Physiology NMJ etc

what is sarcomere

it cause contractionand made of actin and myosin(myofilaments) give striated appearance

what is myofibril

a line of sarcomeres

muscle fiber/myofiber(m cell)

what are many myofibrils

what is muscle fasciculus

many m fibers

epimysium covers what in skeletal m

entire m

perimysium covers what in skeletal m

m fasiculus

endomysium covers what in skeletal m

m fibers - sacrolemma

sacrolemma is what

cell membrane of m cell

myofiber is what

multiple nuclei and has mitochondria

what is sarcoplasmic reticulum

specialized smooth endoplasmic reticullum that regulates uptake and storage Ca

where are actin filaments

attach to Z line composed of actin, tropomyosin, troponin

what are myosin fiflaments

attach to M line

what protein links actin to m cell membrane

dystrophin

muscular dystrophies are what

inherited disorders cause degen of skeletal m tissue

what is DMD

mutation in gene for dystrophin> tears sarcolemma, cause m cell destablization and break down

DMD affects who and symptoms

male recessive, progressive m weakness early childhood

steps of cross-bridge cycle

1. before contraction begins, myosin heads bound ATP, cleave into ADP and phosphate, changing orientation

2. Ca binds to trop C on actin, tropomyosin move and expose myosin binding sites

3. bindingmyosin heads to actin=power stroke pulls actin filaments, shortening sarcomere; myosin heads release ADP and phosphate

4. new ATP binds to myosin heads, detach from actin

5. cycle repeats w sufficient ATP/Ca in sarcoplasm

what is rigor mortis

m contract and become rigid w/o AP; hours after death

why is rigor mortis caused

lack ATP in sarcoplasm

motor unit is what

1 motor n to group m fibers

1 m is innervated by how many motor units

many

where are cell bodies of motor neuron

ventral spinal cord 1-4 segments

small m control has to be exact bc

more n fibers for FEW m fiber(1:2)

large m do not require fine control bc

more m fibers for FEW n fibers (1:200)

Small neurons are what

more excitable

recruit first

slower conduction

excites fewer fibers

Type 1 fiber

fatigue resistant

what are large neurons

less excitable

recruited second

faster conduction

excites many fibers

type 2 fibers

what is staircase effect

strength of contraction increase to plateau

how staircase effect result

increasing levels Ca incytosol due to SR unable reuptake ions quickly enough

what is multiple fiber summation

recruitment different motor units under different stim conditions

smaller motor units stim over larger motor units bc

CNS sends weak signal for m contract - as signal stronger, LMN stim allow bigger contractile strength

what is frequency summation

summation signals in individual m fibers

what s tetanization

contraction strength appears smooth and cont; end goal freq summation

what is tetanus

lockjaw- infection by bacterium clostridum tetani- m spasms

tetanus is transported how

retrogradely and blocks inhibitory signals

sources energy m contraction (highest at top)

cellular macronutrients by oxidative metba

glycogen

phosphocreatine

intramuscular ATP stores

y muscle fatigue results

metab process unable keep up w demand of m fiber work output

type 1 fibers - slow are for

long endurance(distance running)- small diameter, more mit

type 2 fibers are for what

bursts movements(spriniting/heavy lifting)- large diameter

how many months after denervation cause deg appear to m

2 months

in final stage of denervation atrophy, m fibers destroyed and replaced by

fibrous and fatty tissue

what is Ach

NT involved in transmission at NMJ

what is Ach receptor

depolarizes postsynap membrane allowing passage Na ions

what is ach-sterase

enzyme in postsynap membrane designed to destroy ach shortly after released into synaptic cleft

what kind receptor of Ach

nicotinic - ligand gated ion channel

what happens at NMJ

1. AP arrives at terminal, trigger influx Ca cause Ach release NMJ

2. Ach move across NMJ activate receptors causing Na influx in

3. if Na depol, AP intiated

4. AP travel down T-tubules and trigger C release

what is excitation contraction coupling

1. Ap travel down sarcolemma, open vg Na channels to propogate AP down T-tubules

2. AP reaches DHP receptors sense volt change and cause ryanodine recp open

3. when ryan recp open Ca released from cisterna of SR and into sarcoplasm surrounding myofibrils

4. Ca binds to troponin C on actin fils, expose myosin binding sites

5. m contract

what is Botox

bacterial poison dc quantity ach release at NMJ by cleaving poteins involed in exocytosis at synaptic terminal

ach recep agonists do what

stimulate m fiber by ach-like action; activate recp

ach recep antagonists

drugs block transmission at NMJ by inhibit ACH recp

ach-sterase inhib

stim m fiber by inactivating ach-erase

steps skeletal m contract

1. before contraction begins, myosin heads bound ATP, cleave into ADP and phosphate, changing orientation

2. AP arrives axon terminal trigger Ca cause release ACh into NMJ

3. ACh activates ach recep in postsynap, influx Na into cell

4. if infux na cause depol, AP initated

5. excitation-contraction coupling occurs when AP travels down t-tubules-ca released by terminal cisternar of SR and infiltrates associated myofirils

6. Ca binnd to trop C on actin fil, expose myosin binding sites

7. bindingmyosin heads to actin=power stroke pulls actin filaments, shortening sarcomere; myosin heads release ADP and phosphate

8. new ATP binds to myosin heads, detach from actin

9. cycle repeats w sufficient ATP/Ca in sarcoplasm