Case 9 - muscle and movement Flashcards

1
Q

features of skeletal muscle

A

connected to bone
striated
voluntary
high power
usually relaxed

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2
Q

features of cardiac muscle

A

heart
striated
involuntary
high power
pump (cyclic)

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3
Q

features of smooth muscle

A

hollow organs
smooth
involuntary
low power
usually contracted

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4
Q

neuromuscular junction diagram

A
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5
Q

neuromuscular junction diagram

A
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6
Q

what is in a sarcomere

A

a number of different proteins in highly organised structure

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7
Q

how does muscle contract

A

by overlapping the filaments

using energy derived from ATP hydrolysis to power this mechanism which is progressively shortening the distances

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8
Q

what is the thin filament

A

actin

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9
Q

what is the thick filament

A

myosin

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10
Q

where is tropomyosin normally sat

A

over the binding sites for myosin on actin

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11
Q

what has to happen in order fr the myosin to bind to the myosin binding site on actin

A

the binding site has to be exposed. when there is little Ca2+ or none, tropomyosin moves down and covers the binding sites. means that the actin and myosin can’t interact and bind to each other therefore giving no muscle contraction

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12
Q

what is the troponin complex

A

series of regulatory proteins and in the presence of calcium, they help to move that tropomyosin out of the myosin binding site and allows the actin and myosin to interact. you then get ATP hydrolysis that powers the whole process. effectively makes the muscle shorter

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13
Q

striated muscle contraction series of events

A
  1. ATP binds to the myosin head causing the dissociated of the actin-myosin complex
  2. ATP is hydrolysed, causing myosin heads to return to their resting connotation
  3. a cross bridge forms and the myosin head binds to a new position on actin
  4. phosphate is released… myosin heads change conformation resulting in the power stroke. the filaments slide past each other
  5. ADP is released
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14
Q

what happens when there are high levels of calcium

A

you get contraction

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15
Q

diagram with anatomy concerning excitation-contraction coupling

A
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16
Q

what is the plasma membrane

A

the sarcolemma

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17
Q

what are there lots of in the muscle cell

A

myofibrils

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18
Q

what do the invaginations of the plasma membrane form

A

transverse tubules

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19
Q

what interacts with the transverse tubule

A

the sarcoplasmic reticulum cisterns

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20
Q

where does the action potential go

A

goes along the sarcolemma and finds its way down into the T tubules and the T tubule is running very close to the SR. t

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21
Q

where is calcium stored

A

the SR.

when the muscle is relaxed, the Ca2+ will be locked up inside the SR

when the cells contract, Ca2+ will be released

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22
Q

when do we get release of calcium

A

when a wave of depolarisation passes through the T tubule

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23
Q

what does the twitch force depend on

A

how much calcium is released. bigger contraction when more calcium is released

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24
Q

what are the two types of contraction

A

isometric
isotonic

25
what is isometric contraction
a constant length and doesn't actually shorten
26
what is isotonic contraction
a constant load
27
what does isotonic muscle contraction produce
limb movement without change in muscle tension, whereas isometric muscle contraction produced muscle tension without a change in limb movement. most physical activities involve a combination of both forms of muscle contraction, although one form usually predominates
28
more on isometric contraction
contraction is stronger the closer the muscle initial length is to the optimum length a muscle contracts but the joint is controls does not move
29
more on isotonic contraction
contraction is faster the closer the muscle initial length is to the optimum length a muscle contracts and the joint angle it controls increases and decreases while the muscle either shortens or lengthens
30
what is a muscle unit
muscle fibres innervated by a single motor neurone
31
what is a motor unit
muscle unit plus its motor neurone
32
what is a motor neurone pool
collection of neurones innervating a single muscle
33
what is involved in fine control
few muscle fibres per motor unit
34
what is involved in coarse control
any muscle fibres per motor unit
35
how many motor neurones control a muscle
typically about 100
36
what are the features of type 1 muscle
oxidative slow, red slow myosin response time moderate rate of Ca2+ pump transport moderate diameter high oxidative capacity moderate glycolytic capacity reistant to fatigue
37
what are the features of type 2B muscle - 7
glycolytic fast, white fastest myosin response time high Ca2+ pump transport rate large diameter low oxidative capacity high glycolytic capacity non-resistant to fatigue
38
what are the features of type 2A muscles - 7
glycolytic, fast, red fast myosin response time high Ca2+ pump transport rate small diameter very high oxidative capacity high glycolytic capacity resistant to fatigue
39
which muscle type is good for long distance running and why
type 1 fibres are slow and oxidative and tend to rely on aerobic respiration to generate most of their force - long distance run at low speed
40
which fibres fatigue slower than 2B
2A but generate a decent amount of tension
41
what are 2B designed to do
give you high energy. relying on glycolysis anaerobic respiration to give out most of their power.
42
what are the two mechanisms to increase the amount of force
recruitment of motor units firing rate of motor units (shortening the time between action potentials and the contractions sort of add together and the calcium is never fully mopped up by the SR)
43
what is the sequence of recruitment in the gradation of muscle force
S->FR->FF
44
what are the large motor unit properties
motor neurone: large, fast conduction, hard to excite Muscle fibres: many, type 2 (large, fast glycolytic) Activity: recruited if a strong contraction is required, usually inactive
45
what are the small motor unit properties
motor neurone; small, slow conduction, easy to excite Muscle fibres: few, type 1 (small, slow, oxidative) Activity: first to be recruited, frequently active
46
detailed stretch reflex diagram
47
LMN muscle strength
weak
48
what type of paralysis do you get with LMN lesion and why
flaccid - effectively damaged the wiring between the muscle and the spinal cord; cant get a message from the spinal cord to the muscle
49
what is the muscle tone if you have a LMN lesion
hypotonia
50
what is the type of reflex if there is a LMN lesion
hyporeflexia
51
muscle strength in UMN lesion
weakness
52
what type of paralysis do you get in UMN lesion
you get spasticity because the wiring is still there form the muscle unlike in an LMN lesion: can't get the message from the motor cortex to the spinal cord. you get sensitisation of the lower motor neurone pools so that they're responding in the absence of innovation from the motor cortex. that is why you get spastic paralysis
53
what type of muscle tone is there in UMN lesion
hypertonia - thanks to sensitisation to lower motor pools
54
what sort of reflexes do you get. in UMN lesion
hyperreflexia
55
what is Babinski sign
may show a problem in the corticospinal tract. CST is a neural pathway that goes from your brain to spinal cord and helps control your movements. evaluate neuro only in patients above age of 2. the essential phenomenon appears to be recruitment of the extensor hallicus Longus, which consequent overpowering of the toe flexors. the movements of the other joints remain the same
56
how what happens when the corticospinal tract is not functioning
 The corticospinal tract influences the segmental reflex in the spinal cord. When the corticospinal tract is not functioning properly, the result is that the receptive field of the normal toe extensor reflex enlarges at the expense of the receptive field for toe flexion. Toe extension is consequently elicited from what is normally the receptive field for toe flexion.
57
what is the plantar reflex
a nociceptive segmentaal spinal reflex that serves the purpose of protecting the sole of the foot
58
in what conditions has the extensor reflex been observed
hemorrhage, brain and spinal cord tumors, and multiple sclerosis, and in abnormal metabolic states such as hypoglycemia, hypoxia, and anesthesia.[2]