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Exercise Physiology and Pharmacology > Drugs in Sport > Flashcards

Drugs in Sport Flashcards

1
Q

What is the most common type of drug abused in sports?

A

Anabolic agents

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2
Q

What do anabolic agents dd?

A

They promote metabolism and synthesis of complex molecules.

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3
Q

Why do athletes use anabolic agents?

A

They enhance skeletal muscle mass and bone.

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4
Q

Give examples of anabolic agents.

A

Steroids like stanozolol.

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5
Q

What are endogenous anabolic agents?

A

Those that occur naturally like testosterone and other substances in metabolic pathways.

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6
Q

What are exogenous anabolic agents?

A

Those that are man-made like derivatives of testosterone.

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7
Q

What does testosterone interact with?

A

An androgen receptor.

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8
Q

What effects are driven by an activated androgen receptor?

A

Androgenic and anabolic effects.

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9
Q

What are anabolic effects?

A

Protein building in skeletal muscle and bone.

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10
Q

What are androgenic effects?

A

Masculinization in which more masculine features appear.

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11
Q

Where is testosterone in men?

A

The testes

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12
Q

What molecules can be turned into testosterone? Where are they produced?

A

Weak androgens like androsterone and androstenediol that are produced in adrenal glands or ovaries.

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13
Q

What molecule has a higher affinity for the androgen receptor?

A

5 alpha-dihydrotestosterone

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14
Q

Can testosterone be converted into 5 alpha-dihydrotestosterone?

A

Yes, using 5 alpha-reductase

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15
Q

Where can testosterone not be converted into 5 alpha-dihydrotestosterone?

A

In the skeletal muscle because it doesn’t have 5 alpha-reductase.

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16
Q

What are plasma testosterone levels?

A

300-1300 ng/dl (10-50 nM)

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17
Q

How does the female levels of testosterone levels compare to males?

A

Females have 10% of those in males.

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18
Q

How is testosterone found in the bloodstream?

A
  1. Strongly bound to sex hormone binding globulin (SHGB)
  2. Weakly bound to albumin
  3. Unbound
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19
Q

Where is the androgen receptor located?

A

In the cytosol bound to a chaperone/accessory protein.

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20
Q

Explain cellular signaling with testosterone.

A
  1. Testosterone binds to the androgen receptor in the cytosol
  2. This induces a conformational change that releases its chaperone protein
  3. Testosterone x androgen receptor complex diffuse into the nucleus
  4. Dimerizes
  5. Complexes can form around it like co-regulators and transcriptional machinery
  6. This allows for the complex to regulate gene expression
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21
Q

How can testosterone signalling regulate non-genomic effects?

A

The testosterone x androgen receptor complex activates ERK1/2 proteins, which acts as a transcription factor.

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22
Q

Explain testosterone/oestrogen signalling through membrane-bound receptors.

A
  1. Testosterone/oestrogen binds to a membrane-bound receptor (GPCR)
  2. Activates PLC
  3. IP3 is released and binds to ER to release calcium
  4. More calcium = more force = less fatigue
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23
Q

What can testosterone be converted into for women?

A

Oestrogen

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24
Q

What other molecules act on androgen receptors?

A

Anabolic-androgen steroids (AAS)

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25
Q

What happens if you change the hydroxyl group of the cyclopentane ring of testosterone?

A

It changes the bioavailability (absorption/degradation) of the molecule.

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26
Q

What happens if you change the bottom two cyclohexane rings of testosterone?

A

Changes are associated with increased anabolic activity.

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27
Q

Why change the chemistry of testosterone?

A
  1. Slow inactivation
  2. Change the pattern of metabolism (reduce degradation)
  3. Increase lipid solubility (injection and slow release)
    (ALL affect administration routes)
  4. Increase anabolic:androgenic ratio
28
Q

How does stanozolol compare to testosterone in terms of anabolic effects?

A

Much much better with a ratio of anabolic:androgenic affects at 30 compared to testosterone’s 1.

29
Q

How is stanozolol taken?

A

Orally

30
Q

What are the effects of testosterone on muscle?

A
  1. Increase muscle volume
  2. Increase in cross-sectional area of type I and type II fibres (hypertrophy; getting bigger/no difference in proportions)
  3. Increase fibre number (hyperplasia)
  4. Increased lean body mass
  5. Increase in myonuclear number
31
Q

Why is the increase in myonuclear number important?

A

An increase in nuclei means the muscle has more control over protein synthesis and genetic regulation.

32
Q

For the changes in muscle and nuclei associated with testosterone, what comes with it?

A
  1. Increased protein synthesis
  2. Reduced amino acid export
  3. Increased androgen receptor expression
  4. Enhanced released of calcium release from SR and changes in calcium sensitivity of contractile proteins
  5. Changes in muscle architecture like increased pennation
33
Q

What is muscle pennation?

A

The way in which the muscle attaches to the tendons. Fascicles attach in a slanting position to the tendons to allow a higher force but smaller range of motion.

34
Q

What are effects of AAS on females?

A

The produce abnormal development of male sexual characteristics, but also increased distance in terms of strength in their sports.

35
Q

How can anabolic steroids increase exercise tolerance?

A

They decrease muscle damage, and increase both work capacity/fatigue resistance.

36
Q

How are exercise and AAS additive?

A

Because exercise increases androgen receptor expression in skeletal muscle, and thus may enhance the effects of AAS.

37
Q

How are AAS anti-catabolic?

A

Androgens bind with low affinity to glucocorticoid receptors, turning down their ability to perform catabolic actions.

38
Q

What hormones does AAS stimulate?

A

It stimulates the growth hormone-insulin-like growth factor-1 (IGF-1) axis, in which there is a stimulation of GH secretion in the anterior pituitary and a stimulation of hepatic IGF-1 production.

39
Q

What does the stimulation of IGF-1 do?

A

It stimulates muscle formation.

40
Q

What effects does AAS have on the brain?

A

Psychoactive effects like feelings of energy, elevated mood, and aggressiveness.

41
Q

What are the the side effects of AAS?

A

To name a few:
- testicular atrophy (loss)
- cardiovascular disease like stroke or blood clots
- liver dysfunction
- cancer

42
Q

What do stimulants do?

A

They increase alertness, self-confidence and concentration, activate the CNS, reduce fatigue, increase the feeling of energy, and decrease appetite.

43
Q

Why might a stimulant be a performance enhancer?

A

It increases speed, power, endurance, and concentration.

44
Q

What are examples of stimulants?

A

Amphetamine and cocaine.

45
Q

What are stimulants known as?

A

Sympathomimetics, thus increasing our flight/fight responses.

46
Q

CNS stimulants

A

Increase activity of respirator and vasomotor centres.

47
Q

Psychomotor stimulants

A

They increase excitement, euphoria, and motor activity, and decrease fatigue.
ex. amphetamines

48
Q

Why are amphetamines in sports considered unfair?

A

They help in the early stages of exercise (peripheral actions) in which there is an increase in cardiac output, increased blood flow to muscles, and mobilizing energy (inhibition of gut motility).

49
Q

What are monoamines metabolized by?

A

MAO and COMT in the GI tract and liver.

50
Q

What are amphetamines resistant to?

A

MAO

51
Q

What is the advantage of amphetamine in terms of bioavailability?

A

Because they can be taken orally, they are fast acting. For example, they have effects about 1-2 hours after administration.

52
Q

How do MA agents work?

A
  1. Action potential depolarizes the membrane
  2. Calcium flows into the cell
  3. Allows for vesicles to bind to membrane and release MA into the cleft
  4. Interact with post-synaptic receptors
  5. Can act with pre-synaptic to inhibit packing
  6. In cleft, taken back in pre cell for packing or MAO degradation, COMT degradation in the cleft, or taken into post cell
53
Q

How do monoamine-mimetic agents work?

A
  1. Block re-uptake
  2. Enhance release
  3. Actions on pre or post-synaptic receptors
  4. Inhibition of breakdown (MAO)
54
Q

Where does amphetamine act on in the body?

A

Brain, spinal cord, and peripheral sites. NOT a neuromuscular junction.

55
Q

How does amphetamine work at postsynaptic receptors?

A

It has a weak agonism, works at a low affinity to drive their response.

56
Q

How does amphetamine cause blockage of uptake?

A

They can be taken in by uptake 1 mechanisms, reducing uptake of the MA, thus increasing amount in the synapse.

57
Q

How do amphetamines interact with vesicles?

A

They are brought in by a vesicle monoamine transporter (VMAT) and displace the monoamines (NO). Amphetamines are weak bases that increase pH of VMAT to release MA.

58
Q

How does amphetamines interacting with VMAT aid in response?

A

The MA that is removed from the vesicle can leave the presynaptic cell by reversal of uptake mechanisms.

59
Q

Why do amphetamines inhibit MAO?

A

They look similar to monoamine agents.

60
Q

What is the purpose of inhibiting MAO?

A

Less MA metabolized and more attributing to the high concentration in the cytosol and be removed into the cleft.

61
Q

Give examples of monoamines.

A

Dopamine, serotonin, histamine, and noradrenaline.

62
Q

What are trace amine associated receptors?

A

GPCRs, specifically G alpha s, expressed in the CNS dopaminergic and adrenergic nuclei.

63
Q

How do trace amino associated receptors work?

A
  1. Amphetamine interact with TA1 on the membrane of presynaptic cells
  2. The G alpha s subunits dissociates and increases the level of cAMP
  3. Phosphorylation-dependent signalling
  4. Inhibition and internalization of uptake 1 = less MA taken away from synapse
64
Q

How does amphetamine act on performance?

A

Increase strength and anaerobic capacity, increase fatigue resistance, and decreased run times.

65
Q

What are the side effects of amphetamine?

A

Increased heart rate and blood pressure, headaches, distortion of reality and time perception, ruptured blood vessels in the brain and heart, paranoia, etc.

66
Q
A

Exercise Physiology and Pharmacology (9 decks)

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