block 3-muscle adaptations to exercise Flashcards
(29 cards)
neuromuscular junction
-the point at which alpha motor neurones and neurons meet
-they don’t physically meet there’s a gap
-gap = synaptic cleft
- action potentials nee to cross the synaptic clet to propagate down the nerve cell
action at the neuromusclar junction-CHEAT SHEET
Action Potential Arrival: A nerve impulse (action potential) travels down the motor neuron to its terminal.causes depolarisation
Acetylcholine Release: The action potential triggers voltage-gated calcium channels to open, allowing calcium ions to enter the neuron. This influx causes synaptic vesicles to release the neurotransmitter acetylcholine (ACh) into the synaptic cleft via exocytosis.
ACh Binding: Acetylcholine diffuses across the synaptic cleft and binds to ACh receptors on the muscle fiber’s sarcolemma (muscle cell membrane). These receptors are ligand-gated ion channels.
Muscle Fiber Depolarization: Binding of ACh opens the ion channels, allowing sodium ions to enter the muscle fiber and potassium ions to exit. This creates a local depolarization called the end-plate potential.
Action Potential Propagation: If the end-plate potential reaches a threshold, it generates an action potential in the muscle fiber, which propagates along the sarcolemma and down the T-tubules.
Muscle Contraction: The action potential triggers calcium release from the sarcoplasmic reticulum inside the muscle fiber, leading to contraction via the sliding filament mechanism.
ACh Breakdown: Acetylcholinesterase, an enzyme in the synaptic cleft, breaks down ACh into acetate and choline to terminate the signal and reset the system.
excitation-contraction coupling-CHEAT SHEET
The action potential travels along the sarcolemma reaches the pores and then travls down into the T-tubules, triggering calcium release from the sarcoplasmic reticulum. Calcium binds to troponin on the thin filaments, shifting tropomyosin and exposing binding sites on actin. This allows myosin to form cross-bridges with actin, leading to muscle contraction. When calcium is pumped back into the sarcoplasmic reticulum, the muscle relaxes.
Ryanodine receptors-CHEAT SHEET
- on the SR
-coupled to dihydropyridine receptors on T-tubule
-action potential travels down the T-tubules=depolarisation=activates dihydropyridine receptors=changes shape
-the ryanodine receptors change shape and release calcium into the cytosol
-calcium is key to initiate a action potential
-RyR1 = ryanodine receptors:
release calcium from SR into
cytoplasm
structure of the sarcoplasmic reticulum
-sarcoplasmic reticulum surrounds the entire muscle
-areas where the t-tubules and and scaroplasmic reticulum meet is called triads
cross bridge cycling-CHEAT SHEET BECAUSE NEVER REMEMBER
cross-bridge cycling is the process by which myosin and actin interact to produce muscle contraction. It consists of the following steps:
Cross-Bridge Formation: When calcium binds to troponin, tropomyosin shifts to expose actin’s binding sites. Myosin heads, energized by ATP hydrolysis, attach to these sites, forming cross-bridges.
Power Stroke: The myosin head pivots, pulling the actin filament toward the center of the sarcomere. This movement, called the power stroke, releases ADP and inorganic phosphate (Pi) from the myosin head.
Cross-Bridge Detachment: A new ATP molecule binds to the myosin head, causing it to detach from actin.
Reactivation of Myosin: The myosin head hydrolyzes the ATP into ADP and Pi, re-energizing and resetting to its original position, ready to bind to actin again.
This cycle repeats as long as calcium and ATP are available, allowing continuous muscle contraction.
exposure of the actin myosin binding sites-CHEAT SHEET
At rest, tropomyosin blocks actin’s binding sites, preventing cross-bridge formation. When calcium is present (during contraction), it binds to troponin, causing tropomyosin to move and expose the binding sites for myosin.
SERCA-CHEAT SHEET
contractions will continue as long as there is ATP and calcium present
- Contraction is terminated by the return of Calcium to the SR by SERCA
- actively transport calcium ions (Ca²⁺) from the cytoplasm back into the SR using ATP. This reduces cytoplasmic calcium levels, causing muscle relaxation and replenishing SR calcium stores for future contract
what regulates the strength of muscle contraction?
- change the rate at which you fire action potentials
-single action potentials produce a single twitch see slide
-incomplete tetanus= increase the rate at which you fire an action potential e.g. 10 AP/s. you get incomplete relaxation between muscle contractions so the effects of the action potentials are summated even bigger force of contraction. even after contraction, the muscle doesn’t fully relax
-tenatus contraction = increases the rate of firing action potentials even further e.g. 50aps/s= cannot distinguish between single action potentials aps are gfused so doesn’t go down to baseline levels.. muslcle never relaxes
produces its maximum amount of force.
second way to regulate the strength of muscle contraction?
-increase the number of motor units that you recruit
-3 types of motor units:
1) Fast twitch, high force, fast fatigue (type IIx)
2) Fast twitch, moderate force, fatigue resistance, (type IIa)
3) Slow twitch, low tension, fatigue resistant (type I)
hennemans size principle of motot unit requitemnet
-first recrquit the slow motor units
-then the fast twitch unit. 2a
- as more force is required you would the requit the type 2x
-its additative. you you wouldn’t turn one off and on all are activate at the same time
-they are just always requited slow- fast
why is the hennamnas theory true?
- the fibres have different stimulation threshold
-slow motor units has a low stimulation threshold where as faster ones especially type 2x has higher stimulation threshold
how can we see the muscle fibres
- through staining
-can use immunohistochemistry/ staining - we have different proportion of fibre types depending on genetics
-loses them as we get older
Gain in muscle strength
-at the beginng its due to neuralogical changes e.g. 1-3 weeks and then after a while due to muscular hypertrophy(increase in muscle mass) as its need to be consistent
-after a while neurological changes plateus we get to a point where there can be no more changes and the mn muscle strength would be solely on the increase in muscle mass
what neuronal changes occur with training to gain muscular strength
- Improved Motor Unit Recruitment
Strength training improves the brain’s ability to recruit motor units more efficiently.
This includes greater recruitment of large, high-threshold motor units (Type II fibers) that produce more force.
Normally, motor units are recruited asynchronously (some are active, others resting) to avoid fatigue and prevent spasms.
With training, more synchronous recruitment occurs — activating multiple motor units at once.
→ Leads to greater force output, faster rate of force development, and improved ability to maintain steady contractions.
- Increased Neural Drive
Greater activation of motor neurons during maximal voluntary contractions.
Enhanced firing frequency and better coordination between muscles.
→ Contributes to strength gains even before muscle hypertrophy occurs.
inhibition of normal instrinic mechansism= muscle strength
Golgi tendon organs
- Inhibit muscle contraction of the tendon tension too high
- Prevent damage to
bones and tendons
-during exercise threshold in which the golgi tendon is stimulated is higher=orevents the organ from inhibiting muscle contraction earlier on
-reduces inhibitor impulse
-antagonist oppose agonist force in training there’s a reduction in this
unilateral resistance exercise
-where you train only one side of the body
-test strength compared to the other side in many different ways
-used to study muscle strength
-see an improvement in strength in trained leg but also untrained leg because the neurological adaptations are not limited to one side of the body and spill over
mechanisms of hypertrophy
-need to have a higher ratio of muscle synthesis for a long period over muscle breakdown
-Defined as an increase in the volume or mass of muscle fibres without an
increase in cell number.
how muscle protein synthesis is stimulated?
- Feeding – insulin and the branched-chain amino acids – leucine, isoleucine in response to food.
and valine can directly activate protein synthesis - Exercise
-3 hours after exercise you have a really high synthesis of protein synthesis and is still pretty high after 48hours but goes down
-why you should train every 2 days
Akt/mTOR pathway and muscle mass
-e.g. after you eat a meal and you get a secretion of insulin into the cytoplasm. insulins binds to the insulin receptor on the muscle cell and causes autophosphorlation=actives AKT protein and mTOR. controls cell growth= target for cancel cause maybe it can reduce cancer cell growth
-mTor can only be activated if its attached to the lysosome.
-causes proteinntranslation and transcrpition= protein synthesis
how do amino acids activate the AKT/mTOR pathway for muscle growth and also resistance excersise
-e.g. leucine is taken up in the membrane in exchange for glutatmineand activates mTOR directly
- resistance exercise leads to a production of phosphatatic acid= activate mTOR
-diabetes can get muscle synthesis via exercise even if they lack insulin
nuclear domain theory
A cell nucleus can only control a
limited portion of the cell space. Therefore, for a muscle fibre to grow, it would need to add
additional nuclei to maintain the nuclear domain of each nucleus
sateilite cells role?
-satellites are around muscle fibres
-satellite cells activated= migrate into the muscle fibres and repair the damage
-also produce nuclei to siuppoort muscle growth
muscle memory
- The effects of previous
training can be long-lived because - Training results in the
acquisition of new nuclei - These nuclei are then not
lost during detraining - Major implications for how
to handle steroid abuse in
sport. lifetime ban?
-also if you trained when your younger will it have impacts when your older?
