Nervous Coordination And Muscles Flashcards
When does the sliding filament theory stop?
Until actin cannot be moved closer together
OR
When run out of ADP
When enough =muscle remains stimulated by NS (as long as calcium ions released)
what are myofibrils and what is their purpose
fused cells which share a nuclei and cytoplasm
- actin and myosin filaments make up sarcomere in myofibrils
- allow for the movement of the skeleton.
what happens if there is no action potential arriving at the muscle in terms of muscle contraction
no calcium ions released and bound to the tropomyosin
actin-myosin binding sites are not exposed
no muscle contraction
how is the sliding filament theory stimulated and what occurs
-action potential arrives at the muscle
- travels through T tubules into sarcoplasmic reticulum
- action potential causes CA+ protein channels on reticulum to open - CA diffuse into cytoplasm down conc grad
- CA binds to protein attached to tropomyosin = changes shape
- tropomyosin pulled away and actin-myosin binding sites on actin filament exposed
= myosin head binds (ADP)
= cross bridges
how is tension released after myosin head has attached to actin-myosin binding site
TENSION - myosin head changes shape and pulled at an angle
- sliding/ pulling actin filament along myosin
- whilst ADP molecule is released
how is the myosin head recocked
new ATP molecule binds to myosin head
= detaches (changed in shape and no longer complementary)
- calcium ions activate ATPase to hydrolyse ATP to ADP
-provides energy for myosin head to return to original position
what does the H zone, I band, M line, Zline and A band represent
H zone - just myosin filaments
I band - just actin
M line - middle of myosin
Z line - parameter of sarcomere
A band - never moves because myosin doesn’t move during contraction
how are slow twitch fibres designed for aerobic respiration
large stores if myoglobin (stores lots of O2)
rich blood supply
many mitochondria
-contract slower during exercise
how are fast twitch fibres designed for anaerobic respiration
-thicker and more myofibrils
- large store of glycogen
- large store of phospholipids
- high conc of enzymes involved in anaerobic
- short bursts and more powerful contractions
- short and high bursts of ATP
- lactic acid
how are NTs transmitted from neuron to neuron
action potential arrives at synaptic knob (depolarisation)
= opening of volted gated CA channels
- CA diffuse into knob
- vesicles (contain NTs) move towards presynaptic membrane + fuse = NTs released into synapse
- NTs diffuse down conc grad across cleft to post synaptic membrane
- bind to receptors compl on post membrane
- causes NA channels on PS membrane OPEN and NA diffuse from cleft to PS neuron (reach threshold and create action potential)
what happens after the NTs diffuse into next neuron
enzymes break down NTs and reabsorbed to presynaptic neurone to be re sued when another action potential arrives.
why is the flow of NTs unidirectional
vesicles are only found on the PRESYNAPTIC neuron and the receptors complementary to NTs are only found on the surface of POSTSYNAPTIC neuron
information only passed in one direction
explain the transmission of NTs in cholinergic synapses
NT is acetylcholine
enzyme in post synaptic neurone (acetylcholine esterase) hydrolyses it to make choline and acetate
reabsorbed to pre synaptic neurone to make more acetylcholine
