Unit 1 - Muscles Flashcards

1
Q

what is excitation- contraction coupling?

A

process by which a muscle action potential triggers a contraction

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2
Q

how is an endplate potential generated?

A
  • AP in motor axon depolarises nerve terminal opening voltage-gated calcium channels
  • Influx of Ca2+ ions triggers fusion of synaptic vesicles with membrane - releasing acetylcholine into synaptic cleft
  • Acetylcholine binds to the nicotinic receptors causing an endplate potential due to opening of non-selective cation channels
  • When epp reaches threshold, sarcolemma generates AP propagates the entire length of muscle fibre
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3
Q

what is another term for end plate and what type of transmission occurs at this point?

A

neuromuscular junction

- neuromuscular transmission -fast synaptic signally from motor nerve to skeletal muscle

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4
Q

why can miniature endplate potentials be observed when recording?

A

small spontaneous depolarisations reflecting release of acetylcholine from vesicles

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5
Q

what term describes the type of contraction skeletal muscle produces?

A

neurogenic - originates from CNS

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6
Q

what theory is used to describe muscle contraction and explain it

A

sliding filament theory:
- AP spreads along T-tubules causing voltage-gated Ca2+ channels on sarcoplasmic reticulum to open
Ca2+ ions released into sarcoplasm and binds to troponin - causing conformational change which changes its position so displaces tropomyosin exposing myosin head binding site
Myosin head binds to site and dissociates when ATP binds to myosin head
Hydrolysis of ATP causes change in angle of myosin head so it moves to relative to actin - generating force on tendons to which it is attached (power stroke)
This then repeats so cross-bridges break and reform= cross-bridge cycling

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7
Q

what does the amount of force exerted by skeletal muscle depend on?

A
  • cross-sectional area
  • number of active fibres
  • frequency of stimulation
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8
Q

what is:

  • a muscle twitch
  • twitch tension
  • maximal stimulus?
A

muscle twitch= response of a muscle to a single stimulus
t-tension= force developed from stimulus
maximal = stimulus that activates all muscle fibres

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9
Q

what is:

  • summation
  • tetanus/fused tetanus?
A

summation = second stimulus arrives before a muscle has fully relaxed, the total tension increases compared to just a single stimulus

  • If in quick succession, tension summates progressively = tetanus
  • fused tetanus - tension develops smoothly (greater tension - more Ca2+ ions bind to troponin)
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10
Q

what are the properties of type 1 muscle fibres?

A
  • contract/relax slowly
  • Thin
  • Rich in mitochondria/ oxygen-binding myoglobin
  • Rely on oxidative metabolism of fats for energy supply
  • resistant to fatigue due to continuous blood supply
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11
Q

what are the two types of type 2 fibres and give their properties

A

type 2a: fast oxidative-glycolytic fibres
Higher myosin ATPase activity than type 1
thin/rich in mitochondria and myoglobin/ good blood supply - resistant to fatigue
type 2b: fast glycolytic fibres
-large diameter
- develop tension rapidly because high levels of myosin ATPase activity, glycogen and glycolytic enzymes
- Easily fatigued - limited blood supply/ few mitochondria/ myoglobin - pale appearance

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12
Q

what is difference between isometric and isotonic contraction?

A
  • isometric - load prevents shortening

- isotonic - shortens against constant load

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13
Q

why is cardiac tissue described as a functional syncytium?

A

The pacemaker cells of the SA node sets the heart rate by spreading the AP across the whole of the heart since myocytes are tightly bound

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14
Q

what is pacemaker potential? how does it work?

A
  • slow depolarisation that precedes AP- slow activation of sodium current when membrane is repolarised
  • It opposes K+ current so membrane potential becomes progressively less negative- activates calcium current which accelerates rate of depolarisation until AP generated (Ca2+ ions -produce reversal of charge)
  • Repolarisation occurs when calcium permeability falls/ K+ permeability increases so membrane hyperpolarised activating another pacemaker potential (cycle repeated)
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15
Q

why can’t cardiac muscle be tetanised?

A

cardiac AP have long duration between 150-300 ms - therefore mechanical response occurs when depolarised - allows to relax fully

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16
Q

how does EC coupling occur in cardiac muscle?

A
  • AP causes L-type voltage-gated calcium channels to open
  • Ca2+ influx activates ryanodine receptors (calcium release channels) found on sarcoplasmic reticulum
  • rapid release of Ca+ ions( = Ca2+ induced Ca2+ release)
  • leads to contraction (same mechanism as skeletal)
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17
Q

how does relaxation occur in cardiac muscle?

A

Ca2+ ions taken out of cells or back to sarcoplasmic reticulum by Ca2+-ATPase which is regulated by phospholamban:
When protein is phosphorylated, no inhibitory effect on pump so uptake of Ca2+ ions is accelerated - speeding relaxation (lusitropy)

18
Q

what is starling’s law of the heart?

A

The degree to which the muscle fibres are stretched depends on venous return

19
Q

what term describes the change in the rate ?

A

chronotropic

20
Q

what term describes the change in contractility?

A

inotropic

intrinsic contractility of heart = inotropic state

21
Q

what term describes the increase in contractility and describe how this occurs

A

positive inotropic effect
- activation of B-adrenergic receptors by adrenaline leads to calcium influx - generating cAMP/ cAMP activates protein kinase A which phosphorylates calcium channels so open for longer - greater ca2+ release so greater force of contraction

22
Q

where is smooth muscle found?

A

internal/ hollow organs - gut, blood vessels, bladder, uterus

23
Q

describe single unit smooth muscle

A
  • sheets of spindle-shaped cells (fusiform) linked by gap junctions so acts a s functional syncytium
24
Q

how is smooth muscle arranged in alveoli of mammary glands/ small blood vessels?

A

arranged in single layer = myoepithelium

25
Q

what other components are found in smooth muscle?

A
  • loose 3D lattice of microfilaments (actin/myosin) and intermediate filaments
  • dense bodies/ dense plaques
  • caveolae
26
Q

what is the difference between contractile response in single unit and multi unit smooth muscle?

A
  • single unit: myogenic/ spontaneous (involuntary)

- multi unit: activated by motor nerves - not spontaneous

27
Q

how is neurotransmitter released?

A

varicosities along length of axon release neurotransmitters into space

28
Q

where does the ca2+ influx arise from in smooth muscle?

A
  • no T-tubules so arises from calcium channels or sarcoplasmic reticulum
29
Q

how does the contractile response differ between smooth muscle and the other types?

A

it is slower and long lasting in smooth muscle

30
Q

how is EC coupling regulated in smooth muscle?

A

calmodulin

  • binds with calcium to form complex
  • activates myosin light-chain kinase
  • phosphorylates regulatory region on chain so that myosin head can bind to actin and undergo cross-bridge cycling
31
Q

what is tone?

A

steady level of contraction

32
Q

why is tone important and what factors regulate this property of smooth muscle?

A
  • important for maintaining capacity in hollow organs
  • extrinsic: activity in autonomic nerves/ hormones
  • intrinsic: rate of cross-bridge cycling/ response to stretch, metabolites, chemical agents and temperature
33
Q

what is stress relaxation?

A
  • also known as plasticity

- stretch in muscle corresponds with increase in tension then returns to initial value

34
Q

what is reverse stress relaxation?

A

decrease in tension then returns to initial value

35
Q

what else contributes to the property of smooth muscle adjusting to the volume it contains?

A
  • can shorten to two thirds of its initial length due to loose arrangement of microfilaments
36
Q

What is the orientation of muscle fibres in skeletal muscle?

where are the nuclei and why do fibres contain many nuclei?

A
  • longitudinal
  • periphery
  • fusion of myoblasts form a fibre
37
Q

what protein acts as a store of oxygen in the cell?

A

myoglobin
- also a marker for muscle injury - if smooth muscle is broken down releases myoglobin into the blood which is filtered into renal tubules (rhabdomyolysis)

38
Q

what is the difference between concentric and eccentric muscle activity?

A
  • concentric: muscle shortens in length when lifting a weight
  • eccentric: fibres lengthen
39
Q

what is the difference between hyperplasia and hypertrophy?

A
  • hyperplasia: increase in size of muscle by an increase in no of cells in smooth muscle
  • hypertrophy - increase in size of muscle fibres already present
40
Q

how else do skeletal muscles adapt to endurance training?

A

increase in vascularity

41
Q

describe features of cardiac myocyte?

A
  • nuclei centrally located only one in each cell
  • striations due to microfilaments
  • intercalated discs join cells together by gap junctions and adherens junctions (desmosomes)