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KIN 406 > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

The organelle that helps in calcium regulation in the cell is?

a) SERCA
b) T-Tubule
c) Ryanodine Receptor
d) Sarcoplasmic Reticulum
e) Troponin

A

d) SR

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2
Q

Which of the following are potential sources of energy in the cell

a) glycogen
b) fat
c) protein
d) ATP
e) all of the above

A

e) glycogen, fat, protein, ATP

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3
Q

Fastest contracting fiber type in mammals is:

a) Type IIA
b) Type IIX
c) Type IIB
d) Type I

A

c) though only found in rats, humans fastest is IIx

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4
Q

TRUE / FALSE: Determining the number of mitochondria in a fibre is a definitive way of determining fibre type?

A

False

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5
Q

Why would a fibre stain dark during an oxidative enzyme histochemical stain?

a) It contains MHCI
b) it contains high levels of myoglobin
c) it contains a high number of mitochondria
d) it has an extensive capillary network
e) all of the above

A

c) contains a high level of mitochondria

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6
Q

With respect to the motor unit, how can muscle force be increased?

A

Recruit more Motor Units

Increase frequency of stimulation

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7
Q

Which source of ATP has the lowest capacity?

a) oxidative metabolism
b) high energy phosphate transfer system
c) stored ATP
d) anaerobic glycolysis

A

c) Stored ATP

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8
Q

What is the function of a transcription factor?

A
  • transcribes DNA to produce mRNA to produce proteins

* specific binding to a section of DNA sequence that codes for proteins of interest

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9
Q

In the muscle, it would be preferable to:

a) generate new fiber
b) improve/repair existing fibers
c) both would be equally preferable

A

b) improve / repair existing fibers

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10
Q

An important transcription factor involved in promoting myoblast differentiation is?

a) myostatin
b) Mrf-5
c) Myogenin factor 5
d) MyoD
e) All of the above

A

d) MyoD

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11
Q

Which of the following is/are false about muscle nuclei (nuclei found beneath the sarcolemma)

a) there are approximately 100-200 per mm of muscle length
b) they have the same proliferative potential as satellite cells (they can divide)
c) the number of nuclei plays a major role in dictating fibre size
d) a and b are false
e) a b and c are false

A

b) same proliferative potential as satellite cells

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12
Q

What factor(s) is/are a major contributor to muscle strength?

a) fiber type contribution
b) muscle size
c) muscle activation
d) b & c
e) a, b & c

A

d) muscle size and activation

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13
Q

Name another major factor that could potentially influence muscle wasting during aging?

A

Diet

Inactivity

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14
Q

Given the negative consequences caused by the loss of type II fibers during aging, would it be preferable to type I fibers?

A

No
• Type I always activated - fatigue resistant unlike Type II
• Type I have smaller MU allowing for finer movements and finer tuning of muscle force (smaller gradients of force production)
• Type II require faster neural frequency stimulation to induce force summation, unlike Type I

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15
Q

Examining mRNA is important in many cases because?

a) there is a 1:1 relationship between mRNA and protein levels in the cell
b) mRNA levels could influence protein levels
c) provides us an indication of how transcription events are working in the cell
d) b and c only
e) a, b, and c

A

d) influence on protein levels and indicator of transcription events in the cell

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16
Q

Which of the following is not likely to contribute to a slower rate of muscle contraction during aging?

a) slower excitation-contraction coupling events/processes
b) loss of type II fibers
c) altered motor neuron function innervating Type II fibers
d) atrophy of type II fibers
e) none of the above

A

d) atrophy of type II

17
Q

Aging is generally associated with?

a) an increase in the overall proportion of type I fibers
b) more atrophy in type II than type I fibers
c) a greater loss of type I than type II fibers
d) a and c only
e) a and b only

A

e) increased proportion of Type I fibers + more atrophy of Type II

18
Q

TRUE / FALSE: If the body requires fuel in the form of protein it would be better if we tap into type II fibers first

A

TRUE - use Type I all the time, more useful for everyday tasks, and more fatigue resistant

19
Q

Why would inactivity preferentially affect type I fibers to a greater extent?

A

Type I sees stimulation frequently because they are the first ones activated = continued stimulation.
Type II stimulated infrequently so a period of time with inactivity would not be unusual to the muscle fibers, unlike in Type I

20
Q

Which of the following is not likely to occur during inactivity-induced atrophy of a muscle

a) faster rate of contraction for a given force
b) greater atrophy of type II than type I fibers
c) decreased overall muscle force
d) need for a higher frequency of stimulation to reach maximum force
e) both a and b

A

b) greater atrophy of type II than type I

21
Q

If fibre type in a muscle has changed to more type II, why would you require higher frequencies of stimulation?

a) faster relaxation in type II fibers
b) summation occurs at higher frequencies in type II fibers
c) faster rate of Ca2+ update in Type II
d) a and b
e) a b and c

A

e)

22
Q

The muscular dystrophy associated with defects in sarcoglycan structure/function is?

a) Becker MD
b) Duchenne MD
c) Limb Girdle MD
d) Congenital MD
e) none of the above

A

c) Limb Girdle MD

23
Q

What defect is responsible for Becker MD?

A

Deletion of Dystrophin protein

24
Q

Fiber type grouping could be a problem because?

a) recruitment of fibers of one type may be localized to one area of the muscle
b) more fibers per motor unit
c) less metabolic, contractile, and fatigue possibilities in the muscle
d) a and b
e) all of the above

A

e) all of the above

25
Q

What is the difference in muscle fiber changes in atrophic myopathies compared to destructive myopathies

A

Atrophic Myopathies - Decrease in muscle size of all fibers and constant number of fibers
Destructive Myopathies - Destructive of fibers resulting in loss of fiber numbers

26
Q

What are the consequences of inactivity caused atrophic myopathies?

A

Loss of strength
Increased fatigue
Metabolic alterations
Increased frequency of stimulation required for maintaining force

27
Q

What defect is responsible for Congenital MD?

A

Laminin structure/function

28
Q

What defect is responsible for Limb Girdle MD?

A

Sarcoglycans structure/function

29
Q

Overall cause of idiopathic destructive myopathies?

A

Communication failure between skeletal muscle and immune system - destroying skeletal muscle with immune cells and causing longterm inflammation

30
Q

What is the difference in fiber size appearance between small group atrophy seen with motor neuron disease and large group atrophy seen with spinal muscular atrophy

A

Small group = few muscle fibers are affected and undergo atrophy
Large group = majority of muscle fibers undergo large scale atrophy (loss of many more MU)

31
Q

What system does denervation cause?

A

Denervation causes the reversal of the development process - up-regulation of NCAM for re-establishing neural supply by causing branching of nearby axons

32
Q

What stimulates the release of NCAM?

A

Loss of stimulation by removal of nerve supply

33
Q

How does re-innervation affect fibre type grouping?

A

Healthy muscle tissue = random distribution of fiber types
Re-innervation causes grouping of same fiber type clusters causing isolated areas of frequent activation, fewer contractile variations and metabolic phenotypes

34
Q

What happens to muscle fibers with a spinal cord injury?

A

Atrophy of all fiber types

Switching from slow to fast type fibers

35
Q

Describe Malignant Hyperthermia

A

Mutation to the Ryanodine Receptor
Under anaesthetic or stress there is a prolonged release of Ca+ from the receptor causing a prolonged contraction depleting energy stores and producing heat

36
Q

Describe Myotonia

A

Gene defect in muscle Cl channels
Membrane remaining in excitable state causing prolonged contractions (Not as prolonged as with Malignant Hyperthermia because the cell can repolarize itself)

37
Q

Explain fainting goats

A

Fast dynamic movements require fast contraction and relaxation, unable to relax causes the goats to faint with their limbs in maintained contracted state

38
Q

Describe Hyperkalaemic Periodic Paralysis

A

Defect in Na channel, as it stops functioning during excitation and remains open, causing lots of Na to enter cell and upset the membrane gradient. Unable to contract again until the Na gradient is restored to allow for fast depolarization for an AP to occur

39
Q

Describe Hypokalaemic Periodic Paralysis

A

Defect in DHPR, so the electrical activity of an AP is not linked to the release of Ca in the presence of low external K

KIN 406 (2 decks)

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