Lecture 14 - Muscles (2) (Part 1) Flashcards

1
Q

Describe the main similarities and differences between cardiac and skeletal muscle.

A

Similarities:

  • Nuclei are central in both (peripheral in skeletal)
  • Only have 1 contractile cell type
  • Both act as syncytium
  • Both have gap junctions

Differences:

  • Cardiac muscle is striated, smooth is not
  • Smooth doesn’t contain sarcomeres
  • Smooth doesn’t contain troponins
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2
Q

Both cardiac and smooth muscle fibres have 1 central (cardiac sometimes 2), how can you distinguish between the two in H&E stains?

A
  • Cardiac muscle has clear intercalated discs.
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3
Q

How is cardiac muscle innervated?

What are the different types of innervation and how do they affect HR?

A
  • Via the ANS (sympathetic + parasympathetic branches)
  • Para innervates atrium, sympathetic innervates atrium and ventricles
  • Para = decreased HR, sympathetic = increased HR
  • Sympathetic increases HR by activating DHP which leads to increased Ca2+ release through RyR’s.
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4
Q

How is smooth muscle innervated?

How does smooth muscle contract?

A
  • Via the ANS, which causes NT release from varicosities which are released at pre-synaptic clefts.
  • Ca2+ entry occurs and binds to calmodulin. The Ca2+/calmodulin complex activates MLCK which phosphorylates myosin light chains in order for actin to bind and contraction to occur.
  • Ca2+ continues until there is a decrease in IC Ca2+
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5
Q

How is skeletal muscle innervated?

How can recruitment of fibres per motor unit change muscle power?

A
  • Skeletal muscle is innervated by release of ACh at the neuromuscular junction is response to nerve impulses. This binds to sarcolemmal receptors initiating an AP which is propagated along the muscle.
  • Less units recruited per motor unit = less power (therefore useful for fine control muscles), more units = more power (e.g.: for gastrocnemius).
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6
Q

What is the role of Kranocytes in the NM junction?

A

Resides over the terminal Schwann cell on pre-synaptic junction and anchors nerve to the muscle cell.

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7
Q

Describe the series of events that occur in the build up to skeletal muscle contraction.

A
  • Nerve impulse along motor axon leads arrives at NM junction, leading to ACh release which binds to post-synpatic receptors.
  • This opens Na+ channels and influx of Na+ leads to DP of sarcolemma which spreads to t-tubules.
  • Voltage sensor proteins in T-tubule undergo conformational change and release Ca2+ into sarcoplasm
  • Ca2+ binds to TnC and contraction cycle is initiated.
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8
Q

What is Myasthenia Gravis and what does it lead to?

A
  • Autoimmune disease, antibodies block ACh receptor, leads to reduced synaptic transmission and thus intermittent muscle weakness.
  • Symptoms include Ptosis (drooping eyelid)
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9
Q

Describe the basic structure of actin + myosin

A
  • Myosin is a rod-like structure with 2 protruding heads.
  • Actin is a thin filament protein that is composed of F-actin fibres and G-actin globules, with tropomyosin-troponin complex covering binding sites. (therefore actin, tropomyosin and troponin together from the thin filament).
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10
Q

Describe the structure of the functional contraction unit

A
  • Thick filaments run through the middle, thin filaments on the outside, with tropomyosin coiling round the actin helix and a troponin attached to each tropomyosin. Myosin heads extend towards actin filaments in regions of overlap.
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11
Q

How is Ca2+ involved in muscle contraction?

A

Ca2+ binds to TnC leading to a conformational changes that moves tropomyosin away from actin’s binding sites, allowing myosin heads to bind and contraction to occur.

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12
Q

Describe the cyclic sequence of events that occurs during skeletal muscle contraction.

A
  • Myosin heads bind to actin forming cross bridge
  • ADP & Pi release allowing working stroke to occur, myosin head pivots and pulls actin towards M line.
  • New ATP attaches at myosin head level, so cross bridge is detached.
  • ATP hydrolysis starts the process again.
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13
Q

What happens to the length of actin, myosin, sarcomeres and Z-line when muscle contracts?

A

Actin - stays the same length
Myosin - stays the same length
Sarcomere - Shortens
Z-lines - come closer together

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14
Q

What is the origin and insertion points of a muscle?

A
Origin = muscle start point (typically a bone and proximal)
Insertion = muscle re-attachment point (bone, tendon or connective tissue, typically distal).
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15
Q

What are the roles of agonist, antagonists, synergists, neutralisers and fixators in movement?

A
Agonist = primary mover
Antagonist = oppose primary movers 
Synergists = assist primary movers
Neutralisers = prevent unwanted movements agonist can perform
Fixators = holds a body part immobile whilst another part is moving.
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16
Q

What are the 3 types of muscle levers we can have?

A

1) first-class - effort at one end load at another, e.g.: neck muscles in extension
2) second-class - effort at one end, fulcrum at other, e.g.: plantar flexion of foot
3) Third-class - Effort between load + fulcrum, most common in the body, e.g.: biceps

17
Q

What are muscle compartments & what are they based on?

A
  • Muscles grouped together with similar actions, surrounded by thick dense fascia
  • Based on location, e.g.: anterior, posterior, lateral & medial
18
Q

What is compartment syndrome and what are the symptoms?

A
  • When trauma in a muscle compartment causing internal bleeding and exerts pressure on blood vessels and nerves
  • Symptoms = constant localised pain, paresthesia, compartment feels tense and swollen shiny skin.
19
Q

What is muscle tone and how is it regulated?

A
  • Muscle tone is the tension in a muscle at rest
  • Regulated by motor neurone activity, muscle elasticity, use and gravity
  • Improves with exercise.
20
Q

What is the mechanism of muscle hypertrophy?

A
  • Overstretching so A and I bands can no longer re-engage.
  • New muscle fibres produced (from mesenchymal cells) and no sarcomeres added in middle of existing ones so I and A band can engage.
21
Q

What is the mechanism of muscle atrophy?

A

Disuse, surgery or diseases lead to loss of protein, reduced fibre diameter and loss of muscle power.