T3 L3: Physiology of skeletal muscle Flashcards

1
Q

How does muscle grow?

A

By hypertrophy

There is synthesis of myofilaments, addition of sarcomeres, satellite cell activation, angiogenesis, and vascularisation

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2
Q

What is the effect of endurance exercise on muscles?

A

Increased fibre diameter, blood supply, and mitochondrial content

There will be more oxidative enzymes

Fibres will become slower (transformation from IIx to IIa fibres)

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3
Q

What is the effect of non-endurance exercise?

A

Conversion of IIa into IIx fibres

There is increase in IIx fibre size due to increased numbers of sarcomeres and myofilaments

Results in much larger muscle

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4
Q

What is the effect of ice on muscles?

A

It reduces swelling by reducing perfusion

Good after an acute injury like a sprain, or after overuse injury

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5
Q

What is the effect of heat on muscles?

A

It helps to relax and loosen muscles

Used before activities that irritate chronic injuries like strains because it increases blood flow

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6
Q

What is the mechanism behind Aspirin?

A

It inhibits COX which reduces the synthesis of prostaglandins and part of the arachidonic acid

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7
Q

What are the side effects of blocking prostaglandins and arachidonic acid?

A

Gastro-intestinal adverse effects

Eg. stomach bleeding, ulcers

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8
Q

What are the anabolic effects of testesterone?

A
  • Increases protein synthesis
  • Decreases catabolism
  • Reduces fat (increases BMR and increases differentiation to muscles rather than fat cells)
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9
Q

What is catabolism?

A

Breaking down of large molecules

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10
Q

What is BMR?

A

Basal metabolic rate

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11
Q

What are the effects of anabolic steroid abuse?

A

They’re used to increase muscle size and strength.

Large doses are needed

Male- testicular atrophy, sterility, baldness
Female- breast/uterus atrophy, menstrual changes, facial hair, deepening of voice

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12
Q

What is the effect of bed-rest of muscles?

A

Weight-bearing muscles atrophy

  • Decreased muscle protein synthesis
  • Myofibrillar breakdown
  • Reduced strength
  • Loss of type I fibres

Transition of type I to type IIa

Treated by resuming minor activity early

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13
Q

How does a contracture form?

A

If the limb is immobilised for a long period of time, the process of growth is reversed so sarcomeres are removed and the muscle shortens

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14
Q

Why do multinucleate cells not divide?

A

Because mitosis with multiple nuclei is usually impossible

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15
Q

How are muscles regenerated?

A

Satellite cells are activated which proliferate, differentiate, and fuse onto fibres and contribute to forming multinucleate myofibers

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16
Q

What are the progenitor cells of muscles?

A

Satellite cells

17
Q

What is myalgia?

A

Muscle pain caused by injury, overuse, infections, or autoimmune

18
Q

What is myopathy?

A

Muscular weakness due to muscular fibre dysfunction

19
Q

What is paresis?

A

Weakness, partial loss, or impaired voluntary movements,

20
Q

What are fasciculations?

A

Involuntary large visible neurogenic twitches in single motor units
-Usually occur in lower motor neurone diseases

21
Q

What are fibrillations?

A

Small involuntary myogenic spontaneous contractions of individual muscle fibres

Can be identified by electromyography

22
Q

What is rhabdomyolysis?

A

Rapid breakdown of skeletal muscle

Causes: trauma, drugs, hyperthermia, ischaemia to skeletal muscle

Symptoms: muscular pain, vomiting, confusion, dark urine

23
Q

What is the treatment for Rhabdomyolysis?

A

Intravenous fluid to treat shock and haemodialysis to clear the blood

24
Q

How is Rhabdomyolysis diagnosed?

A

Urine will be very dark and will be tested for myoglobin

Hyperkalaemia is tested for because when muscle cells lyse, they release K+

25
Q

What is myasthenia gravis?

A

Progressive muscle weakness and fatigability

Caused by a depletion of nicotinic ACh receptors because of autoimmune destruction of the receptors

26
Q

What are some initial symptoms of myasthenia gravis?

A

Ptosis and diplopia because those muscles are so weakened

27
Q

What is the treatment for myasthenia gravis?

A

-AChE inhibitors
Eg. Pyridostigmine increases ACh activity at the NMJ
Eg. Edrophonium is used for diagnosis because it should temporarily improve symptoms

  • Thymectomy reduces 70% of symptoms
  • Immunosuppressive drugs
  • Plasmapheresis: removal of anti-AChR antibodies from the blood
28
Q

What is Spinal muscular atrophy (SMA)?

A

AKA floppy baby syndrome

It’s caused by the death of lower motor neurones in the anterior horn of the spine

Aetiology: autosomal recessive gene

29
Q

What is meant by fibre type grouping?

A

Different types of muscle fibres grouped together

30
Q

What is malignant hyperthermia?

A

A rare genetic susceptibility to gas anaesthetics causing SERCA to work too hard

Symptoms: increased O2 consumption, CO2, acidosis, tachypnea, muscles overheat, the body overheats, muscles are damaged (rhabdomyolosys), hyperkalaemia, muscles become rigid

31
Q

What is the treatment for malignant hyperthermia?

A

Dantrolene sodium will stop the abnormal calcium release by inhibiting the ryanodine receptor

32
Q

What is Gower’s sign?

A

A sign of muscular dystrophy where the patient is too weak to stand up so has to use their hands

33
Q

What is duchenne muscular dustrophy?

A

An X-linked disease caused by a mutation on the dystrophin protein