skeletal focus terms

epimysium

surrounds entire muscle

parimysium

bundles of cells

endomysium

individual muscles

how is it voluntary

it is connected to somatic conscious neurons

part of skeletal that has striations

myofibril

sarcomere

from Z-Z

H zone

just thick filaments

I band

just thin filaments

A band

all thick filaments

sliding filament theory

myosin head starts in relaxed stage, up with ATP

ATP splits and head resting position pushed forward

myosin head gets binded to actin

power stroke makes ADP release, pushing myosin head up

ATP binds back making myosin head go back to relaxed stage

contraction

motor neuron sends action potential to axon terminal next to muscle fiber

calcium enters axon terminal. Voltage gated calsium channels open and calcium enters nerve terminal triggering vescicles to release acetyl choline

acetylcholine then crosses synaptic cleft and binds to receptors on muscles motor end plate, opening sodium channels, depolarizing the muscle membrane

action potential travels down t-tubules allowing the electrical signal to go through into the fiber

voltage sensors then activate calcium release, flooding into sarcoplasm

calcium binds to troponin, changing shape making tropomyosin move for myosin head to bind to actin

myosin attached to actin and power stroke happens.

resting membrane potential

-90

muscle fiber tension

takes longer

has delay before contraction

coraterols

axon branch from motor unit

what shortens when contraction happens

sarcomere

fused tetanus

it keeps a straight line of being on

twitches summate

two bumps together

unfused tetanus

bumps and bumps, doesnt go fully down

what stores ATP

creatine phosphate stores the phosphate to give to ADP on myosin head when needed

myoglobin protein

in muscle cell

binds to oxygen

single polypeptide

higher affinity for oxygen then hemoglobin

rapid onset fatigue

intense excersize

lactic acid gets built up and changes the PH

t-tubule conduction fails

cross bridge blockage

slow onset fatigue

same as rapid onset fatigue but from long term moderate exercise

more likely due to decreased glycogen/glucose availability

isometric

while muscle contracts, length does not change

like tug of war

concentric isotonic

shortens muscle

not based on how hard it contracts but on comparison/load overcoming

eccentric isotonic

tug of war and loosing

load exceeds tension

lengthening

slow oxidative

weak

oxidative phosphorylation

aerobic

weak

fast glycolytic

strong

anaerobic (glycolysis)

tend to get energy from strength from glycolysis

muscle fatigue from lactic acid creation

atrophy

muscle shrinks and weakens

first loss of myofibrils then cells start to die

harder to regenerate later

hypertrophy

muscles bigger

stimulate increase in myofibrils

muscles grow and sometimes make more

cramps

involuntary tetanic contraction

tetanus

decreased extracellular calcium causing weaker membrane potential (depolarize) opening sodium channels

clostridium tetani is the bacteria that cause it

boyulism

blocks acetyl coline

decreased muscle contraction and tone, leading to flacid paralysis

caused by clostridium botulinum

muscle dystrophy

genetic

alters proteins that hold muscles

myasthenia gravis

due to loss of ach-receptors on muscle cell surfaces

typically an autoimmune reaction where antibodies attack the receptors

results in weakening EPP’s