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physiology > muscles > Flashcards

muscles Flashcards

1
Q

name the 3 different types of muscles tissue and their difference structures

A

3 types of muscle tissue
– Skeletal (attached to bones) = 40% body wt.
– Cardiac (heart & great vessels).
– Smooth (hollow vessels & organs)

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2
Q

what is the difference between striated and non-striated muscles

A

S: highly ordered arrangement of contractile proteins
NS: less ordered…

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3
Q

which muscle types are straited and which are non striated

A

NS: smooth
S: skeletal and cardiac

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4
Q

why do the muscles have different microscopic appearance

A

different functions

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5
Q

which muscle can relax and recover quickest and slowest: provide a order

A

skeletal> cardiac >smooth

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6
Q

describe what happens during a flexion

A

triceps muscle relaxes
biceps muscle contracts (flexors)

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7
Q

describe what happens during an extension

A

triceps muscle contracts (extensor) biceps muscle relaxes

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8
Q

what is an antagonistic pair and what is a good example of it

A

each reverses the action of the other

e.g. flexion and extension

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9
Q

what is the muscle equivalent of a muscle cell

A

muscle fiber

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10
Q

what is the muscle equivalent of a cell membrane

A

sarcolemma

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11
Q

what is the muscle equivalent of a cytoplasm

A

sarcoplasm

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12
Q

what is the muscle equivalent of a modified E.R

A

sarcoplasmic reticulum

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13
Q

describe the ultrastructure: where is the sarcomere

A

Z line to Z line

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14
Q

how are sarcomeres arranged

A

Highly ordered filament arrangement - ensures efficient interaction

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15
Q

name the 2 filament tpes

A

thick, myosin
thin actin

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16
Q

describe arrangement of thin filaments

A

2 polymer helices, F and G actin

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17
Q

what is the metaphorical description of thin and thick filaments

A

double string of pearls-A, thin
golf clubs in a bag’ -M, thick

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18
Q

(thin) what is the F actin function

A

no diretionality

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19
Q

(thin) what is the G actin function

A

myosin binding site

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20
Q

(thin) what is the function of tropomyosin

A

guards binding site

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21
Q

(thin) function of nebulin

A

separate 2 thin helices, align actin

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22
Q

describe the sarcomeres within the smooth muscles

A

No ‘sarcomeres’, but caveolae

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23
Q

(sarcomere) what is the function of titin

A

elasticity and stabilizes myosin

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24
Q

what does calcium do within the power stroke

A

binds to TN and shifts exposing binding site of G actin, allows for power stroke

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25
Q

fibre types Fast, fatigable

A

glycolytic (sparse mitoch/myoglobin)

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26
Q

fibre types - Slow, fatigue-resistant

A

oxidative (high mitoch/myoglobin)
Exercise & Fatigue

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27
Q

name 2 types of contractions

A

neurogenic and myogenic

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28
Q

difference in the 2 types of contractions: neurogenic and myogenic

A

N: skeletal muscle contracts when M.N activated
M: Cf cardiac muscle & most smooth muscle, contracts spontaneously

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29
Q

Latent period- what is it

A

schematic of the series elastic component

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30
Q

what are the 5 components force generation depends on

A
  1. Initial length of muscle
  2. Degree of activation (no. active muscle fibres)
  3. Rate of contraction (fibre type, fast/slow)
  4. Frequency of stimulation
  5. Cross-sectional area of muscle
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31
Q

Frequency of stimulation: describe single twitch freq

A

well spaced

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32
Q

does tension always induce movement and explain the mechanisms behind this

A

no due to isotonic contraction, muscle contracts, shortens and creates enough force to move load

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33
Q

on a force velocity relationship graph where is the isotonic and isometric contractions

A

isotonic contraction in the middle and isometric o at 0 velocity of shortening

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34
Q

what is the difference between isometric and isotonic contraction

A

No external load -> max rate of shortening -> isotonic.
* Max load -> no shortening -> isometric

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35
Q

what does a greater load mean for contraction speed

A

– Greater load -> slower shortening.

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36
Q

true or false: isotonic means no movement and no power/work

A

false it is isometric,

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37
Q

what is the most efficient fraction and percentage of rate of shortening

A

1/3 max rate of shortening.
* For humans, efficiency of most frequently used leg muscles
– = ~20-25% max rate of shortening

38
Q

what does tension muscle fibre equation

A

no. myofibrils/ muscle fibre

39
Q

what does resistance training do to the muscle fibre

A

increases number of myofibrils
increase x sectional area of individual muscle fibres

40
Q

true or false resistance training increases in number of muscle fibres

A

false it increase cross sectional area no number of fibres

41
Q

which types of muscles have quicker contraction rates

A

skeletal>cardiac>smooth

42
Q

(smooth muscle) contractile organisations: how does the multi-unit contract and how (separately or together)

A
  • predominant
    – cells connected by gap junctions
    3D clusters of smooth cells
    – activity in one cell -> others -> single functional unit.
  • all contract together as single unit
43
Q

(smooth muscle) contractile organisations: how does the multi-unit contract (separately or together)

A

Multi-unit
– cells not connected by gap junctions
- each stimulated separately as multi unit

44
Q

(smooth muscle) contractile organisations: single unit examples

A

gut, uterus, bladder ANS, activity strongly influenced by circulating hormones (e.g. epinephrine)

45
Q

(smooth muscle) contractile organisations: multi unit examples

A

intrinsic muscles of eye (iris/lens), skin piloerectors, lge blood vessels

46
Q

(smooth muscle) contractile organisations: single unit contraction type

A

– spontaneous rhythmic contractions, originate in pacemaker areas. = MYOGENIC CONTRACTION

47
Q

(smooth muscle) contractile organisations: multi unit contraction type

A

activated by nerve activity only -> similar to skeletal muscle
motor units. = NEUROGENIC CONTRACTION

48
Q

Typical smooth muscles organisations

A

single unit & multi-unit organisation

49
Q

smooth muscle vs cardiac muscle : what initiates contractile properties

A

S: actin/myosin - contractile proteins
C: cardiac AP - myogenic

50
Q

smooth muscle contraction; what are dense bodies

A

where the diagonal filaments bundles of actin and myosin intersect

51
Q

Excitation/contraction coupling: contraction of muscles

A

calcium enters from SR and ECF to phosphorylate calmodulin
from inactive to active myosin light chain kinase
MLCK + ATP = active myosin ATPase
ATPase + actin = increased muscle tension

52
Q

relaxation of smooth muscles

A

calcium pumped out using ATP into ECF and SR through pump Na+/Ca2+ exchanger and Ca2+ pump
Ca2+ drops off calmodulin
active to inactive calmodulin
myosin phosphatase takes Pi off myosin head
myosin ATPase activity decrease –> inactive myosin
= decreased muscle tensions

53
Q

what is the difference between myosin phosphatase and kinase

A

kinase activates proteins and phosphatase deactivates

54
Q

true or false: calcium can diffuse through membrane from ECF and SR into the cell for smooth muscle contraction

A

no, Calcium is pumped out using ATP against conc. grad. for smooth muscle relaxation

55
Q

caveolae function in smooth muscle

A

small invagination that concentrate Ca, so that it can readily flood in

56
Q

(smooth muscle) difference between slow wave, pacemaker potentials and pharmacochemical coupling

A

SW: fire AP when threshold is reached
P: depolarise when threshold is reached
PC: when chemical signals change muscle tension without changing membrane potentials

57
Q

(smooth muscle) provide examples of slow wave, pacemaker potentials and pharmacochemical coupling

A

SW + P : Ca channels open and contract
P: hormone/paracrine factors e.g. histamine or nitric oxide

58
Q

(smooth muscle) what triggers the regulation of contractions process from ECF

A

signal ligands such as ANS transmitter circulating hormone
and depolarization or stretch

59
Q

(smooth muscle) what does this regulation of contractions process from ECF trigger

A

membrane receptors, membrane channels, and store operated Ca2+ channels

60
Q

(smooth muscle) what do membrane receptors trigger

A

modulatory pathways –> alter MLCK/myosin phosphatase
alter actin associated proteins
increase IP3 –> sarcoplasmic Ca2+ release
–> cell response

61
Q

(smooth muscle) what do membrane channels trigger

A

increase Ca2+ entry –> cell response

62
Q

(smooth muscle) what do store operated Ca2+ channels trigger

A

decreased intracellular Ca2+ stores
–> cell response

63
Q

cardiac muscles: what are intercalated disks

A

allow cells to attach to each other and communicate with each other- disk between 2 adjacent cells

64
Q

cardiac muscles: what do intercalated disks contain

A

gap junctions for electrical contractions

65
Q

cardiac muscles: describe the structure of cardiac muscle

A

one nucleus, gap junctions and desmosomes many mitochondria for energy

66
Q

cardiac muscles: what do desmosomes do

A

are strong attachments to support the powerful contractions

67
Q

action potential skeletal muscle and what does repeated activity cause

A

skeletal : AP before tension generated

causes summation & tetanus

68
Q

cardiac muscles: action potential duration

A

refractory period is very long (compare to skeletal, 15-5x longer)
this means that cannot get multiple stimuli in a healthy heart

69
Q

cardiac muscle: where is the AP and why is tetanus not possible

A

AP during tension generated: Tetanus impossible due to long refractory period

70
Q

what’s the different roles of skeletal and cardiac muscle during contraction

A

s: triggers contraction
c: dictates length of contraction

71
Q

how to increase the freq of membrane potential in Sino atrial cell

A

sympathetic stimulation, noradrenaline activating only Sino atrial cells through β1 adrenoceptors

72
Q

how to increase heart rate

A

increase the freq of membrane potential in Sino atrial cell

73
Q

difference in membrane potential graph in SA cells when heart rate increases and decreases

A

increases: faster depolarisation and hyperpolarisation
decrease: slower depolarisation and hyperpolarisation

74
Q

how to decrease heart rate

A

decrease the freq of membrane potential in Sino atrial cell

75
Q

how to decrease the freq of membrane potential in Sino atrial cell

A

Parasympathetic stimulation/acetylcholine
- slows pacemaker cells
-through muscarinic ACh receptors

76
Q

Sino atrial membrane potential: adrenoreceptor β1 function and muscarinic Ach receptor function

A

increase Ca2+ and I.f flow for sympathetic stimulation
decrease Ca2+ and I.f flow for sympathetic stimulation

77
Q

what is a membrane potential made up of in a Sino atrial cell

A

membrane potential = pacemaker potential (1) and action potential (2)

78
Q

Sino atrial membrane potential: what happens at the start and end of pace maker potential

A

start: not Na+ in, I.f channels open
end : Ca2+ in, channels open , threshold potential, I.f channels close

79
Q

Sino atrial membrane potential: what happens at the rise, peak, point of hyperpolarisation of action potential

A

rise : Ca2+ in, I.f channels close
peak : Ca2+ channels close and K+ channels open
point of hyperpolarisation: K+ channels close

80
Q

what is the chronotropic effect vs the inotropic effect on heart muscle

A

chronotropic effect : change of rate
inotropic effect : change of force through increase cotnractility

81
Q

true or false: the positive ionotropic effect is due to sympathetic stimulation and occurs by change in length
explain answer

A

false, without any length change cause the receptors on surface change intrinsic ability of muscle cell to contract

82
Q

what is the positive negative ionotropic effects

A

positive = increased contractibility
negative = decreased contractibility

83
Q

Sino atrial membrane potential: describe the cascade of reactions to increase contraction force

A

adrenoreceptor β1 stimulation - increase cAMP - activates PKA - phosphorylation of V-G Ca2+ Channels - longer open time - increase Ca2+ influx/AP = increase contraction force

84
Q

what is the sarcomere proportional to

A

blood volume returning to heart

85
Q

skeletal vs cardiac: which has higher tension at a set sarcomere length (not 100%)

A

skeletal does over cardiac

86
Q

describe 2 functional benefits to length tention relaationship

A

more venous return (e.g. exercise) -> stretch -> more
forceful contraction
more blood pressure in left vent -> more venous return -> more forceful contraction

87
Q

what does venous return mean

A

flow of blood from the periphery back to the right atrium, hence cardiac output

88
Q

what is Starling’s Law of the Heart

A

heart pumps out all blood received.

89
Q

describe the internodal pathway: Electrical conduction system of the heart

A

SA node; AV node, A-V bundle, bundle branches, Purkinje fibres

90
Q
A

physiology (10 decks)

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