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Biol 1412 > Topic 10 > Flashcards

Topic 10 Flashcards

1
Q

Excitable muscle

A

respond to stimulus by producing action potentials

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2
Q

Contractile muscle

A

can shorten, thicken

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3
Q

Extensible muscle

A

stretch when pulled

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4
Q

Elastic muscle

A

return to regional shape after contraction or extension

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5
Q

4 muscle functions

A
  • movement
  • posture, facial expression
  • heat production
  • protection of viscera
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6
Q

Each muscle fibre innervated by only..

A

1 neuron

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7
Q

Axon of motor neuron branches to..

A

innervate several muscle fibres. 1 neuron is about 150 fibres within the same whole muscle

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8
Q

Motor unit

A

single motor neuron and ALL the muscle fibres it innervates

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9
Q

Neuromuscular junction structure

A
  • presynaptic cell (neuron) with ACh (nt) in vesicles
  • postsynaptic cell (muscle) membrane (sarcolemma) specialized region with ACh receptor (=motor end plate)
  • two membranes speared by synaptic cleft
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10
Q

Neuromuscular junction function first step

A

AP reaches axon terminal and synaptic end bulb of neuron

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11
Q

Neuromuscular junction function second step

A

Ca enters via voltage gates and causes exocytosis of ACh

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12
Q

Neuromuscular junction function fourth step

A

chemical gates open and Na enters so end plate potential (EPP= depol. GP)

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13
Q

Neuromuscular junction function fifth step

A

PP causes opening of Na voltage gates on adjacent sarcolemma which creates an AP and propagates along sarcolemma

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14
Q

1 AP neuron equals..

A

1 EPP and 1 AP always!

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15
Q

In a relaxed muscle ..

A

tropomyosin covers myosin binding on the actin and the myosin head is activated

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16
Q

Myosin head activation 3 steps:

A
  • excitation of muscle fibre (electrical event)
  • excitation-contraction coupling (electrical to mechanical event)
  • contraction (mechanical event) = sliding filament mechanism
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17
Q

Excitation of muscle fibre

A

a) sarcolemma depolarized - EPP –> AP

b) AP propagates down t-tubules to deep within fibre

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18
Q

Excitation-contraction coupling

A

c) AP in t-tubules cause release of Ca (coupling agent) from terminal cisterna of sarcoplasmic reticulum (SR) via mechanically gated channels
d) Can binds to troponin
e) troponin-tropomyosin complex moves, exposing myosin binding sites on actin

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19
Q

Contraction = sliding filament mechanism

A

f) activated myosin heads attach to binding sites inaction (cross bridge formation)
g) energy stored in myosin head released -myosin head pivots (=POWER STROKE), ADP+Pi are released. Actin slides over myosin toward centre of sarcomere
h) ATP attachés to myosin head, causing its release from actin + pivots = RECOVERY STROKE
i) myosin head reactivates (ATP –> ADP + Pi)
j) if Ca in cytosol remains high, these steps repeat (as many times to shorten the sarcomere)

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20
Q

Sliding filament mechanism 3 steps

A
  1. sarcomeres shorten: H zone, I band shorten. A band = same length
  2. Myofibrils shorten = muscle shortens
  3. thin actin and thick myosin my-filaments remain same length
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21
Q

Relaxation 4 steps

A
  1. Act broken down by AchE on motor end plate (facing cleft)
  2. SR actively takes up Ca (Ca ATPase)
  3. ATP binds to and release myosin heads
  4. tropomyosin moves back to cover myosin binding sites on actin
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22
Q

ATP necessary for 4 reasons

A
  • cross bridge release (ATP not broken down)
  • activation of myosin (ATP –> ADP + Pi) + power stroke
  • pump Ca into SR
  • fibre Na K ATPase activity
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23
Q

Rigor Mortis (stiffness of death)

A
  • myosin heads still activated even after death and can bind to actin
  • ATP production gradually stops (no O2)
  • starts 3 hrs after death (max 12 hrs)
  • gradually subsides over days as cells break down
24
Q

Extracellular Ca as clinical application

A

-stabilizes Na+ voltage gates (keeps them closed in the absence of APs) ∴ if extracellular Ca++ low (pregnancy, lactation) – gates open & Na+ enters fibre → cramps (contractions)

25
Q

Conditions/substances resulting in flaccid paralysis:

A
  • myasthenia gravis
  • curare poisoning
  • botulism
26
Q

Myasthenia gravis

A

decrease in Ach receptors (autoimmune). use AchE inhibitors to increase binding to remaining receptors

27
Q

Curare poisoning

A

prevents Act from binding to receptors (was used in surgery)

28
Q

Botulism

A
  • improper canning= clostridium botulinum
  • prevents exocytosis of Ach
  • used to control blinking, cross eyes
29
Q

Substances resulting in muscle contractions

A
  • nicotine: binds to receptors and mimics Ach effect. causes muscle spasms
  • black widow spider venom: massive release of Ach and stops breathing
30
Q

Muscle tension

A

force exerted by a muscle or muscle fibre and determined by # of cross bridges formed

31
Q

Muscle tension affected by single stimulus

A

produces a twitch (not normally occurring in skeletal muscle)

32
Q

Twitch

A

weak contraction and relaxation

33
Q

4 steps of single stimulus

A
  • 1 stimulis = 1 AP
  • latent period (associated with excitation)
  • contraction period: high tension, cross bridge formation + sliding filaments. much Ca release from SR on stimulation, but taken back rapidly by SR CaATPase (not max tension reached)
  • relaxation: decrease tension, Ca pumped into SR, ATP release myosin
34
Q

2nd stimulus arrives before complete relaxation of 1st stimulus

A
  • muscle AP over but uptake of Ca by SR not complete, so second stimulus causes release of more Ca, adding to that already in cytosol (more myosin heads can attach)
  • produces 2nd contraction with higher tension (wave summation)
35
Q

Rapid sequence of stimuli

A
  • tension increases further (high Ca availability so wave summation)
  • partial relaxation between contractions produces quivering (incomplete tetanus)
36
Q

High frequency of stimuli

A
  • no relaxation between contraction contractions (complete tetanus)
  • highest tension: all troponin saturated with Ca + fibre warm (ATP synthesis) works faster
  • occurs normally in body
37
Q

Fibre length: resting length

A

most optimum: max # of cross bridges formed upon stimulation (max tension)

38
Q

Fibre length: shorter

A

thin filaments overlap and interfere with cross bridge formation (fewer cross bridges form and decrease tension)

39
Q

Fibre length: stretched

A

not all myosin heads near actin binding sites (fewer cross bridges form and decrease tension)

40
Q

Size of fibre

A

thicker = more myofibrils/fibre and more tension

41
Q

2 types of fibres in a muscle

A
  • fast: contract/relax rapidly (white w little myoglobin)

- slow: contract/relax slowly (red w more myoglobin)

42
Q

In a whole muscle tension is affected by

A
  • number of fibres contracting
  • # fibres/ motor unit
  • muscle size (more fibres and myofibrils)
  • fatigue
43
Q

Number of fibres contracting

A

more active motor units = high tension (small motor units recruited first)

44
Q

Number fibres/motor unit

A

more fibres/unit = higher tension

45
Q

Muscle tone

A

low level of tension in a few fibres that develops as different groups of motor units are alternately stimulated over time (firmness to muscle)

46
Q

2 types of whole muscle contraction

A
  • isotonic

- isometric

47
Q

Isotonic

A

muscle changes length (elbow flex). tension exceeds the resistance of load lifted. uses ATP

48
Q

Isometric

A

muscle length starts constant. tension less than required to move load, but tension increases (cross bridges form but no shortening). uses ATP

49
Q

Muscle metabolism is

A

energy for contraction

50
Q

Muscle metabolism during resting conditions

A
  • fatty acids used to produce ATP (anerobic)

- storage of glycogen, creatine phosphate, and little ATP

51
Q

Muscle metabolism during short term exercise (< 1 min)

A
  • primarily anaerobic
  • use available ATP creatine phosphate used to produce ATP
  • muscle glycogen –> glucose –> pyrvric acid –> anaerobic pathway –> lactic acid
52
Q

Muscle metabolism during long term exercise

A
  • ATP from aerobic pathway
  • glucose from liver
  • fatty acids: used more as exercise continues
  • O2 sources: blood hemoglobin and muscle myoglobin
53
Q

Physiological muscle fatigue

A
  • inability to maintain tension

- fatigue decrease ATP uses (protective)

54
Q

Physiological muscle fatigue due to..

A
  • depletion of energy supplies
  • build up of end products
  • failure of APs: increase K in t tubules during rapid stimuli and disturbs MP, stops Ca release from SR
55
Q

Psychological fatigue of muscle fatigue

A

failure of CNS to send commands to muscles (due to lactic acid)

56
Q

EPOC

A

excess post exercise O consumption

57
Q

EPOC: O2 used to

A
  • replenish stores of glycogen, C P, O2, on Hb. myoglobin.
  • convert lactic acid to pyruvic or glucose
  • higher body temp from exercise = higher O2 demand

Biol 1412 (15 decks)

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