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Muscle physiology Flashcards

(85 cards)

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1
Q

Motor unit

A

Alpha motor neuron + all the muscle fibres it innervates

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2
Q

Type I muscle fibres are:

A

Slow

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3
Q

Type II muscle fibres are:

A

Fast

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4
Q

Size principle

A

Small oxidative units recruited first because of their lower threshold, large glycolytic motor units last

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5
Q

Neuromuscular junction

A

Motor axon synapses on the motor end plate of the motor neuron. The axon loses its myelin sheath and splits into multiple branches.

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6
Q

2 distinct domains of the postsynaptic folds

A

Crests and depths of the folds

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7
Q

The crests of the postsynaptic folds have:

A

High concentration of AChRs, rapsyn and utrophin

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8
Q

Rapsyn

A

AChR clustering proteins

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9
Q

Utrophin

A

Ubiquitous dystrophin

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10
Q

The depths of the postsynaptic folds have:

A

High concentration of voltage gated sodium channels

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11
Q

Presynaptic events at the neuromuscular junction

A

1) AP reaches nerve terminal
2) Depolarisation opens VGCCs
3) Ca+2 influx
4) Increased Ca+2 triggers vesicle exocytosis and ACh release

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12
Q

Vesicle cycling and release

A

1) Vesicles filled
2) Vesicles form vesicle cluster
3) Filled vesicles dock at active zone
4) Vesciles are primed
5) Ca+2 triggered fusion-pore opening
6) Vesicles undergo exocytosis
7) Recycling of vesicles

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13
Q

3 ways vesicles can be recycled

A

Local reuse
Fast recycling
Clathrin mediated endocytosis

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14
Q

Postsynaptic events at the neuromuscular junction

A

1) ACh binds transmitter gated channels
2) Channels open
3) Na+ inflow, K+ outflow
4) Depolarisation of motor endplate
5) VGNCs open
6) Na+ inflow
7) Depolarisation
8) Propagated muscle AP

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15
Q

AChE

A

Acetylcholinesterase

Anchored to collagen fibrils of basement membrane

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16
Q

AChE works by:

A

Rapidly hydrolysing ACh with water to form choline and acetate
Choline diffuses back to presynaptic terminal and is reabsorbed

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17
Q

3 presynaptic examples of abnormal neuromuscular transmission

A

Lambert-Eaton syndrom
Diabetes
Botulinum and tetanus toxins

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18
Q

2 postsynaptic examples of abnormal neuromuscular transmission

A

Myasthenia Gravis

Alpha toxins

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19
Q

Myasthenia Gravis key points

A

Autoimmune - antibodies attack AChRs
Reduces number of functional receptors and inhibits AP initiation
Treated with anti-AChEs and immunosuppressants

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20
Q

Botulism key points

A

Botulinum toxin released by Clostridium botulinum
Toxins bind presynaptic terminal, are internalised and catalyse cleavage and inactivation of vesicle release system
Blocks depolarisation induced quantal release
Recovery only occurs when nerve terminals grow new sprouts to escape toxins and form new contacts with the muscle fibre

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21
Q

4 characteristics of skeletal muscle

A

Excitable
Contractile
Extensible
Elastic

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22
Q

Epimysium

A

Surrounds entire muscle

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23
Q

Perimysium

A

Surrounds entire fascicle

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24
Q

Endomysium

A

Surrounds each muscle fibre

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25
Sarcolemma
Cell membrane of the muscle fibre
26
Na+ concentrations inside and outside cell
Inside: 10 mM Outside: 145 mM
27
K+ concentrations inside and outside cell
Inside: 145 mM Outside: 4 mM
28
Ca+2 concentrations inside and outside cell
Inside: 0.1 microM Outside: 1.5 mM
29
Transverse tubular membrane system
Deep invaginations of sarcolemma into myocyte | Conduct propagated APs and result in localised contracture of filaments
30
T-tubule location
Either side of myosin strip at junction of overlap between A and I bands
31
Triad
T-tubule + 2 terminal cisternae of the sarcoplasmic reticulum Essential for synchronised excitation-contraction coupling
32
Sarcoplasmic reticulum function
Stores Ca+2
33
3 major classes of SR calcium-regulatory proteins
Luminal calcium binding proteins SR calcium release channels Sarcoplasmic reticulum Ca+2 ATPase pumps (SERCA)
34
Basic unit of contraction
Sarcomere
35
A band
Both thick and thin filaments | Anisotropic
36
I band
Only thin filaments
37
Z line
Electron dense region in the middle of the I band
38
H band
Only thick filaments
39
M line
Electron dense region in the middle of the H band
40
Actin filaments attach:
At the Z line
41
Myosin filaments attach:
At the M line
42
Thick filament composition
Myosin pairs oriented in opposite directions, staggered around fibre
43
Thin filament compostion
Two strands of F-actin twisted together with tropomyosin molecule lying along the helix in a groove
44
Titin
Acts as a spring connecting myosin to Z line
45
Heads of myosin are present along the sarcomere except in:
The H zone
46
Nebulin
Helps align thin filaments
47
3 parts of troponin complex
TnT TnC TnI
48
TnT
Troponin tropomyosin | Positions complex on tropomyosin molecule
49
TnC
Troponin calcium | Contains Ca+2 binding sites
50
TnI
Troponin inhibitor | Binds actin and inhibits myosin head from binding to the actin binding site in the process
51
Troponin complex + tropomyosin =
Ca+2 sensitive switch
52
Roles of ATP in cross-bridge cycle
ATP + myosin binding breaks link formed between actin and myosin ATP hydrolysis provides energy for cross-bridge movement
53
6 steps of cross-bridge cycle
1) Myosin bound to actin 2) Myosin dissociation 3) ATP hydrolysis 4) Conformational change 5) Power stroke 6) Myosin binds actin
54
Describe Step 1 - Rigor state of the cross-bridge cycle
Myosin is tightly bound to actin at the actin binding site. The myosin head is at 45° relative to the filaments
55
Describe Step 2 - Myosin dissociation of the cross-bridge cycle
ATP binds nucleotide binding site on the myosin which changes the configuration of the myosin head and allows it to dissociate from the actin binding site
56
Describe Step 3 - ATP hydrolysis of the cross-bridge cycle
ATPase activity of myosin hydrolyses ATP into ADP + P. At this stage, both products are still bound to myosin which is unbound from actin.
57
Describe Step 4 - Relaxed state of the cross-bridge cycle
Myosin head swings over and binds weakly to a new actin molecule, changing the angle from 45° to 90° relative to the filament. ADP and P are still bound to myosin.
58
Describe Step 5 - Power stroke of the cross-bridge cycle
P dissociates from the myosin head which causes the head to rotate on its hinge back to 45°. It is still attached to the same position on the thin filament and therefore pushes the thin filament back with it - therefore power stroke.
59
Describe Step 6 - Repositioning of the cross-bridge cycle
After power stroke the ADP dissociates from the myosin head. With this conformational change the myosin forms the rigor state attached to the actin once again.
60
At rest, tropomyosin prevents:
Interaction between actin and myosin
61
Troponin C has ____ Ca+2 binding sites
4 | 2 high affinity and 2 low affinity
62
The binding of the 2 extra Ca+2 to troponin C causes:
The conformational change in the troponin complex which allows tropomyosin to shift in respect to the actin filament
63
The mechanical coupling hypothesis
High density of dihydropyridine receptors in tetrads opposite 4 ryanodine receptors in SR terminal cisternae. Depolarisation of TT membrane flips DHPR, inducing conformational change in RyR which allows them to become open Ca+2 channels. Therefore DHPRs are essential for excitation-contraction coupling.
64
4 benefits of voltage dependent excitation contraction coupling
1) Rapid kinetics 2) No dependence on current flow 3) No reliance of diffusion of substances from sarcolemma 4) Activation can occur in absence of extracellular Ca+2
65
Isometric contraction
No external shortening takes place Same length Force of weight = force developed by muscle
66
Isotonic contraction
Movement takes place | Same force
67
2 types of isotonic contraction
Concentric | Eccentric
68
Concentric contraction
Force of weight is less than force developed by muscle | Muscle shortens
69
Eccentric contraction
Force of weight is more than force developed by muscle | Muscle lengthens
70
Force velocity relationship
Load opposing contraction increases so velocity of shortening decreases
71
Force = ?
Mass x Acceleration
72
Work = ?
Force x Distance
73
Power = ?
Work / Time
74
Type 1 slow twitch fibres
Red due to myoglobin Lots of mitochondria Resistant to fatigue Abundant in postural muscles and endurance athletes
75
Type 2a fibres
``` Fast oxidative Hybrid of type I and II fibres Red, lots of mitochondria Anaerobic and aerobic More prone to fatigue than type I ```
76
Type 2b fibres
``` Fast glycolytic White Anaerobic Fatigue rapidly Lots of power ```
77
3 causes of muscle weakness
Muscle fatigue Muscular dystrophy Sarcopenia
78
Muscle fatigue
Failure to maintain required or expected power output | Reduced muscle performance
79
Central fatigue
Muscle fatigue resulting from decreased activation from CNS and decreased number of motor units recruited
80
Peripheral fatigue
Muscle fatigue resulting from affected cellular mechanisms that control force such as smaller Ca+2 transient, reduced Ca+2 sensitivity of myofilamentsand slower crossbridge cycling
81
Proposed causes of fatigue
Accumulation of metabolites | Depletion of muscle energy supplies
82
4 key metabolite products that could accumulate
Lactic acid Extracellular K+ Inorganic phosphate ROS
83
4 key products that could be depleted
Glucose Creatine phosphate ATP Oxygen
84
Duchennes muscular dystrophy
Mutation in dystrophin gene causes loss of dystrophin Increased membrane permeability leads to skeletal muscle weakness and degeneration Respiratory failure common around age 20
85
Sarcopenia
Age related loss of muscle function | Muscle mass/body mass ratio decreases leading to significant loss of strength

Musculoskeletal (9 decks)

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