9 - muscle and movement Flashcards
1
Q
location (typical), morphology, control, type of work, and activity (typical) of skeletal muscle
A
- location = connected to bone
- morphology = striated
- control = voluntary
- type of work = high power
- activity (typical) = usually relaxed (however does have a basal muscle tone)
2
Q
location (typical), morphology, control, type of work, and activity (typical) of cardiac muscle
A
- location (typical) = heart
- morphology = striated
- control = involuntary
- type of work = high power
- activity (typical) = pump (cyclic)
3
Q
location (typical), morphology, control, type of work, and activity (typical) of smooth muscle
A
- location = hollow organs
- morphology = smooth
- control = involuntary
- type of work = low power
- activity = usually contracted (varies)
4
Q
describe what happens in full at a neuromuscular junction
A
- AP arrives
- voltage-sensitive Ca++ channels open
- Ca++ enters the cell
- vesicle fusion - ACh exocytosis
- ACh diffusion in the synaptic cleft
- ACh-sensitive cation channels open
- Na+ in and K+ out
- end-plate membrane depolarises — End Plate Potential (EPP)
- AP forms = stimulus for muscle
5
Q
thick vs thin filaments
A
thick - myosin
thin - actin
6
Q
where does energy to shorten the muscle come from?
A
ATP hydrolysis
7
Q
what shortens in a muscle contraction?
A
sarcomere
8
Q
label this sarcomere
A
9
Q
what makes up a muscle?
A
muscle cells or fibres = myofibrils = myosin + actin (myofilaments; thick and thin)
10
Q
what are the myosin binding sites like at rest?
A
covered up by tropomyosin due to the absence of Ca++ — therefore actin and myosin can’t interact
11
Q
what is the troponin complex and what does it do?
A
- regulatory proteins — TnT, TnC and TnI
- help moves tropomyosin out of binding sites in the presence of Ca++
12
Q
what parts of the thin and thick filaments bind when they interact?
A
myosin head binds to actin filament at myosin binding site
13
Q
describe the steps in a striated muscle contraction starting from the previous contraction
A
- ATP binds to myosin head, causing the dissociation of the actin-myosin complex
- ATP is hydrolysed, causing myosin heads to return to their resting conformation
- a cross-bridge froms and myosin head binds to a new position on actin
- P is released. myosin heads change conformation, resulting in the power stroke. the filaments slide past each other
- ADP is released
14
Q
what triggers a muscle contraction?
A
increase in Ca++ —> exposes binding sites —> contraction
15
Q
what forms the T-tubules?
A
invaginations of plasma membrane (sarcolemma)
16
Q
what does the AP spread along in excitation-contraction coupling?
A
the sarcolemma
17
Q
what stores the Ca++ at rest and then releases it when the T-tubule is depolarised?
A
sarcoplasmic reticulum
18
Q
what pump is active at rest?
A
NaK pump
19
Q
what is the Ca++ released through?
A
Ca++ release channels
20
Q
increase in Ca++ = ?
A
stronger force of contraction
21
Q
what are the 2 types of muscle contraction? how are they different?
A
isometric = muscle stays at constant length (but still generates force) (eg. lifting hand up against a table)
isotonic = muscle shortens (eg. weight lifting)
22
Q
contraction is stronger and faster the…….?
A
closer the muscle initial length is to the optimum length
(too stretched/already contracted = worse contraction)
23
Q
what is a muscle unit?
A
muscle fibres innervated by a single motor neuron
24
Q
what is a motor unit?
A
muscle unit plus its motor neuron
25
what is a motor neuron pool?
collection of neurons innervating a single muscle
(UMN synapses on pool of LMNs - not 1 on 1)
26
fine vs coarse control
fine = few muscle fibres per motor unit
coarse = many muscle fibres per motor unit
27
typically a muscle is controlled by about ___ motor neurons — cell bodies in the spinal cord or brainstem
each motor neuron controls ___-___ muscle fibres scattered over the muscle
- 100
- 100-1000
28
type 1 muscle fibres:
myosin speed, Ca++ pump transport rate, diameter, oxidative capacity, glycolitic capacity, fatigue
myosin = slow
Ca++ pump transport rate = moderate
diameter = moderate
oxidative capacity = high
glycolytic capacity = moderate
fatigue = resistant
29
type 2B muscle fibres:
myosin speed, Ca++ pump transport rate, diameter, oxidative capacity, glycolitic capacity, fatigue
myosin = fastest
Ca++ pump transport rate = high
diameter = large
oxidative capacity = low
glycolytic capacity = high
fatigue = non resistant
30
type 2A muscle fibres:
myosin speed, Ca++ pump transport rate, diameter, oxidative capacity, glycolitic capacity, fatigue
- myosin = fast
- Ca++ pump transport rate = high
- diameter = small
- oxidative capacity = very high
- glycolytic capacity = high
- fatigue = resistant
31
what type of muscle fibres are resistant?
type 1 and 2A
32
what muscle fibre type has the highest oxidative capacity?
type 2A
33
what type of muscle fibre has the fastest myosin?
type 2B
34
what muscle fibre type has the largest diameter?
type 2B
35
what kind of respiration do type 1 muscle fibres use? use?
aerobic — long distance at low speed — fatigue resistant
36
why do type 2B muscle fibres tire quickly?
rely on glycolysis
37
how can you increase muscle force?
1. increase recruitment of motor units
2. increase firing rate of motor units
38
what can you recruit?
- fewer/more units
- units of different sizes
39
the CNS is lazy - you have to teach it to recruit more motor units. when is this evident?
1st few months of weight training == can lift more weight but dont see muscles getting bigger
40
large vs small motor unit motor neuron
large = motor neuron is large, fast conduction, hard to excite
small = motor neuron is small, slow conduction, easy to excite
41
large vs small other unit muscle fibres
large - many, type 2 (large, fast, glycolytic)
small - few, type 1 (small, slow, oxidative)
42
large vs small motor unit recruitment/activity
large - recruited if a strong contraction is required, usually inactive
small - first to be recruited, frequently active
43
describe the stretch reflex
1. tendon tap
2. stretch muscle
3. stimulate muscle spindles
4. excite motor neuron —> agonist muscle contraction
excite inhibitory interneuron —> antagonist muscle relaxation
44
what type of afferents in stretch reflex?
Ia, II
45
what type of efferent in stretch reflex?
Aa efferent
46
what type of motor neuron in stretch reflex?
a
47
lower vs upper motor neuron lesion properties
muscle strength, paralysis, muscle tone, reflexes
> lower:
muscle strength = weakess
paralysis = flaccid
muscle tone = hypotonia
reflexes = hyporeflexia
> upper:
muscle strength = weakness
paralysis = spastic
muscle tone = hypertonia
reflexes = hyperreflexia
48
why can you get twitching in a lower motor neuron lesion?
muscles respond to circulating ACh
49
why do you get spastic paralysis and hypertonia in an upper motor neuron lesion?
sensitisation of LMN pools — respond in absence of innervation from motor cortex (still have wiring from spinal cord to muscle)
50
why do you get hyperreflexia in an UMN lesion?
loss of a descending inhibitory pathway — get re-emergence of primitive reflexes
51
what do the ventral and dorsal parts of the somite give rise to?
ventral — bone, cartilage, tendons
dorsal — skeletal muscle
52
skeletal muscles from in _____?
subsequent waves
53
what do invaginations of the cell membrane do?
increase SA = more receptor for ACh
54
where are motor neurons found in spinal cord?
in anterior horn of spinal cord
55
AP propagates along membrnae via _____ until it reaches ____
Na+ channels
T-tubule
56
what is electrically coupled to T-Tubule?
sarcoplasmic reticulum
57
what do type 1 muscle fibres contain to make them resistant to fatigue?
myoglobin — captures O2 and releases it when needed
58
describe a muscle strain
- commonly referred to as a “pulled” muscle
- this injury can happen when the muscle is overstretched, overused, or used improperly
59
describe a muscle tear
- larger injury in which a muscle and the blood vessels that supply it are torn
- typically takes a significant amount of force to cause this type of injury
60
what is rhabdomyolysis?
a serious condition that occurs when muscle fibres die and their contents are released into the bloodstream
61
what can rhabdomyolysis result in and why?
kidney failure — kidney responsible for filtering put the muscle byproducts
62
symptoms of rhabdomyolysis
muscle pain, weakness, dark urine
63
causes of rhabdomyolysis
- crush injuries
- car accidents
- heatstroke
- infections
- intense exercise
- seizures
- use of cocaine or amphetamines
64
what is muscle contusion?
- also referred to as a muscle “bruise”
- occurs when a blunt object strikes the body and crushes underlying muscle tissue, but does not break the skin
- typically cause pain, swelling, and decreased range of motion
65
muscle damage and regeneration
66
what degrades and digests the debris of dead muscle?
neutrophil
67
M1 macrophage classically divides into what? what do they promote?
1. via IL-6 — satellite cell (like a stem cell) —> promotes regeneration
2. M2 macrophage —> promotes inflammation
68
what are chronic types of muscle damage?
69
what is muscular dystrophy?
an X-linked recessive disease (more common in males) caused by mutation of dystrophin gene = the largest known gene coding for a cytoskeleton protein
70
what is muscular dystrophy characterised by?
degeneration of skeletal muscle due to absence f dystrophin on muscle fibre membrane
71
what happens to the calf in later stages of muscular dystrophy?
pseudohypertrophy of the calf — due to severe inflammation of gastrocnemius
72
morphology of dystrophic muscle
73
what is dystrophin?
- coded for by the DMD gene
- cytoplasmic protein
- connects the sarcomeres to the membrane and other proteins to the basal lamina
- protects from stress in contraction
74
what happens in the absence of dystrophin?
- increased probability that muscle membrane will be damaged
—> Ca++ influx
—> hypercontraction
—> activation of Ca protease — destroys fibre
75
what are the 2 forms of muscular dystrophy disease?
1. mild form = Becker’s form — inframe mutation — amino and carboxyl left intact
2. severe form = Duchenne’s form — frameshift mutation — protein not made
76
what replaces fibres in muscular dystrophy?
fat infiltration and fibrosis
