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Body Logistics > Lecture 17 - Muscle structure and function > Flashcards

Lecture 17 - Muscle structure and function Flashcards

1
Q

How do the types of muscle divide ?

A

Striated and non-striated

Striated is Skeletal - myoglobin present, voluntary control, direct nerve muscle communication

or Cardiac - myoglobin present, involuntary control, indirect nerve muscle communication

Non striated is smooth muscle - myoglobin abesnt, involuntary control, No direct nerve muscle communication

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2
Q

Outline the structure of Skeletal Muscle

A
  • Epimysium(deep fascia) -Around muscles, creating muscle compartments
  • Perimysium–Around fascicles
  • Endomysium–Around individual muscle fibre

blood vessels in between fasicles

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3
Q

muscle compartments - give ya knowledge

A

limbs divided into compartments by deep fascia

  • Trauma to one compartment can lead to compartment syndrome:
  • Internal bleeding confined to a single compartment • Build up of pressure
  • Compresses blood vessels and nerves, leading to ischaemia and pain
  • Treated by fasciotomy–Relieves pressure
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4
Q

what is the role of myoglobin?

what is Rhabdomyolysis ?

A

Myoglobin is the O2 transport/breif storeage molecule in the striated muscle

Rhabdomyolysis - skeletal muscle necrosis due to a crush injury

myoglobin released into the kidney causes kidney damage

release of intracellular K+ —hyperkalamia
results in potentially fatal cardiac arrhythmias

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5
Q

give some knowledge on skeletal muscle histology

A

Cells are cylindrical, unbranched and multineucleate

neucli are lined along edges

mitochondria appear as long dark streaks
see stripes along the fibers - rest between the myofibirls

can have transverse and longnitudinal views - cut in different planes of muslce

fibers surrounded by a thin layer of connective tissue with cappilaires and nerves

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6
Q

describe / draw the structure of a Sacromere unit
what contracts the muscle
how does it contract

A

a sarcomere is Z band to Z band

made of central myosin and peripheral actins

H zone is the myosin only section

M line is the center of the sacromere and myosin unit

I band is the actin only section and Z band

A Band is total length of myosin unit , with Actin crossover

relaxed - larger H zone and I Band
Contract H zone and i band shrinks as actin and myosin come together
A band remains the same as its just myosin length

be able to identify zones on a histogram - check this

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7
Q

Explain the Striated Muscle Contraction and Sliding Filament Theory

A
  1. Myosin cross bridge attaches to the actin myofilament

ADP and Pi bound to the myosin head
Myosin head is in the high energy configuration

  1. Working stroke - myosin head pivots and bends as it pulls the actin filament sliding it toward the M line

ADP and Pi are released

  1. ATP joins to myosin head - now in low energy configuration - it is not bound to the actin fillament

ATP joining to the myosin head the cross bridge detached from actin

  1. As ATP hydrolyisis (split) occurs to create ADP and Pi bound to the Myosin Head

the myosin head is Cocked - ready to bind to thin actin filament - go to step 1.

this is triggered by ….

Ca2+ binding to troponin C
Tropomyosin Shifts from Actin, exposing the myosin binding sited
Myosin pulls actin fillaments towards M line via a sliding filament mechanism - this requires ATP hydrolysis

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8
Q

What is the T tubule system ?

A

Transverse tubules with terminal cisternae of SR (contains Ca2+) either side forms a traid, conntected by the branching cisternae struture

action potiential travels along t tuble and can cause ca2+ to be released into the nerve cell

singal from neurons will induce Ca2+ release over the contracting Sacrolemma

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9
Q

what is Excitation - contraction coupling ?

A
  • Action potential of motor neurone reaches NMJ
  • Depolarisation causes voltage-gated Ca2+ions to open, leading to Ca2+ influx and consequent release of ACh from the synaptic knob
  • ACh binds to nicotinic AChRs, leading to Na+influx(voltage-gated Na+ channels also open) • Depolarisation spreads locally over sarcolemma and into T tubules
  • Voltage-gated Ca2+channels open, causing Ca2+ release into sarcoplasm
  • Calcium-induced calcium release (see ICPP)
  • Ca2+ binds to troponin C and contraction cycle initiated
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10
Q

what is cardiac muscles structure ?

Histology ?

A

Cells are cylindrical branched - contract in both directions either side of an intercalated disc, to obtain a 3D contraction

central neucli - 1 or 2 per cell
branching system
no t-tubule system
only one cell - cardiomyocyte that communicate through gap junctions/intercalated disc

intercalated discs - Gap Junctions which couple neighbouring myocytes forming a functional syncytium

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11
Q

use of biochemical markers to do with the heart, what are they ?

A

• Cardiac troponin I/T -Gold standard for diagnosing MI • Released by necrotic cardiac myocytes

  • Creatine kinase (CK) –Can be raised due to: • Myocardial infarction
  • Rhabdomyolysis
  • Intramuscular injection
  • Vigorous physical exercise
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12
Q

what is the structure of smooth muscle

A

• Cells are spindle-shaped (fusiform) with a single central nucleus
• No sarcomeres or T tubules
Strechy
• Contraction still relies on actin-myosin interactions –More sustained, requires less ATP - via a cross lattice structure in the cell, causing tightening

little dots on histogram are called dense bodies

smooth muscle is in gut and around arterioles/capillaries

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13
Q

what is the basic principle of muscle growth and repair ?

A
  • Striated muscle cells –Cannot divide, but can increase in size (hypertrophy)
  • No regenerative capacity
  • Smooth muscle cells – Can divide
  • Can regenerate
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14
Q

name and define your sarco terminology

A

Sarcolemma: The outer membrane of a muscle cell
Sarcoplasm: The cytoplasm of a muscle cell
Sarcosome: The mitochondrion
Sarcomere: The contraction unit in striated muscle
Sarcoplasmic reticulum: The smooth endoplasmic
reticulum of a muscle cell

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15
Q

what are the types of muscle fibers

A

slow, fast and intermediate

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16
Q

explain the differences between the slow and fast and intermediate muscle fibers ?

A

each fascicle will have at least one of each

Slow twitch - are red - lots of myoglobin, lots of energy production - many mitochondira and cytosomes
Fast twitch are white -quicker to use then stop - eyelid muscles blinking

Slow fibers - smaller diameter , fast fibers thicker diameter

Fast fibers - larger colour , fatigue easily

17
Q

what are pukunjie fibers ?

Not vital

A

Purkinje fibres are large cells with:

  • abundant glycogen
  • sparse myofibrils
  • extensive gap junction sites

The Purkinje fibres conduct action potentials rapidly (3-4 m/s, compared to 0.5 m/s for cardiac muscle fibres)

This rapid conduction enables the ventricles to contract in a synchronous manner

18
Q

differences and similarities of smooth muscle and cardiac

A

Differences
• Smooth muscle does not contain sarcomeres
• Electrical conduction - specialised cells/routes in cardiac muscle
• No troponins in smooth muscle

In common
• Nuclei are central not peripheral
• Only one contractile cell type
• Act as a syncytium (wave-like function)
• Myocytes communicate through g
19
Q

what is the the thin fillament made of

A

formed of actin
tropononinc (tnI,TNc(Ca2+ binds), Tnt)
tropomyosin

ca2+ binding to Tnc - conformational change - moves myosin out the way from actin binding site - mysoin head can bind

20
Q

what is different about the center of the sacromere

A

myosin is devoid of myosin head,so binding cannot occur

21
Q

summaries the whole contraction process from ach releas to contraction ?

A

howd it go ?

22
Q

what is muscular hypertrophy ?

A

muscle growth

Overstretching
such that the A and I bands can no longer re-engage
• New muscle fibrils are produced
• New sarcomeres are added in the middle of
existing sarcomeres
• New muscle fibres arise form mesenchymal cells

23
Q

what is muscular atrophy

A

muscle loss

Disuse
e.g. bed rest, limb immobilisation, sedentary behaviour, age, etc.
Surgery
e.g. denervation of muscle
Disease
Muscular dystrophies
• Loss of protein, reduced fibre diameter, loss of muscle power

24
Q

what are the clinical correlates of muscle dysfunction ?

A

• Duchene muscular dystrophy - mutation to dystrophin - too much Ca2+ enters cells - cell lysis
creatine kinase and myoglobin very high in blood
Muscle cells replaced by adipose tissue
• Rhabdomyolysis
• Myocardial infarction - creatine kinase or TnI is high in blood if this has happened
• Botulism and organophosphate poisoning - sludge and mtwtf

Body Logistics (20 decks)

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