muscle physiology Flashcards

1
Q

Describe the macroscopic organisation of skeletal muscle..

A

myocyte
wraped in endomysium
collection of these myocytes make a bundle wrapped in perimysium **
multiple perimysiums wrapped in
epimysium **

all connective tissue layers come together to form thick connective tissue layer - tendons and ligaments.

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2
Q

describe the microscopic organisation of skeletal muscle…

A

myocytes consists of
* many microfibrils = thick and thin filaments made of actin and myosin. Give it a striated appearance.
* Sarcoplasmic reticulum
* surounded by plasma membrane with invaginations (T tubules) - in close contact with sarcomere and SR.
* many mitochondria
* glycogen stores

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3
Q

describe the structure of the sarcomere…

A

basic contractile unit of the muscle cell
consists of thick and thin filaments
thin filaments = actin + tropomyosin + troponin
Thick filaments = myosin

regular overlapping pattern, many arranged in parrallel in skeletal muscle giving a striated appearance

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4
Q

describe the interactions between tropomyosin, troponin and actin and myosin..

A

tropomyosin is a strand like protein bound to actin and blocks the binding site for myosin head.

troponin I, C and T are also bound to tropomyosin via troponin T

when troponin C binds Ca it causes a conformational change that puls the tropomyosin away from the binding site

myosin heads have an ATP binding site and a actin binding site.

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5
Q

functions of skeletal muscle

A

posture
movement

BMR - increasing body temp

venous return - leg muscle contraction

some sphincters are skeletal - bladder, rectum and swallow

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6
Q

describe the process of activating NMJ…

A
  1. action potential
  2. depolarisation causes N type VG Ca channel to open
  3. Calcium enters the cell
  4. calcium attaches to sypnatotagmin and activates SNARE proteins on pre-filled vescicles
  5. these fuse with presynaptic membrane releasing Ach
  6. ACh released into synaptic cleft and can bind post synaptic receptors
  7. these ionotrophic receptors are now activated and open to allow cations to flow into the muscle causing depolarisation
  8. this activate muscle contraction via excitation contraction coupling.
  9. Ach can also bind pre-synaptic receptors and lead to vesicles moving from reserve pool to the readily realasble pool such that the next action potential can continue to sitmulate muscle contraction and fatigue isnt seen
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7
Q

describe excitation contraction coupling…

A

this is the process of action potential being generated in a myocyte and the activation of sarcomeres to cause muscle contraction

the AP travels down and is propagated through T tubules
this takes the depolarisation to the depths of the muscle and throuhgout
VG L type Ca channels are present in T tubule and allow Ca to enter
there is also Ca-induced Ca release whereby Ca induces opening of ryanodine receptors to allow further calcium to enter

calcium then binds to Troponin C and causes a conformational change whcih pulls tropomyosin away from the actin exposing the myosin binding site

myosin can now bind to actin to form a cross bridge.
ATP on myosin head is hydrolysed giving energy for a power stoke.

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8
Q

describe the process of cross bridge cycling and the sliding filament theory..

A

calcium binds to Troponin C and causes a conformational change whcih pulls tropomyosin away from the actin exposing the myosin binding site

myosin can now bind to actin to form a cross bridge. ADP is attached to its head.
ADP is replaced by ATP causing detachment and instantly hydrolysis of ATP causes power stroke and reattachment at a site further along
This process is repeated to bring actin filament in closer, shortening the sarcomere.

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9
Q

how is muscle contraction terminated?

A

no further ACh released
Ach is hydrolysed by acetylcholinesterase within synapse and metabolites are taken up by pre-synaptic terminal

nACHR therefore close
no further AP
no further release of Ca

calcium is pumped back into the SR by SERCA and Na/Ca exchanger.
calcium levels drop and detach from troponin C
hence myosin binding sites are one again unavailable and the sarcomere relaxes.

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10
Q

describe the proces of removal of Ach from the cleft

A

acetylcholinesterase
into choline and acetic acid

reabsorbed and reproduce Ach.

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11
Q

resting membrane potential of skeletal muscle…

A

-90mV

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12
Q

what is a motor unit?

A

motor neuron Aa and all the muscle fibres it innervates

depending on function this may be few fibres (fine movements) or many fibres (gross movements)

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13
Q

what is a motor end plate ?

A

the point at which a nerve innervates a myocyte - usually just one end plate

has folded membrane to increase S.A for AchR
has more AchR than required - redundancy

synapse is small to promote fast diffusion

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14
Q

how is Ach synthesised and stored in vesicles?

A

choline + acetylCoA = acetylcholine
catalysed by choline acetyltransferase

transported into vesicles in exchange for H+

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15
Q

what is meant by extra junctional nACHR ?

A

these are nACHR that are produced after injury - usually burns/ nerve injury
they are usually fetal type and very sensitive to depolarising NMB hence can result in hyperkalaemia
not sensitive to non-depolarising, sometimes larger dose of this needed.

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16
Q

subunits of nACHR…

A

2a, B, g, d = fetal

e instead of g in adult .

17
Q

what are the different types of muscle fibres?

A

type 1
* slow twitch, aerobic, many mitochondira, low power, fatigue resistant, used for posture.

type 2a
* fast twitch aerobic, medium force, many mitochondria.

type 2b
* fast twitch glycolytic, anaerobic, a lot of force but tire quickly. more glycolysis enzyme

18
Q

what happens in MH?

A

defect in ryanodine
uncontrolled calcium released
uncontrolled muscle cell contraction - tetany

uses lots of ATP, O2
produces lots of CO2, heat
muscle tires and becomes anaerobic - acidosis
muscle injury - hyperkalaemia , rhabdo

19
Q

describe the contraction of smooth muscle cells.. describe how nitric oxide influences this…

A

action potential
depolarisation
calcium via VG channels

calcium binds calmodulin
ca-calmodulin complex activates MLCK
phosphorylated Myosin –> contraction

nitric oxide: cGMP activates PKG

20
Q

resting membrane potential of smooth muscle and action potential duration…

A

-50mV

no T tubules so not as quick - gradual response

21
Q

how is smooth muscle contraction regulated?

A

intrinsic pacemakers scattered amoungst smooth muscle layers.

ANS
vagus - ACH - increases contraction
sympathetic NS - a1 - vasoconstriction, B2 - vasodilation.

22
Q

how does B2 cause vasodilation?

A

Gs
increase PKA
phospholates MLCP to activate it

23
Q

compare and constract cardiac, skeletal and smooth muscle..

A

skeletal
* striated
* voluntary
* multinucleated, long cylinderical
* short AP (5ms)

cardiac
* striated
* involuntary
* single nucleus
* branching and gap junctions
* longest AP duration (300ms)
* different T tubule organisation
* different ryanodine
* many mitochondria and more vascular.

smooth
* non striated
* involuntary
* single nucleus
* spindle shape arranged in sheets.
* long duration AP (100ms)
* does not have troponin - instead calmodulin and myosin light chain kinase
* no T tubules

24
Q

what drugs affect the NMJ?

A

NMBA
acetylcholinesterase inhibitors - neostig, edrophium, organophos
Mg and aminoglycosides inhibit N type Channels presynaptically