstroke : Myosin heads move into position to bind actin and “flex” , which shortens the muscle fibre releasing ADP in the process.
4) ATP binds the empty site where ADP was released and causes detachment from actin
5) ATP hydrolization Causes myosin to return to the relaxed position.
6) If there is sufficient calcium and ATP present, the process repeats.

19
Q

ABCDE picture process

A

A ) Tropomyocin is wrapped around actin. Myocin has a molecule of ADP attached to it
B) tropomyosin is twisted to show myocin binding sites in the presence of calcium
C) myosin hitsw actin which causes the tension generation and slides the fliaments closer together. ADP gets the boot “powerstroke”
D) Wth ADP gone, there is an open binding site which ATP binds to while there is contraction
E) As soon as myosin and ATP bind, it uses energy (hydrolizes ATP) to stretch itself back out - releases from actin

20
Q

Rigor Mortis

A

ATP needs to be hydrolyzed to get into a relaxed state. When ATP runs out, we stay contracted for a few hours.

21
Q

T/F Ca2+ binds to troponin which moves tropomyocin

A

T : Troponin is the boss

Ca2+ is bound to troponin at rest/ neutral state.

22
Q

What happens as Calcium is pumped out of the cytoplasm?

A

Ca2+ dissociates from troponin.

  • due to a function of Ca- ATPase, Calcium is pumped back into the sarcoplasmic reticulum or cisterns of T-tubules
  • conformational change brings troponin back to neutral , hiding myosin binding sites.
23
Q

Tetanus

A

Continous muscle contraction : we use this all of the time to keep us upright. Ie) posture muscles.

24
Q

Muscle Twitch

A
  • occurs when a muscle fiber is stimulated to contract by a single action potential . (one very quick action potential).
  • twitch begins after depolarization, but before repolarization is complete. * important for the summation of contractions.
    duration of the twitch dependent on the muscle fiber (fast for fine motor movements or slow for sustained gross movements)

twitch occurs in approx 5ms while full relaxation takes 25ms

25
Q

Summation of muscle contraction

A

length of depolarization is shorter than duration of contraction
contractile mechanism does not have a refractory period
repeated stimulation before contraction causes a additive/summation effect (which has greater tension than a single twitch)

  • if it happens fast enough, individual responses fuse and go from single contractions to tetanus.
26
Q

When is the muscle the longest? Relation to tension

A

Longest at rest

  • tension proportional to the number of actin-myosin crossbridges formed
  • fewer actin-myosin associations available when the muscle is stretched.
  • less capacity for filament movement if the muscle is already contracted. ( no where for it to go, already overlapped)
27
Q

Types of Muscle Tissues

A

Skeletal : Striated , voluntary , attached to bone, innervated, troponin present.

Cardiac : Striated , involuntary, heart, no innervation needed for contraction, troponin present

Smooth Muscle : non-striated , involuntary, inside walls of tubular organs, most are innervated but not needed for unit smooth muscle, troponin does not exist in smooth muscle.

28
Q

Skeletal Muscle

A

Skeletal : Striated , voluntary , attached to bone, innervated, troponin present.

29
Q

Cardiac Muscle

A

Cardiac : Striated , involuntary, heart, no innervation needed for contraction, troponin present

30
Q

Smooth Muscle

A

Smooth Muscle : non-striated , involuntary, inside walls of tubular organs, most are innervated but not needed for unit smooth muscle, troponin does not exist in smooth muscle.

31
Q

Smooth Muscle contraction differs from other muscle contraction because :

A
  • lack of troponin
    Ca2+ still released
  • influx of calcium sue to voltage gated/ligand membrane channels.
    -effluc of Sarcoplasmic reticulum stores through Ryanodine Receptor or IP3 receptor.
32
Q

Smooth Muscle Contraction

A

Myosin needs to be phosphorylated to activate myosin ATPase.
Ca2+ binds to calmodulin which activates myosin light chain kinase (MLCK)
Process of muscle contraction is then similar to that of other muscle tissue.

33
Q

Smooth Muscle Relaxation

A

Myosin is dephosphorylated via myosin light chain phosphatase (MLCP)
- which is regulated via GRCR and cGMP pathways
Removal of intracellular Ca2+ results in dissassociation of the Ca2+ - calmodulin complex which triggers relaxation

34
Q

Plasticity of Smooth Muscle

A

Force/tension different in smooth muscle
Initial stretch of unitary smooth muscle is met with an increase in tension
If stretch is maintained, smooth muscle becomes tolerant to it and tension decreases

  • smooth muscle is resistant to change but doesn’t do a lot about it. ie_ bladder sends signals (via nerves) that it is stretching, but you can override it until it reaches a certain capacity. eventually ceiling will be hit cusing involuntary contraction
35
Q

Phosphocreatine

A

Used for the first split second of muscle contraction. The rest comes from ATP

36
Q

ADP energy

A

ADP powers the first few seconds of muscle contraction through anerobic phosphrylation of ADP

37
Q

ATP energy in contraction

A

During rest or low muscular effort, excess ATP is used to restore CrP stores

38
Q

Lipids and Fatty acids

A

primary source of energy during low to moderate intensity exercise.
uses beta oxidation for <60% max

39
Q

Carbohydrates and muscle contraction

A

primary source of energy for moderate to high intensity exercise. (above 60% man)
Most of the energy for CrP and ATP resynthesis provided by glucose

40
Q

Oxygen debt

A

Metabolic needs of the muscle are on (need energy) of off (at rest).
Compensatory ventilation responses take time. ex) increased rate of respiration after you are climbing the stairs.

This happens when we are more metaboliccaly active and don’t have enough O2

We have evolved to preemtively increase our breathing to increase 02 consumption to offset the O2 debt

41
Q

Oxygen debt when muscular exertion is high

A

Aerobic resynthesis of ATP cannot keep up with the ATP utilization.
Phosphocreatine used to resynthesize ATP via creatine kinase
Fastest system : (Phosphagen > Glycolysis > Mito CHO >Mito FFA

42
Q

LActate and Oxygen Debt

A

Anerobic breakdown of glucose to lactate occurs during all intensities of exercise.
- overall contrubution to ATP decreases as level of intensity increases

43
Q

Factors that limit physical exertion

A
  • Low O2 availability via the blood
  • low number of mitochondria
    -Cardiovascular system is the more limiting in a vacuum.
    Respiratory is theroretically not limiting , but we must account for pollution, smoking, respiratory diseases etc.
44
Q

Temperature Regulation during exercise exertion

A

Heat is released during exertion which is challenging for homeostasis
1) sweating evaporative cooling.
iss ) dehydration and reduced blood volume.

2) Increased cutaneous blood flow promotes heat loss via convection
issues : decrease in peripheral resistance and diversion of blood away from muscle
- fall in venous BP may decrease blood flow to the brain

3) adaptation - body adjusts to a hot climate over time.