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Locomotor & Exercise > Skeletal Muscle Function & in Ageing > Flashcards

Skeletal Muscle Function & in Ageing Flashcards

1
Q

What are the 3 basic motor unit types?

A

fast-fatiguable (FG, IIX), fast-resistant (FOG, IIA), slow (SO, I)

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2
Q

Type I muscle fibres

A

slow oxidative; slow-twitch, small force, high resistance to fatigue

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3
Q

Type IIA muscle fibres

A

fast oxidative/glycolytic; fast-twitch, medium force, high resistance to fatigue

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4
Q

Type IIX muscle fibres

A

fast glycolytic; fast-twitch, large force, low resistance to fatigue

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5
Q

Fast muscle fibres are ______ in size and fatigue _______

A

larger, more easily

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6
Q

Slower muscle fibres are _______ in size and are fatigue ________

A

smaller, resistant

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7
Q

What are ‘pure’ muscle fibres?

A

have one type of MyHC ie either fast or slow

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8
Q

What are ‘hybrid’ muscle fibres?

A

contain multiple forms of MyHC ie combinations of fast and slow

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9
Q

T/F Muscles are static units

A

False; muscle fibres are highly malleable and change their properties based on thes timulus they receive

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10
Q

T/F Within our muscles there is either only pure fibres or hybrid fibres

A

False; there is a combination of pure and hybrid

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11
Q

T/F Slow contracting muscle (eg soleus) do not contain any fast-twitch (IIA or IIX) fibres

A

False; they contain relatively smaller amounts but they are still present

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12
Q

What is the role of myostatin?

A

Negative regulator of muscle mass; if it is inhibited it results in muscle hypertrophy

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13
Q

What is the role of myostatin in muscle wasting?

A

In muscle wasting disorders eg inflammatory environments, myostatin levels rise contributing to atrophy of muscle

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14
Q

What is spinal muscular atrophy (SMA)?

A

Loss of motor neurons and dendritic contracts to muscle results in atrophy and loss of function

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15
Q

T/F Cachexic weight loss can directly cause death

A

True; >20% of cancer-related deaths are attributable to cachexia as loss of muscle mass over 40% is fatal

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16
Q

T/F Cachexia impairs patient respons to chemo and radiotherapies

A

True

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17
Q

T/F Muscle is an endocrine organ

A

True; it produces and releases different hormones into the circulation

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18
Q

In cachexia and critical illness myopathy, muscle

A

atrophies and has disrupted architecture

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19
Q

What is critical illness myopathy?

A

An inflammatory environment associated with infection sets of a cascade of signalling pathways leading to degradation of muscle protein and atrophy over a matter of days

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20
Q

T/F Muscle fibres cannot switch types

A

False; eg stimulation of a fast twitch muscle like TA with low-freqeuency slow-twitch type innervation can change it from FF to SO

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21
Q

What is sarcopenia?

A

Age-related muscle wasting with associated loss of muscle function

22
Q

What changes in ageing are associated with sarcopenia?

A

disuse, changing endocrine function, chronic diseases, inflammation, insulin resistance, nutritional deficiencies or dietary changes

23
Q

T/F Cachexia is the same as sarcopenia

A

False; cachexia may be a component of sarcopenia, but sarcopenia is specifically age-related

24
Q

Diagnosis of sarcopenia should be considered in

A

older patients with observed declines in physical function, strength, or overall health

25
Q

Initial criteria for sarcopenia diagnosis are

A

bedridden, cannot independently rise from chair, gait speed less than 1m/s

26
Q

What changes accompany loss of muscle mass in ageing?

A

Increase in non-contractile material - connective tissue and fat; change in architecture of the muscle

27
Q

Which type of physical activity, running or weightlifting/explosive force events declines faster in ageing?

A

Weight lifting/quick contraction activities that are dynamic and require a lot of muscle power decline at an even greater rate

28
Q

What is muscle weakness?

A

Inability to develop initial force appropriate for the circumstances eg unable to rise from a chair

29
Q

Muscle strength declines steeply beyond age

A

50

30
Q

T/F Slow muscles are more susceptible to age related changes

A

False; fast muscles

31
Q

What are the mechanisms of age-related motor unit remodelling?

A

loss of fast type II motor unit innervation results in death of fast-twitch muscle fibres; expansion of type I motor units innervates fast fibres and converts them to slow fibres

32
Q

What is intrinsic weakness?

A

With ageing, force produced per CSA of muscle fibre is decreased

33
Q

What is fibre-type grouping?

A

selective loss of fast motor units leads to loss of checkerboard pattern of fast and slow fibre distribution

34
Q

Fibre-type grouping is seen in

A

neuromuscular disorders AND sarcopenia

35
Q

What is the cause of the slowing of contraction and relaxation of muscle with age?

A

impaired release and reuptake of Ca2+ by the SR

36
Q

T/F Age-related changes in speed of contraction occur concurrently with atrophy

A

False; these changes occur well before there is significant loss of muscle mass

37
Q

What happens to motor neurons with ageing?

A

MNs are lost, numbers and diameters of motor axons decrease; some fibres die, others survive due to sprouting from slow fibres

38
Q

What changes occur at the NMJ with age?

A

widening of the end-plate, longer nerve terminals, fewer side branches - futile remodelling

39
Q

What changes occur to nerves in ageing?

A

Increase in connective tissue between axons, aberrant small diameter axons, dysmyelination

40
Q

What is responsible for the stiffening of muscles with age?

A

Muscles lose their elasticity because connective tissue increases between muscle fibres

41
Q

Strength training in the elderly increases what type of fibres?

A

type II (fast)

42
Q

What contributes to the inability to combat sarcopenia even with optimal strength training?

A

Decreased circulating levels of anabolic hormones - GH, IGF-1, testosterone - compromises efficiency of muscle regeneration or repair of daily wear and tear

43
Q

What characterized DMD?

A

Generalized weakness and muscle wasting affecting limb and trunk muscles first; calves are often enlarged; elevated CK levels

44
Q

What is Gower’s sign?

A

due to weakness of limb muscles, need to walk self off of floor up the thighs to stand, can’t just stand using limb muscles

45
Q

What changes occur to the appearance of muscle in DMD?

A

loss of fibres, variable size of remaining fibres, significant fibrotic infiltration (fat and CT)

46
Q

DMD is caused by

A

multiple mutations on dystrophin gene (X-linked) causing deficiency in dystrophin expression, a ctyoskeletal protein

47
Q

What is the normal role of dystrophin?

A

Ctyoskeletal protein involved in shock absorption and force transmission by anchoring actin to transmembrane proteins, anabolic signalling blood flow signalling via connection to laminin

48
Q

What is the difference in dystrophin in Becker MD?

A

there are significant amounts of abnormal, smaller stable fragments that confer some stability to muscles

49
Q

Dystrophin is postulated to have a structural role in stabilizing the ________ during contraction via the ________

A

sarcolemma; dystrophin-glycoprotein complex (DGC)

50
Q

What are costameres?

A

Lattices of DGC on the cytoplasmic face of the sarcolemma that join sarcomeres to laminin in the EXM`

51
Q

What is the result of loss of costameres in DMD?

A

Membrane fragility and disruption causing instability in the muscle fibres - membranes tear on activation leading to fibrosis of ECM and leakage of calcium ions which can activate muscle destruction (proteases, phospholipases)

52
Q

What is the role of BPG-15 in DMD?

A

Increases HSP-72 (HSPs help fold misfolded proteins) to improve SERCA levels (takes up Ca into SR) to improve muscle function

Locomotor & Exercise (11 decks)

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