Muscle Flashcards

1
Q

What are the types of muscle and how are they differentiated?

A

Skeletal (Striated, Voluntary)
Cardiac (Striated, Involuntary)
Smooth (Unstriated, Involuntary)

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2
Q

What is myoglobin and what is it’s specific function?

A

Protein with a single haem group that binds to O2 (single-subunit of Haemoglobin)
Present in Striated muscle to transfer O2 to muscles (Higher affinity at lower pH - when there’s higher [CO2])

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3
Q

What is the structure of skeletal muscle?

A
Muscle fibres surrounded by endomysium
Muscle fibres bundled into fascicles
Fascicles are surrounded by perimysium
Groups of fascicles bundled into skeletal muscle
Muscles are surrounded by epimysium
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4
Q

What is the structure of muscle fibres?

A

Contain myofibrils of thin actin and thick myosin filaments

Myofibrils are divided into sarcomeres and surrounded by outer membrane sarcolemma

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5
Q

Describe the sections of a sarcomere

A
A-band (dark): length of myosin
I-band (light): length of actin only
H-zone: length of myosin only
Z-disc: connection point for actin
M-line: middle point of sarcomere
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6
Q

Describe the features of hypertrophy

A

Replacement > Destruction of muscle fibres
Increase in fibre diameter (more contractile proteins)
Increase in number of sarcomeres

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7
Q

Describe the features of atrophy

A

Replacement < Destruction of muscle fibres
Decrease in fibre diameter (less contractile proteins)
Decrease in number of sarcomeres

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8
Q

What causes hypertrophy/atrophy?

A

Changes in the rate of metabolism
Changes in the frequency of stretching (contraction/relaxation)
Changes in the amount of innervation

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9
Q

Describe the features of actin filaments

A
Dimers of actin form a double helix
Coils of tropomyosin surround actin for reinforcement and blocking myosin
Troponin complex (TnI, TnT, TnC) attached to every tropomyosin controls attachment of actin to myosin
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10
Q

Describe the features of myosin filaments

A

Many individual myosin molecules group to form a filament

Each myosin molecule contains 2 myosin heads in regions of potential overlap (none in the H-zone)

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11
Q

Describe the stages of muscle contraction

A

1) Attachment of the myosin head to actin filaments:
Additional Ca2+ binds to TnC of the troponin complex
Displaces tropomyosin away from the actin filaments allowing binding of myosin
2) Working stroke:
Myosin pulls actin toward the m-line, releases ADP and Pi
3) Low-energy configuration:
ATP binds to myosin heads releasing actin
4) Preparation:
ATP is hydrolysed but not released, ‘cocking’ the myosin head
(This will repeat as long as there is Ca2+)

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12
Q

What happens to the regions of a sarcomere during contraction?

A

H-zone shortens
I-band shortens
A-band is constant but moves closer to Z-discs

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13
Q

What are markers for:

Cardiac muscle damage and skeletal muscle damage?

A

Cardiac: Increase in troponin levels
Skeletal: Increase in Creatine Kinase levels

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14
Q

What is sarcolemma and what is it’s specific function?

A

Outer membrane of myofibres (formed from T-tubules and sarcoplasmic reticulum)
T-tubules which conduct the Action Potential
Sarcoplasmic reticulum contain Ca2+ which is released to bind to TnC
T-tubules form triad with adjacent terminal cisternae of sarcoplasmic reticulum

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15
Q

After post-synaptic depolarisation by VGNaC’s how does Ca2+ get released?

A

Action potential travels down T-tubules causing conformational change of voltage-sensing proteins
Conformation change of proteins opens gated Ca2+ channels of adjacent terminal cisternae
Rapid efflux of Ca2+ into sarcoplasm

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16
Q

What are muscle spindles?

A

Intrafusal muscle fibres surrounded by a capsule facilitating proprioception
3 neurones:
Gamma - keeps fibre taught
Type Ia sensory - rate of change of muscle length
Type II sensory - position of muscle

17
Q

What special structure do cardiac muscle cells contain?

A
Intercalated discs (allows contraction of cardiac muscle simultaneously):
Fascia adherens (connect sarcomeres via anchoring actin filaments)
Desmosomes (prevent separation of muscle fibres by binding actin filaments)
Gap junctions (allow passage of ions, continuing the AP and depolarisation between sarcomeres)
18
Q

What is the difference between hypertrophy and hyperplasia?

A

Hypertrophy: Increase in cell size
Hyperplasia: Increase in cell number

19
Q

What are Natriuretic peptides and what causes their release?

A
Natriuretic Peptides (reduce hypertension)
Distension from hypertension (from hyperbole is) causes their release
20
Q

What are the effects of ANP and BNP?

A

Decrease the level of Renin (causes increase in blood pressure)
ANP: Increases Glomerular Filtration Rate (kidneys)
BNP: Increases vasodilation

21
Q

What does a reduction in Renin cause?

A
Reduction of Renin, causes reduction of Angiotensin II (which activates aldosterone - mineralocorticoid)
Increases Diuresis (Excretion via urine) and natriuresis (Excretion of Na), which decreases blood volume as water also leaves, lowering blood pressure
22
Q

Describe the features of smooth muscle

A

Unbranched: fusiform
Unstriated: no sarcomeres/T-tubules
Involuntary: under autonomic nervous control (still use myosin/actin)

23
Q

How does each type of muscle cell regenerate?

A
Skeletal muscle (cannot divide) - 
Satellite cells differentiate into skeletal muscle cells  and can undergo Mitosis (hyperplasia) or fuse with existing muscle fibres (hypertrophy)
Cardiac muscle (cannot regenerate) -
Following damage, fibroblasts invade area, divide and lay down scar tissue
Smooth muscle (can regenerate) -
As cells can divide (hyperplasia) and grow (hypertrophy)