MT1 Flashcards

0
Q

What is an athlete’s phenotype determined by

A
  1. Their genes (can’t change)
  2. How much of each gene is made into RNA
  3. How much of each RNA is made into protein
  4. How active the protein is
    - -> can change 2-4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What is phenotype

A

Genotype and environment (what you see)

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

How do you get from DNA to protein?

A

Transcribe DNA to hnRNA, then process hnRNA to mRNA
Translate mRNA to a nascent protein
Post translational modification of a nascent protein to an active protein

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

What is translation

A

mRNA to protein

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

What is transcription

A

DNA to mRNA

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

What is a SNP

A

Single nucleotide polymorphism

= variation of the sequence of a gene by one base pair

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

If you change your DNA you change your ?

A

Performance

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

What is DNA

A
  1. Two strands of genetic code
  2. Made up of sugars and phosphates (backbone) and nucleotides or bases (rings of the ladder)
  3. The 4 bases in DNA are
    • cytosine (C)
    • guanine (G)
    • adenine (A)
    • thymine (T)
  4. The bases compliments each other such that A binds to T and C to G
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the human genome

A
  1. Contains ~3.1467 billion base pairs
  2. This DNA is stored into 23 chromosome pairs
  3. These 23 chromosomes contain approximately 24000 genes
  4. These 24000 genes encode for between 300000 to 2 million proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are chromosomes made up of

A

Genes

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

DNA packaging affects what?

A

Gene expression

- a more “open” DNA is easier to make more DNA of

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

What are the two types of gene sequences

A

Exons

Introns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Exons

A

Made into mRNA

EXons are EXpressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Introns

A

Are spliced out; important for stability and protein make up

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

Promoter

A

Tells is how much, when, and where to make the mRNA

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

What is a nascent protein

A

An inactive protein, does nothing

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

What is epigenetics

A

Lifestyle and environment - how your environment affects your genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does epigenetics affect our genetic code

A

While our DNA code in our genes does not change, our lifestyle and environment can affect how our genes are expressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is DNA expression controlled

A

By DNA methylation and acetylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Epigenome

A

Which genes are made into RNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What can epigenetics help explain

A
  • lasts longer than the training effect
  • “muscle memory”= someone who has trained in the past gains muscle mass and/or endurance faster than someone who hasn’t
  • some of the effects of living/running at altitude
  • altered epigenetics could explain why taking PEDs at one point might improve training/performance much later in life, after the direct effect (and detection) of the drug is long gone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

General function of insulin receptor

A

Moves things to membrane
Or
Scaffolding/docking protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

General function of S6K1

A

Protein kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

General function of Raptor

A

Identifies substrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

General function PI3K

A

Lipid kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

General function of mTOR

A

Protein kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

General function of PIP3

A

Moves things to membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

General function Vps34

A

Moves membranes
Or
Lipid kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

General function of Rag A

A

Moves things to membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

General function mSIN1

A

Moves things to membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

General function Notch

A

Change transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

General function Rictor

A

Identifies substrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

State the overload principle

A

Strength gains occur with systematic and progressive resistance of sufficient frequency, intensity and duration to cause adaptation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

In general, how does “epigenetics” decrease expression of a gene?

A
  1. As we change our environment (training, PEDs, etc) this can change our Epigenome (which genes are made into mRNA)
  2. This is controlled by DNA methylation and acetylation
  3. To decrease expression of the gene epigenetically we would close the DNA around a specific promoter by altering the degree if methylation/acetylation
34
Q

What are the ways that we can decrease transcription of a gene?

A
  1. Close the chromatin by demethylating/acetylating DNA
  2. Make less of an activator or more of a repress or
  3. Make less of a co-activator
  4. Decrease the activity of an activator
  5. Increase the activity of a repressor
  6. Move an activator out of the nucleus or move a repressor in the nucleus
35
Q

Briefly, how do amino acids increase mTORC1 activity?

A
  1. Amino acids enter the cell through an AA transporter
  2. The increase in aa in the cell causes Rag A/B to bind to GTP and activates Vps34
  3. Rag A/B boun pd to GTP is active, binds to raptor and moves mTOR to Rheb (Rab7 positive membranes)
  4. When together with Rheb, mTOR becomes activated and phosphoralates S6K1 and 4EBP
  5. Active Vps34 causes the Rab7 positive membrane to move around more
  6. This increases the likelihood of mTOR interacting with Rheb, activating mTOR
36
Q

Why does IGF-1 gene expression in muscle cause muscle growth when increasing circulating IGF-1 does not?

A
  1. Over-expressing IGF-1 in muscle increases the amount of IGF-1 in a muscle 47 fold without changing IGF1-1 in the muscle
  2. Increasing circulating IGF-1 by taking growth hormone results in only a 4 fold increase
  3. Over expressing the gene also keeps IGF-1 high 24 hours/day
  4. With continuously high IGF-1 levels there is continuously high mTORC1 activity, whereas a transient increase has little effect in mTORC1
37
Q

In elite athletes, what is the best predictor of endurance performance? How would you measure it?

A
  1. In elite athletes, the best predictor of endurance performance is power/velocity at lactate threshold
  2. This is measured by performing a graded exercise test while measuring blood lactate
  3. Power/velocity at lactate threshold is the power/velocity when lactate begins to accumulate at greater than linear rates with increased intensity
38
Q

Will AAS increase muscle mass?

A

Yes they will

39
Q

How do AAS increase muscle mass

A
  1. Increase protein synthesis
    - mechanism at this point is unknown, but AAS do result in an increase in mTORC1 activity
  2. Decreased protein degradation
    - competitive inhibitor of the cortisol receptor
    - by decreasing cortisol binding of the receptor this results in a decrease in atrogenes and other genes that induce muscle breakdown
40
Q

What precautions do you give a male athlete considering taking AAS

A
  1. Using steroids will decrease the length of your career due to injury
  2. AAS will increase aggression. This is good for batting (increases reaction time) but bad in day to day life
41
Q

Why is taking AAS bad

A
  1. While the steroids have a positive effect on muscle mass and strength, they have a negative effect on connective tissue
  2. The result is that the incidence of significant injury is much greater than someone who does not use steroids
  3. Ethics/getting caught
42
Q

What is transcription

A

The conversion of genetic code of a gene from DNA into RNA

- going from storage form of the code to functional form

43
Q

What is an enhancer

A

Binds proteins to enhance transcription

44
Q

What is a silencer

A

Binds proteins to repress transcription

45
Q

What is the promoter

A

The region of the DNA that signals how much RNA will be made from the gene

46
Q

What are transcription factors q

A

Protein factors that bind to DNA and change the rate of transcription

47
Q

What are co activators

A

Protein that do not bind DNA, but adjust the activity of transcription factors

48
Q

What is RNA degradation controlled by

A
  1. Processing
    - capping
    - polyadenylation
    - splicing
  2. Modulating RNA stability
  3. MicroRNA
49
Q

What is initiation

A

The small ribosomal subunit binds to the mRNA cap and then scans to find the start site. At the start site, it is joined by the big subunit to make the ribosome. Translation begins.

50
Q

What is elongation

A

The ribosome translates th RNA code into an amino acid sequence (protein). Fr every 3 pieces of RNA (codon) a specific amino acid is added to the end of the protein chain

51
Q

What is termination

A

The ribosome reaches a stop codon and the protein is released

52
Q

How does mTORC1 regulate initiation of translation

A

It phosphoralates 4EBP and S6K1

53
Q

What are post transcriptional modifications

A
  1. Phosphorylation/de phosphorylation
  2. Acetylation/ de
  3. Ubiquitination
  4. Oxidation/reduction
  5. Ligand/nucleotide binding
54
Q

What is Ubiquitination

A

It target a a protein for degradation, it acts like a tag marking the protein to be degraded.

55
Q

What causes hypertrophy

A

Load

56
Q

What are the three aspects of strength

A
  1. Size
  2. Neural components
  3. Connective tissue
57
Q

What does IRS1 bring to the membrane

A

PI3Kinase

58
Q

What is PI3K target?

A

PIP2, makes it into PIP3

59
Q

What does pip3 bring to the surface

A

PDK1

PKB

60
Q

What does PDK1 do

A

Phosphoralates pkb

61
Q

What does PKB do. How does it get activated

A

When it is phosphoralated by both PDK1 and mTORC2 then it can inhibit the inhibitors

  • phosphorylates and inhibits TSC1/2 complex
  • phosphorylates and removed PRAS40 from mTORC1
62
Q

What does growth hormone do

A

It has NO DIRECT effect on muscle size and strength

  • it actually increases the amount of water you hold in your body, so your muscles appear bigger
  • it does improve your ability to recover
63
Q

Briefly, how does the resistance exercise pathway work

A

By some unknown mechanism, resistance reservist phosphorylates TSC1/2 complex and moves it away from the lysosomes
- when it moves away, Rheb is now GTP bound and can activate mTORC1

64
Q

How is the majority of force transferred

A

Laterally

65
Q

What do actin and myosin do

A

They create force, but do not produce tension

66
Q

What are mechanoreceptors? What are their function with mTOR?

A
  • length sensors (costameric proteins)
  • tension sensors (Titin, Muscle Lim protein)
  • stretch activated channels
    => an increase in any/all of these lead to TSC1/2 being phosphorylates and mTOR being activated
67
Q

What happens when you lose dystrophin

A

You get a large decrease in lateral force transmission and more injuries

68
Q

What is testosterones main effect

A

Blocking glucocorticoids therefore blocking protein breakdown
- testosterone also increases the number of satellite cells

69
Q

What is myostatin. What does it do

A

A feedback protein that regulates the amount of muscle you have

  1. Controls muscle fiber number
    - regulates muscle fiber proliferation
  2. Controls muscle fiber size
    - regulates mTOR activity
    - regulates transcription of genes important in growth
70
Q

What does training do with myostatin

A

It decreases myostatin. mRNA

71
Q

Myostatin pathway summary

A

Myostatin binds to ALK and ActIIB together, when ALK is bound to myostatin it phosphorylates Smad 2/3. With Smad 2/3 phosphorylated, it can bind to Smad 4. Smad complex enters nucleus and decreases transcription

72
Q

What inhibits myostatin

A

Ski, sno and notch inhibit the Smad complex in the nucleus

73
Q

GPF5 pathway summary

A

GPF5 binds to ALK3 and BMPR1 and when bound ALK3 phosphorylates Smad 1/5/8. This can bind to Smad 4 and this Smad complex goes into the nucleus and activates Mighty. Like a protective mechanism, keeps am injured muscle from shinr I making away to nothing
Also, helps set your baseline. Someone with more Smad 1/5/8 will be a bigger individual

74
Q

Smad signaling competition

A

Whether there is more Smad 2/3 or Smad 1/5/8 determines which Smad that Smad 4 binds to.

75
Q

As you increase exercise intensity which fuel do you primarily use

A

Sugars, carbs,

76
Q

At lower. Intensity of exercise, which fuel source of you use most

A

Fat

77
Q

If you have higher sympathetic nervous system activity, which fuel source is used

A

More sugar

78
Q

How does diet and exercise history dictate fuel use

A

If in a high fat, low carb diet you have more fat so more likely to breakdown fat as fuel
- more endurance exercise = more mito, so more fat as fuel

79
Q

How does blood flow dictate fuel use

A

A decrease in blood flow caused by Sns stimulation (vasoconstriction) causes a decease in flow to adipose tissue so less fat used

80
Q

What does epinephrine stimulate for fuel purposes

A

It similes glycogen phosphatase= breaks down glycogen into glucose
- more flucosw because of epinephrine so a decrease in need for fat

81
Q

Lots of epinephrine stimulate what

A

Alpha adronergic receptors, causes vasoconstriction, less blood flow to everywhere except muscle because muscle metabolizes override the stimulation and cause local vasodilation

82
Q

How do you calculate Vo2 max

A

SVmax x HRmax x a-Vo2

- SV is what we can change to increase our Vo2 max