Exam 3: Chapter 21: Movement and Muscles at Work Flashcards

1
Q

striated muscle makes up what percentage of tissues in vertebrate?

A

about 50%

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2
Q

Mammalian cardiac muscle contracts _____ times per minutes.

A

30-700

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3
Q

Adult muscle cells are in what state of division. What does this mean?

A

They are in a post-mitotic state. This means that they are capable of adaptation but not division.

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4
Q

Muscles add bulk by _____

A

hypertrophy, addition of proteins

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5
Q

With disuse, muscles will ______

A

atrophy; loss of cells

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6
Q

Strength training muscles will add more ________, result in more __________.

A

Strength training will add more actin and myosin, resulting in the formation of more myofibrils. Can also add more nuclei.

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7
Q

Hypertrophied muscle nuclei are connected to _______/

A

Muscle memory .: Muscles trained at an earlier time, return to earlier strength w/ less effort than before

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8
Q

Leg muscles of distance runners develop…

A

more and larger mitochondria, making more ATP.

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9
Q

Endurance training can cause the formation of more _____ around their muscles.

A

Capilaries

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10
Q

How do muscles from endurance training differ from that of strength training.

A

They (endurance training muscles) do not have the hypertrophy of strength training athletes.

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11
Q

Muscle phenotypes depend on….

A

it’s actions

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12
Q

Slow twitch muscle fiber characteristics:

A

narrow diameters, using aerobic metabolism, predominates in endurance exercise

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13
Q

example of endurance exercise

A

long-distance running, cycling, and swimming

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14
Q

slow twitch muscle fibers action and forces

A

repetitive actions and low forces; economically apply isometric force and involved isotonic contractions

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15
Q

example of strength traning

A

stair running or weight-lifting

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16
Q

strength training uses what type of muscle fibers

A

fast-twitch muscle fibers

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17
Q

Fast-twitch muscle fibers use what type of metabolism

A

anaerobic (without oxygen)

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18
Q

repetition and forces of strength training

A

fewer repetitions and larger forces

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19
Q

different muscle fibers have different _______. What does this influence?

A

isoforms; influence the muscles functional properties

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20
Q

2 important molecules for muscle fibers

A

myosin heavy chain and the thick filament and the Ca2+-ATPase pump of the SR

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21
Q

SO type 1 fibers

A

have many mitochondria and are fatigue resistant

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22
Q

FOG muscle fibers

A

have fatigue resistance

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23
Q

4 main characteristics of FG fibers

A

contract 10x faster than SO, have few mitochondria, large diameters, and fatigue quiclkly

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24
Q

Motor units are made up of…

A

each muscle type with the motor neurons that connect them

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25
Q

How can motor units be converted?

A

Can be converted from one type to another by cross-innervation

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26
Q

Motor units recruit in a fixed order:

A

SO, FOG, and lastly FG

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27
Q

what determines a muscles’s contractile performance?

A

power output, which changes in response to use and disuse

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28
Q

how is mechanical power generated determined?

A

forced produced in a muscle multiplied by the velocity of shortening

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29
Q

velocity of shortening _______ as the load _______.

A

decreases, increases

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30
Q

Power output of most muscles is maximal when…

A

the muscle shortens to 20-40% of Vmax

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31
Q

power is measure in what unit?

A

watts

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32
Q

Endurance training elicits….

A

changes in fiber type, increasing capillary density and mitochondrial density

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33
Q

Normal people have what ratio of fast to slow muscle fibers

A

50/50

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34
Q

Marathoners have much higher ________ fibers and few _____.

A

higher slow fibers and few fast fibers

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35
Q

Sprinters have more _______ fibers

A

fast fibers

36
Q

exercise training can cause…

A

increases in capillary density, increases in mitochondrial density, a convergence between fiber types, especially types IIa and IIx

37
Q

endurance training leads to what change in capillaries?

A

can lead to a larger number of capillaries contacting muscle

38
Q

angiogenesis

A

the vascularizing of the muscle

39
Q

vascular endothelial growth factor

A

produced by exercised muscles, stimulates angiogenesis

40
Q

Mitochondria in response to endurance training

A

endurance training increases the number of mitochondria

41
Q

Changes mitochondria that lead to less fatigue

A

changes in the structural and enzymatic proteins of the mitochondria

42
Q

more mitochondria allow the cells to…

A

use more oxygen

43
Q

How do new mitochondria get fuel? What does this allow for?

A

use more fat as fuel instead of glucose; saves glycogen and produces less lactic acid

44
Q

3 types of genes that contribute to muscle phenotypes

A
  • contractile protein genes (myosin isoforms)
  • angiogenesis genes (growth factors like VEGF)
  • mitochondrial genes
45
Q

what does transcriptional coactivator PGC-1a do

A

coactivates a number of transcriptional factors; enhances mitochondrial biogenesis, muscle fiber conversion, and angiogenesis

46
Q

PCG-1a1 is required for

A

production of VEGF and angiogenesis

47
Q

What does B-adrenergic sympathetic stimulation happen with

A

happens with exercise, induces PGC-1a1

48
Q

resistance/strength training causes? What does it not cause?

A

It causes changes in hypertrophy and changes in fiber types and it does NOT cause increases in aerobic capacity or capillary density at muscles

49
Q

strength training can result in? What does this mean? What affect does detraining have?

A
  • fiber type changes, gene expression changes, type IIa over IIx
  • This means there is a decreased amount in myosin heavy- chain (Mhc) IIX and increased amount of myosin heavy- chain IIa
  • De training has the opposite effect with Mhc IIx levels increasing beyond pre- training values
50
Q

PGC-1a4 is made with strength training and what does this isoform do?

A

this isoform downregulates myostatin and upregulates IGF-1

51
Q

combined resistance and endurance training can…

A

improve performance

52
Q

hypertrophy can also occur in ______ muscles. When else can it occur?

A

cardiac; occurs during development, but also with exercise and pregnancy

53
Q

how does cardiac muscle hypertrophy occur?

A
  • proteins are added to myofibrils
  • adds sarcomeres to myofibrils
  • results in thicker heart walls and larger heart chambers, especially the left ventricles
54
Q

hypertrophy of cardiac muscles result in

A
  1. enhanced cardiac function
  2. more oxygen taken up by myocytes
  3. higher force and speed and contraction
  4. greater stroke volume
55
Q

Effects of endurance exercise on the heart

A

makes greater wall thickness and internal diameter of the heart

56
Q

Effects of strength/resistance training on the heart

A

increases wall thickness

57
Q

effects of pregnancy on heart

A

blood volume may increase by 50%

58
Q

effects of hibernation on heart

A

decrease in heart rate, ventricular tissues atrophies 26%, and pathological atrophy may occur with high BP

59
Q

unused muscle will

A

break down

60
Q

major cause of atrophy

A

enzymatic breakdown of proteins

61
Q

response to muscle atrophy

A

both mitochondria and nuclei decrease, less actin mRNA, cytochrome C mRNA, and oxidative enzymes

62
Q

humans experience atrophy in

A

microgravity; disuse atrophy from weightlessness during space travel

63
Q

17 days in space resulted in what changes in muscles (results were taken before and after the trip)

A

Muscle size and strength decreased: soleus muscle was 70% type I fibers, loss occurred in both thick and thin fibers, decrease in fiber diameters (even though sarcomere length was similar in both samples)

64
Q

161-192 day space flights resulted in

A

20% decrease in type I fibers, fiber composition changed from slow to fast

65
Q

starting at age 40, humans lose how much muscle mass?

A

1-2% muscle mass each year

66
Q

What is sarcopenia? What is a key factor?

A

age related muscle loss, death of motor neurons in the spinal cord is a key factor and debranching is a part of it

67
Q

what percent of motor neurons die by normal aging?

A

10-15%

68
Q

muscle mass loss can cause issues with

A

balance and posture, resulting in falls and injury

69
Q

what can help slow muscle mass loss in old age

A

continued strength training

70
Q

endurance training can lessen

A

loss of mitochondria, helping with cell metabolism

71
Q

what type of diet can help retain muscle?

A

nutrition with plenty of protein

72
Q

some animals experience little or no disuse atrophy: how? Muscles lost accounts for what percentage of their strength?

A
  • bears (hibernate 5-7 months and although inactive have little disuse atrophy); may recycle nitrogen from urea into amino acids used in protein synthesis
  • 25-30% of their strength
73
Q

maintaining muscle mass is important for

A

controlling homeostasis

74
Q

myostatin

A

growth factor (GDF-8), controls muscle mass; negative regulator, its inactivity results in more muscle mass

75
Q

animals with GDF-8 mutation

A

“double muscled”, both copies of the gene normal are thin; humans with mutation would be very strongly muscled

76
Q

PI3K-Akt1 pathway

A

Akt1 controls the balance between synthesis and atrophy a protein kinase cell signaling enzyme with a role in protein synthesis and cell survival; its role can be stimulate by use or not and hormones

77
Q

IGF-1

A

stimulates PI3K and Akt1

78
Q

Akt1 is activated by

A

phosphorylation; stimulates protein synthesis and then also acts as a negative regulator in the nucleus

79
Q

GH and androgens

A

also stimulate protein synthesis

80
Q

When the muscle is inactive and leads to atrophy what is happening?

A

the PI3K-Akt1 pathway isn’t function, Akt1 is suppressed by glucocorticoids from the stress response

81
Q

Mechanical power=

A

Force produced in a muscle x shortening velocity

82
Q

What is shortened velocity influenced by?

A

The myosin isoforms expressed by the motor units of the muscle

83
Q

Power is the product of…..

A

force and velocity

84
Q

What is maximum forced produced by a muscle proportional to?

A

The cross- sectional area of the contractile elements

85
Q

Steps in P13K- AKt1 pathways

A
  1. Strength work stimulated IGF-1 release: When muscle exerts force on a load, it secretes IGF-1, which binds its receptor and triggers molecular pathways for protein synthesis
  2. IGF-1 stimulated P13K and AKt1
  3. AKt1 is activated by phosphorylation
  4. This stimulates protein synthesis and then also acts a negative regulator in the nucleus