Physiology of Muscle -Brownell Flashcards

1
Q

What are the 3 types of motor proteins?

A
  1. myosin: actin==> basis of skeletal, cardiac and smooth mm contraction
  2. kinesins: microtubule motors that walk intracellular organelles along microtubules
  3. dyneins: microtibule motors that cause the bending of cilia and flagella

defects in any of these will lead to diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a muscle fiber? How is it developed?

A

Muscle fiber=1 muscle cell

developed by fusion of myoblasts into multinucleate myotubes, differentiation into mm fibers

fixed # of mm fibers at birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which myofibril band is where actin and myosin overlap?

A

A band- think of it as the “active” band

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is titin?

A

The large elastic protein that connects thick filaments to A discs in mm myofibrils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does CapZ do?

A

form the Z disc, and binds the (+) end of actin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What couples electrical depolarization to contraction?

A

the DHP/ryanodine complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the process of muscle contraction

A

ACh from the motor neuron is released in to the neuromuscular junction (short distance). this binding of the ACh receptor allows for the depolarization of the mm through Na+ influx and the formation of an action potential. The action potential propagates and in the t-tubule changes the DHP receptor conformation, releasing Ca2+ from the sarcoplasmic reticulum

The Ca2+ binds to trpoonin allowing actin-myosin binding and a power stroke formation–> actin slides towards the center of the sarcomere

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What can cause an increase in muscle contraction tension?

A

increase in frequency of action potentials

==> can lead to tetany=maximum contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the rate limiting factor for most physiological processes? How is this overcome in muscle contraction?

A

diffusion distance

for muscle contraction, the distance must be in micrometers or smaller (between motor neuron terminal and ACh receptor on mm).

=> the T-tubule and DHR and RyR allow for the Ca2+ to be held right next to them so it can be released quickly and effectively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is the initiation of contraction different in smooth muscle from skeletal mm?

A

smooth mm couples electrical depolarization to contraction by a second messenger mediated process (MLCK) (myosin light chain kinase)

much SLOWER than skeletal mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How can ATP for muscle contraction be generated (3)?

A
  1. creatine phosphate (quickly release stored energy–> only enough for 8 twitches)
  2. glycolysis
  3. oxidative phosphorylation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the major differences in fast and slow twitch muscle fibers?

A

Fast twitch:

  • glycolytic, anaerobic ATP synthesis
  • large diameter
  • pale in color
  • easily fatigued
  • e.g. escape reflex mm, jumping mm.

Fast oxidative:

  • fast
  • oxidative phosphorylation
  • fatigue resistant
  • e.g. walking
  • medium diameter

slow twitch:

  • beta oxidative (aerobic ATP synthesis)
  • smaller diameter
  • dark red color due to myoglobin (vascularized)
  • fatigue resistant –> sustained contraction
  • e.g.: postural mm.
  • numerous mitochondria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is negative feedback used in controlling muscle contraction?

A

-ALL skeletal mm contraction is under negative feedback control.

-the set point (intended movement) is the central command to move.
the body senses current movement and amplifies (motor neurons) the signals to get output appropriate for the set point .

this output can be affected by environmental factors–> negative feedback of movement (sensory)

cannot have precision without negative feedback!!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the fastest nerve fibers? Where are these found and why?

A

1a (muscle spindle)

1b (golgi tendon organ)

largest diameter, fastest fibers here because need fast feedback in the somatosensory system!

these fibers are responsible for sending the afferent information to cerebellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is responsible for the re-efference (error correction) in muscle movement?

A

the cerebellums signals to the alpha and gamma* motor neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When does muscle fatigue occur? What are the 2 types of fatigue?

A

30% ATP depletion

central and peripheral fatigue

17
Q

What is myasthenia gravis? How is it treated?

A

autoimmune suppression of the post-synaptic NACh receptors–> will present with weakness (fatigue)

tx: pharmacological inhibition of ACh esterase

18
Q

What is Lambert-Eaton Syndrome?

A

Autoimmune attack of presynaptic Voltage-gated channels for Ca2+ which blocks ACh vesicle exocytosis (triggered by Ca2+)

also leads to less NT release and weakness

19
Q

What is the difference between Duchennes Muscular Dystrophy and Beckers Dystrophy?

A

Duchennes (x-linked) =unexpressed gene for dystrophin protein

Beckers (x-linked) =Dystrophin is partially functional

20
Q

What is the function of dystrophin? How is the body affected in pt’s with Duchennes?

A

dystrophin gives the body structural integrity

normally, nNOS (attaches to dystrophin) triggers NO release when there is tension on dystrophin which causes vasodilation

without dystrophin, you lose this vasodilation reflex and get less NO generation and less vasodilation

21
Q

What is Amyotrophic Lateral Sclerosis?

A

Degenerative motor neuron diseases with associate effects on muscle atrophy.

Progressive degeneration from lower motor neuron to upper motor neuron

22
Q

What are the differences between fatigue and rigor mortis?

A

peripheral fatigue:

  • 30% ATP depletion
  • sufficient ATP to drive Ca2+ transport
  • [ADP]/[ATP]=too high to drive crossbridges–> no movement

rigor mortis:

  • complete depletion of ATP
  • no Ca2+ transport
  • crossbridges cannot dissociate (stuck in contracted state)
  • occurs 3 hours postmortem and persists up to 72 hours
23
Q

What determines muscle fiber type, distribution and size? How was this proven?

A

The motor neuron that innervates it! (determined during development)

when you take a fast motor neuron and attached it to a slow muscle, it will become fast muscle

24
Q

What does denervation atrophy lead to?

What does disuse atrophy (e.g. bedridden) lead to?

A

denervation: type grouping–> fast and slow muscle fibers will group together

disuse atrophy: smaller, “angular” fast fibers