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Locomotor > Skeletal muscle: ageing and disease > Flashcards

Skeletal muscle: ageing and disease Flashcards

1
Q

List the factors that control muscle mass?

A

Nutritional status

Hormones

Genetics

Innervation

Inflammation

Oxidative stress

Blood flow

Exercise

Disease

Protein synthesis and degradation

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2
Q

What are the three fibre types present in muscle?

A

Fast fatiguable

Fast resistant

Slow

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3
Q

Describe the difference in twitch responses between FF, FR and S muscle fibres?

A

FF: fast twitch

FR: fast twitch

S: slow twitch

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4
Q

Describe the difference in fatiguability between FF, FR and S muscle fibres?

A

FF: fatigue rapidly

FR: fatigue slowly

S: do not fatigue

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5
Q

Describe the concept of muscle fibre malleability?

A

Fibres exist as either pure (one type of MHC) or hybrids (multiple forms of MHC)

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6
Q

What determines the composition of MHC in a muscle fibre?

A

Varies according to stimuli

Composition reflects function

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7
Q

What are the goals of intervention to attenuate muscle wasting?

A

Attenuate muscle atrophy

Promote muscle strength

NOT: increase muscle fatigue

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8
Q

Give an example of a genetic influence on muscle mass?

A

Myostatin: negative regulator of muscle mass

Knockout > increase muscle mass

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9
Q

Describe the situtations which may lead to disuse muscle atrophy?

A

Hindlimb underweighting

Immobilisation

Limb casting

Prolonged bed rest

Spaceflight

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10
Q

Describe the effect of denervation on muscle mass?

A

Denervation atrophy

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11
Q

Describe cancer cachexia?

A

Severe wasting and weakness in many cancer patients

Disruption of muscle architecture

Affects up to 80% lung, pancreatic and GIT cancer patients

Reduces QoL

Impairs response to chemo and radiotherapy

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12
Q

Loss of how much muscle mass is fatal?

A

40%

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13
Q

Describe why muscle wasting is thought to occur so rapidly in the ICU?

How is this being combatted?

A

Inflammatory environment > cascade of signalling pathways > favour protein degradation

Occurs over days

Treatment with electrical stimulation and exercise in the ICU

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14
Q

Describe the outcome of loss of muscle mass in disease states and old age?

A

Compromises QoL and survival

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15
Q

Describe sarcopenia?

A

Age-associated loss of skeletal muscle mass and function

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16
Q

Describe the cause of sarcopenia?

A

Multifactorial: disuse, endocrine changes, chronic diseases, inflammation, insulin resistance, nutritional deficiencies

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17
Q

In which patients should a diagnosis of sarcopenia be considered?

A

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

Bedridden, cannot rise from a chair or measured gait speed <1 m/s

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18
Q

Describe the functional effects of sarcopenia?

A

Descreased running performance

Descreased performace in explosive events

Eventually impacts upon personal care, feeding and domestic duties

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19
Q

Describe the changes that occur in muscle during sarcopenia?

A

Decreased muscle mass

Increased connectove tissue and fat

20
Q

Define weakness?

A

Inability to develop an initial force appropriate for the circumstances

21
Q

At what age does loss of muscle strength usually onset?

A

50

22
Q

Which muscle types are most affected by sarcopenia?

A

Fast muscles more affected than slow

23
Q

Describe the effect muscle fibre denervation and reinnervation with a new fibre type?

A

Muscle fibre changes to match new innervation

24
Q

Describe the chnages in speed of contraction that occur with ageing?

When do these changes occur?

A

Changes in Ca handling (impaired release and reuptake) > speed of contraction affected

Occurs before severe muscle wasting

25
Q

Describe how motoneuron losses in ageing are handled?

A

Type IIB fibres most susceptible > may be renervated by axonal sprouting from slow fibres, or may cease functioning

26
Q

Describe the changes that are thought to occur in motoneurons with ageing?

A

Demyelination

Remodelling of motor end plates

Increased connective tissue

Smaller diameter axons

27
Q

Are the changes that occur in sarcopenia reversilbe?

Can they be attenuated?

A

Generally not reversible

Can be attenuated with strength training

28
Q

Describe the effects of strength training in the elderly?

A

Significant increase in muscle strength

Significant hypertrophy

Increase lean total body mass

Increase in muscle fibre area

29
Q

What are the adaptations that occur in strength training in the elderly thought to be an effect of?

A

Combination of neural adaptations and muscle hypertrophy

30
Q

Describe the hormonal changes that occur with ageing that may have an effect on muscle mass and strength?

A

Decreased circulating levels of anabolic hormones: GH, IGF-1, testosterone

Compromises efficiency of muscle regeneration and repair

31
Q

Describe the age of onset of DMD?

A

2-6 years

32
Q

Describe the inheritance of DMD?

A

X-linked recessive

33
Q

Describe the pattern of onset of DMD?

A

Generalised weakness and muscle wasting affecting limb and trunk muscles first

Calves often enlarged

Progresses to affect all voluntary muscles

34
Q

Why are the calves enlarged in the initial stages of DMD?

A

During early stages, muscles are breaking down and repairing well

Fewer fibres are present, but they are hypertrophied

35
Q

Describe the clinical features of DMD?

A

Lordotic and waddling gait

Gower’s sign

36
Q

Describe the changes in the muscle that occur during DMD?

A

Loss of fibres

Variable fibre size

Infiltration of fibrosis

37
Q

What is the cause of DMD?

A

Mutation in dystrophin gene on Xp21 > deficiency in dystrophin expression

38
Q

Describe the dystrophin-glycoprotein complex?

A
39
Q

Describe the physiological role of dystrophin?

A

Structural role in stabilising sarcolema during muscle contraction

Also a receiver and transducer of signals

40
Q

Describe the age of onset of BMD?

A

Adolescence or adulthood

41
Q

How do the symptoms and presentation of BMD differ from DMD?

A

Almost identical, but less severe

Significant heart involvements

42
Q

Describe how the cause of BMD differs to DMD?

A

X linked recessive mutation in dystrophin gene, but some dystrophin still produced

Many abnormal, smaller molecules

Also some larger, useful proteins

43
Q

Describe the effect of loss of dystrophin on myofibre function and organisation?

A

Disorganised costameres > enhanced membrane leak

Increased oedema

Inappropriate cystolic Ca and ROS generation

Increased ECM deposition

44
Q

Describe the effect of costamere dysfunction on force transmission?

A

Muscle contraction > no force transmission

45
Q

Are dystrophic muscles more susceptible to contraction induced injury?

Why/why not?

A

There is support for this hypothesis

Membrane disruption allows influx of Ca, leads to hypercontraction and necrosis

High incidence of branching

46
Q

Describe the biochemical signs of DMD and BMD?

A

Elevated serum CK (marker of muscle damage)

Increased Evans blue dye uptake (membrane disruption)

47
Q

Describe the treatment targets of muscular dystrophy?

A

Correct genetic defect (gene therapy)

Cell therapy (myoblast transfer, stem cells)

Prevention of secondary consequences (corticosteroids)

Locomotor (28 decks)

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