muscle adaptation, damage and repair lecture (NMSK3)

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37 Terms

1
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Describe the mechanisms of hypertrophy and atrophy in skeletal muscle

















2
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Describe the mechanisms of repair and regeneration in muscle fibres























3
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Describe the major causes and consequences of disease in skeletal muscle




















4
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Outline the causes and effects of:

  • congenital and inherited myopathies

 


  • endocrine and nutritional factors in myopathies



  • exertional myopathies














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Describe what is meant by sarcopenia

























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LO1: what happens when a limb grows/ becomes immobilised?

they dont undergo hyperplasia - number of cells stay the same

  • disease atrophy

  • contraction can be permanent

  • cells (fibres) can become longer or wider but not more numerous


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LO1: how can you reduce likelihood of muscle tearing?

warm up muscles before exercise - allows them to stretch rather than snap

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LO1: hypertrophy/ hyperplasia meaning

hypertrophy = calls increase in size

hyperplasia = increase number of cells

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LO1: Aplasia meaning

incorrect cell number

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LO1: hypertrophy details

muscle fibre increases in size

  • myofibrils size increase

  • myofilament size increase

  • muscle circumference = muscle mass indicator


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LO1: Atrophy meaning

reduction in muscle volume/ mass - may be generalised/ limited to certain muscles

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LO1: what happens if you overtrain one muscle area/ skill?

increase mass of that muscle only

increase one type of fibre - not a good range of skill

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LO1: what muscle type is specific to humans?

2

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LO1: factors that cause hypertrophy and atrophy

anabolic factors (growth hormones)

building up the muscle (some damage = good - leads to inflammation → increase fibrils, late onset muscle soreness = good)


catabolic factors

breaking down muscle

  • disuse

  • denervation (nerves active during rest, activity = increase frequency. loss of background noise may cause muscle to shut down - can be fixed with physio)

  • disease

  • malnutrition


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LO1: how does mechanical stimulus produce increase in fibre size?

stimulated by growth hormone

IGF-1 (insulin-like growth factor 1)


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LO2: Trauma’s impact on muscle tissue

cause inflammation

all soft tissues can scar

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LO2: what are satellite cells

most common skeletal muscle stem cells

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LO2: When are satellite cells activated?

following damage

proliferate + differentiate to form muscle cells and daughter cells

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LO2: stages of repair of canine muscles

















1: 3 days after injury

  • lost muscle cells

  • clusters of activated satellite cells

2: 5 days after injury

  • myotubes formed - can go on to differentiate into muscle cells

3: 7 days after injury

  • regenerating fibres back to normal size


<p>1: 3 days after injury</p><ul><li><p>lost muscle cells</p></li><li><p>clusters of activated satellite cells</p></li></ul><p>2: 5 days after injury</p><ul><li><p>myotubes formed - can go on to differentiate into muscle cells</p></li></ul><p>3: 7 days after injury </p><ul><li><p>regenerating fibres back to normal size </p></li></ul><p></p>
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LO2: impact of nerve damage?

motor nerve damage

lack of innervation of muscle

muscle undergoes atrophy

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LO2: example of nerve damage











stringhalt - excessive flexion in 1/ both hindlimbs

severe cases - muscles can tetanise

  • can lead to muscle atrophy


<p>stringhalt - excessive flexion in 1/ both hindlimbs </p><p>severe cases - muscles can tetanise</p><ul><li><p>can lead to muscle atrophy </p></li></ul><p></p>
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LO2: recurrent laryngeal nerve














L – Recurrent laryngeal Nerve courses round aortic arch

R – Recurrent laryngeal Nerve runs around subclavian artery

<p><span>L – Recurrent laryngeal Nerve courses round aortic arch</span></p><p><span>R – Recurrent laryngeal Nerve runs around subclavian artery</span></p>
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LO2: detection of muscle damage?

Myoglobinuria:

O2 binding protein in muscle

excessive amounts of myoglobin in urea

too much can cause kidney damage - myoglobin leaks into kidney

creatine kinase:

enzyme used by muscles

increased levels can indicate muscle damage/ wasting

creatine = like energy battery

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LO3/4: polymyositis

inflammatory disease

generalised inflammatory myopathy

muscle damage thought to result of cell-mediated immunity

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LO3/4: Masticatory muscle myositis (MMM)

inflammatory disease

focal inflammatory myopathy - selectively affects muscles of mastication (2M fibres)

clinical signs:

Trismus (lock jaw)

fox like contour of the head

prominence of zygomatic arch

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LO3/4: congenital + inherited myopathies













not inflammatory

duchenne muscular dystrophy

mutation in gene coding for membrane protein dystrophin (x linked recessive disorder)

leads to degeneration/ regeneration resulting eventually in failure of respiratory muscles

<p>not inflammatory </p><p>duchenne muscular dystrophy </p><p>mutation in gene coding for membrane protein dystrophin (x linked recessive disorder)</p><p>leads to degeneration/ regeneration resulting eventually in failure of respiratory muscles </p>
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LO3/4: endocrine myopathies examples

hypothyroidism

cushings disease (hyperadrenocorticism)

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LO3/4: hypothyroidism

Clinical signs of weakness, stiffness, reluctance to move decreased exercise tolerance and muscle wastage

Muscle biopsies show atrophy of type II fibres

Problems with carbohydrate metabolism which interferes with glycolytic metabolism

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LO3/4: cushings disease

Clinical signs of muscular weakness, stiff gait, muscle atrophy and inability to walk in dogs

Selective atrophy of type II fibres

Break down of muscle proteins & inhibition of muscle protein synthesis

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LO3/4: nutritional myopathies

usually large animals

E.g. Selenium/vitamin E deficiency

Clinical signs:

Still birth

Weak calf – stiffness and inability to stand

Disease of calves, lambs, swine and foals

Doesn’t often affect carnivores

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LO3/4: exertional Myopathies

“Myofiber damage occurring as a result of exercise stress as the primary cause”

Exertional rhabdomyolysis in the horse (sporadic or recurrent)

Clinical signs include: 

  • muscle injury, myoglobinuria, weakness, recumbency in heavy horse breeds

  • Episodic muscle pain, sometimes swelling and reluctance to move in light horse breeds

Can occur with minimal exercise in susceptible individuals

Unknown etiology – possibly due to a metabolic myopathy

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LO3/4: metabolic myopathy

Equine Polysaccharide storage myopathy

  • Abnormal accumulation of glycogen in the muscles

  • Glycogen synthase 1 mutation

Clinical symptoms, recurrently exertional rhabdomyolysis (tying up or painful muscle cramps)

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LO5: What is a motor unit?













A single α-motor neuron and all of the corresponding muscle fibres it innervates.

inter-dependent

<p><span>A single α-motor neuron and all of the corresponding muscle fibres it innervates.</span></p><p><span>inter-dependent</span></p>
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LO5: motor unit sizes

vary

eye muscles→ 3: 1 | muscle: nerve

hamstring→ 300: 1 | muscle: nerve

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LO5: why are there different motor neurone sizes?

depends on how specific the movements need to be.

eye = very specific movements

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LO5: sarcopenia

Atrophy associated with aging is known as Sarcopenia:

Loss of motor axons

Denervation

Degeneration/regeneration

Loss of motor fibres/axons

Motor-unit size

Fibrosis

IGF-1?

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summary: most important aspects

Mechanisms of hypertrophy and atrophy

Investigated what happens when there is repair and regeneration following injury

Looked at some major causes and consequences of disease in skeletal muscle

Looked at what is meant by sarcopenia