block 9- drugs in sports Flashcards
(24 cards)
anabolic agents
-Promote metabolism & synthesis of complex molecules
-Enhance skeletal muscle mass and bone
-Most commonly steroids (stanozolol = 15% of steroids)
-endogenous naturally occurring* testosterone and substances in metabolic pathways .Exogenous* derivatives of testosterone
-acts directly on androgen receptors
-banned at all times
testosterone
- has both androgenic effects= masculinization
anabolic effects=protein building in skeletal muscle and bone - higher percentage in men
testosterone-cellular signalling
-Testosterone binds to the androgen receptor located in the cytosol and has a chaperone/accessory protein
-binding causing the release of the androgen receptor from the chaperone protein
-adrogen receptor free to translocate from cytosol to nucleus
-in the nucleus acts as a transcription factor=regulates the transcription of genes
changing the chemistry of testosterone
Chemical modifications are made to testosterone to:
Slow its inactivation in the body
Alter metabolic pathways (e.g., reduce breakdown by the liver)
Increase lipid solubility → allows for injection with slow release
Boost the anabolic:androgenic ratio → maximize muscle-building effects while minimizing masculinizing effects
effects of testosterone administration on muscles
-increased muscle volume = found in MRI scams of quads
-iIncreased cross-sectional area of type I (48%) andtype II (36%) fibres (ie. fibre hypertrophy)- no difference in proportions = seen in muscle bippsies
Increased myonuclear number
What are these morphometric changes associated with?-GUESS
Reduced amino acid export (increased reutilization?)* Increased protein synthesis* Increased androgen receptor expression
what does fibre hypertrophy and hypoplasia account for-COME BACK
They both contribute to increased muscle strength through:
Fiber hypertrophy: ↑ size of existing muscle fibers
Fiber hyperplasia (to a lesser extent in humans): ↑ number of muscle fibers
Enhanced Ca²⁺ handling:
Greater release from sarcoplasmic reticulum
Possible ↑ sensitivity of contractile proteins to calcium
Changes in muscle architecture:
↑ pennation angle (fiber orientation) → allows more fibers to pack into a given muscle area, enhancing force generation
muscle pennation
In pennate muscles, fascicles (muscle fibers) attach to the tendon at an angle rather than running straight
This arrangement:
Allows for more muscle fibers in a given area → greater force production
Comes at the cost of a smaller range of motion and slower shortening speed
issues associated with Anabolic steroids
abnormal developmentof male sexual characteristics)Severe and can be irreversible1986European Champion(aged 20)Heidi KriegerDepression, attempted suicide,gender reassignment in mid 1990s
how can anabolic steriods increase exercise tolerance?
- gives you the ability to work harder for longer
-decrease muscle damage and so increase fatigue reststance
-increases collagen syntheis sand bone mineral density - additive effects=exercise increases androgen receptor expression in skeletal muscle- may therefore enhance effects of AAS
What are the complementary anabolic actions that support muscle growth and performance?
Possible antagonism of glucocorticoids:
Androgens may block or reduce the muscle-wasting (catabolic) effects of stress hormones like cortisol
They bind (weakly) to glucocorticoid receptors, but the real significance of this is still unclear
Stimulation of the GH–IGF-1 axis:
Androgens can increase secretion of growth hormone (GH) from the anterior pituitary
GH then stimulates the liver to produce IGF-1, which promotes muscle protein synthesis and growth
Psychoactive effects:
Increased energy, motivation, aggression, and mood may indirectly support harder training
⚠️ But negative psychological effects (e.g., irritability, mood swings) are also possible
side effects of AAS
-not that important lol but cann look up off you care.
how can people avoid the drug beeing detected via drug testing
-Drink lots to dilute urine sample DiureticsA dding chemicals to urine samples Sample substitution’ Toxin removers’ (consumed)Devices (often designed to deliver a fake urine sample)-design drugs that are not detectable
stimulants
-increase alertness, self-confidence and concentration
-activate the CVS, reduce fatigue and feeling of increased energy
-mixed evidence of increased speed, power,endurance and concentration
-generally activate the sympathetic nervous system fight or flight response e.g. increased HR = seen as a potentially unfair advantage
-prohibited in competitions
why are stimulants difficult to avoid ?
-effects are temporary and difficult to avoid
-diet (e.g. coffee or over the counter medicines)
-produced by metabolism of other compounds
different types of stimulants
CNS stimulants: little effect on mental function, increase activity of respiratory and vasomotor centres, increase reflex excitability – little used in sport
Psychomotor stimulants: excitement and euphoria, increase motor activity,reduce
fatigue=Includes: amphetamines, cocaine and methylxanthines eg. caffeine
Sympathomimetic amines: potentiate effects of sympathetic NS
use of amphetamines in sports
Performance-enhancing effects (considered an unfair advantage):
Peripheral effects (early exercise phase):
↑ Cardiac output
↑ Blood flow to muscles
↑ Energy availability (mobilizes stored fuel)
↓ Gut motility (less digestive interference during performance)
Central nervous system effects:
↑ Locomotor activity (movement)
Feelings of euphoria, alertness, and excitement
↓ Appetite (anorexia)
May cause repetitive or stereotyped behaviors
⚠️ Significant risks and side effects, including addiction, heart problems, anxiety, and potential for disqualification
amphetamines structure
Structurally similar to noradrenaline (norepinephrine) and dopamine
Act as indirect sympathomimetics:
Don’t directly bind to receptors like those neurotransmitters
Instead, they increase the release or block the reuptake of noradrenaline and dopamine
Mimic the sympathetic nervous system (“fight or flight” effects)
Can be chemically modified (e.g., MDMA/ecstasy) to alter potency or detectability
why would a person not just take noradrenaline and dopamine to activate the sympathetic nervous system and not amphetamines?
Because noradrenaline and dopamine are rapidly broken down in the body:
Metabolized immediately by enzymes like MAO (monoamine oxidase) and COMT (catechol-O-methyltransferase) in the gut and liver
This makes them ineffective when taken orally
In contrast:
Amphetamines are chemically stable and resistant to MAO/COMT
They are orally active, can be snorted, and are well absorbed through the small intestine
They act indirectly, increasing the release and availability of noradrenaline and dopamine in the brain
generally how does neurotransmitters work into the synapse with the case of MAO
-MOA (monoamine vesicles) are synthesised locally within pre synaptic cell and packaged into vesicles.
-when the membrane is depolarised, calcium influx= cause the fusion of vesicle to the synaptic cell= neurotransmitter into the synaptic cleft which interacts with the post-synaptic cell and has an effect
-need to be able to release neurotransmitter quickly and remove quickly to be able to reuse the synapse e.g. atch which is broken done in the synaptic cleft
-MAO is removed by transported by uptake which takes it back into the pre synaptic cell or uptake 2 which takes MAO into support cells where it can be broken down by enyzymes
how do amphetamines work?
Site of action: Amphetamines do not act at the neuromuscular junction (where nerves meet muscles)
→ They work primarily in the brain, spinal cord, and autonomic nervous system
Cell entry:
Enter presynaptic neurons via Uptake-1 transporters or by diffusing across the membrane
Main effect:
Trigger the release of noradrenaline and dopamine by:
Entering vesicles via vesicular monoamine transporters (VMAT)
Displacing neurotransmitters, pushing them out into the synaptic cleft
May also block reuptake of neurotransmitters, but release stimulation is the dominant effect
Additional effect:
May inhibit MAO enzymes, slowing the breakdown of noradrenaline and dopamine
➤ Overall: They indirectly stimulate the sympathetic nervous system by flooding the synapse with neurotransmitters
TAARS and amphetamine action
-TAAR= trace amine-associated receptors
-amphetamines have the ability to activate TAAR receptors
-results in the inhibition of uptake 1 and so more neurotransmitter and less uptake
effects on ampetamines on athletic performance
-taken to enhance mood and perfoemance
-evudence is sparse some people report it to increase strength md anaerobic capacity etc
-acute side effects = increased HR and BP
-diso=tortion of reality and time perception=misjudgemment
-chronic side effects = paranoia,blood vessel damage etc…
clinical uses of amppphetamine
-know vaguely
-Clinical uses of amphetamine
ADHD (attention deficit hyperactivity disorder; particularly in children)
Mechanism(s) unclear – may involve dopaminergic pathways
Go to fullsize image
Narcolepsy – patients suddenly & unpredictably fall asleep
Genetic or developmental abnormalities in brain catecholamine regulation
Amphetamines used to prevent excessive daytime sleepiness
Often combined with:
* sleep hallucinations
* sleep paralysis
* cataplexy (sudden uncontrollable loss of
muscle tone/control)
Ocular actions – dilate pupil and reduce intraocular pressure
Nasal decongestants – vasoconstriction to reduce mucosal swelling
Chronic fatigue syndrome Poorly understood condition - muscle and joint pain, cognitive difficulty, chronic mental and physical exhaustion.
