Physio Exam #4 Review

alpha

neuron associated with a skeletal muscle contraction

skeletal muscle

made up of extrafusal muscle fibers

motor end plate

muscle post synaptic membrane

ach

chemical that allows the end plate potentials to continue

nicotinic

type of receptor on the sarcolema that binds to Ach and allows Na+ to pass through

Na+

ion allowing end plate potential

alpha motor neuron

releases Ach to go to the sarcolema

acetylcholine esterase

breaks down Ach into acetyl and choline

choline

picked up by the terminus and repackaged into Ach → more conserved

lower motor

type of neuron that an alpha motor neuron is

depolarization

the 1st wave → allows Na+ in through VS channels

repolarization

the 2nd wave → allows K+ out through VS channels

Ca++

enters neuron through VS channels → allows for the release of Ach

Ca++ pump

responsible for moving Ca++ out of a neuron

transverse tubule

channels that go deep into the muscle cells

sarcoplasmic reticulum

storage for Ca++ in a skeletal muscle

depolarization

action that opens VS channels to let Ca++ out of the sarcoplasmic reticulum

Ca++ pump

responsible for the movement of Ca++ into the sarcoplasmic reticulum

thick filaments

made up of myosin, an ATPase → where E is put into “setting the trap” of attaching myosin head to thin filaments

rod, hinge, head

3 parts of a myosin

thin filaments

made up of actin, each has a myosin binding site

tropomyosin

protein thread gate to block cross bridge before it is ready

troponin

hinge proteins

TnC

where Ca++ binds on a troponin

TnT

tropomyosin binding on troponin

TnI

inhibitor region of troponin

spiral

arrangement of actin on a thin filament

Ca++

“key to unlocking the hinge gate” → once unlocked, pulls back tropomyosin so myosin can bind to actin

ATP binding

breaks the mysin/actin cross bridge to release E

sarcolema

PM of the muscle

sacromere

skeletal muscle body → unit of contraction

myofibril

one row of sacromere

nebulin

protein responsible for making sure that thin filaments are lined up → attach to the Z line

titen

protein that makes sure the thick filaments line up and aren’t bend → ensures muscle elasticity

z line

holds together thin filament, pulled together during a contraction

m line

holds together thick filaments, grabs thin filaments in a contraction

h line

“sunny region” thick filaments only

striated muscle

skeletal and cardiac muscle → alternating light and dark bands

A band

dark band → entire thick filaments

I band

light band → thin filaments only

ATP

needed to set myosin head

70%

the landmark = max E percentage

anaerobic

above 70% = glycolosis → pyruvate → lactate → 2 ATP => pays back the O2 debt through the heart and liver

lactate

goes into the blood and becomes lactic acid

aerobic

below 70% = glycolysis = glucose → pyruvate (Krebs +ETC)

creatine kinase

adds phosphate to creatine to make phophocreatine

phosphocreatine

stored for short bursts and recycle ATP

twitches

Ach generates end plate potential → release Ca++ burst → movement

elastic

muscle wanting to go back to its original shape

isometric

same length → tension, no shortening or length change, plotted time vs tension through Ca++ IN/OUT

isotonic

same tension → plotted length vs time, longer latent period

latent period

period of time before muscle movement → overcoming elastic forces for muscle to start shortening (in isotonic)

lengthening

muscle gets longer, not shorter

Ca++

as long as it is present, increase in cell cross bridges → Ach → EPP allows more more twitches

tetany

sustained contraction allowed by a summation in twitches

fatigue

drop in energy levels, short duration or long duration

short duration

type of fatigue → increase H+ and P

long duration

type of fatigue → decrease in glycogen

optimal length

where overlap between thick and thin filaments generates the most force

30%

percentage change for any movement

60%

contraction % that is too contracted

175%

contraction % that is stretched too far → no overlap

alpha motor neurons

innervate extrafusal muscle fibers

slow and fast oxidative

aerobic type fibers

fast glycolytic

anaerobic type fibers

slow oxidative

undergoes the Krebs cycle and has high myoglobin, first recruited, smallest diameter, last to fatigue

fast oxidative

undergoes the Krebs cycle and has high myoglobin, 2nd recruited, middle diameter, 2nd to fatigue

fast glycolytic

undergoes glycolysis and has low myglobin, 3rd recruited, largest diameter, 1st to fatigue

aerobic fibers

“runners” more metabolically efficient → the dark meat

anaerobic fibers

“body builders” → white meat

smooth muscle control

innervation or cajal cell pacemakers

innervation

type smooth muscle control → release Ach + generate EPSP (muscerinic #1) → bind SM → works as a unit

cajal cell pacemaker

tpye smooth muscle control → slow leak Na+ channel leak until threshold → send AP through gap junctions

caveoli

depressions in the fusiform (instead of T tubules) in smooth muscle

fusiform

round cells making up smooth muscle (instead of striated fibers)

extracellular fluid

location of Ca++ in smooth muscle

unitary gap junctions

connect fusiform in smooth muscle → allow SM to work as a unit & allows communication btwn them

cajal cell

pacemaker of the SM

latch mechanism

contraction from for SM → allows it to stay contracted

calmodulin

SM replacement for TnC → binds to Ca++

myosin kinase

adds phosphate allowing for a contraction in SM → cross bridge as long as phosphate is present

myosin phosphatase

removal of phosphate allows for SM to relax

dense bodies

attach thin filaments together in SM

myosin

cross bridge and latch to actin → in SM is not ATP based, but phosphate based

cardiac muscle

Z lines, TnC, and tropomyosin

Ca++ source in cardiac muscle

sarcoplasmic reticulum, T tubles

t tubules

25x larger in cardiac muscle, extracellular source of Ca++

sarcoplasmic reticulum

inctracellular source of Ca++ in cardiac muscle

gap junctions

make up the intercalated discs of cardiac muscle

vena cava

where the blood enters the side of the

SA node

generates an electrical signal that causes the upper heart chambers (atria) to contract

AV node

transmits the heart's electrical signal from the atrium to the ventricle, optimizes the coordination of each heartbeat

internodal bands

communicate signals between the SA and the AV node

interatrial bands

allows for the atria to contract at the same time

connective tissue

valves on the same plane, holding them in place, and electrically separating the atria and the ventricles

tricuspid

valve between the right atria and ventricle, prevents backflow into the right atria

pulmonary semilunar

valve between the right ventricle and the pulmonary artery

pulmonary, systemic, coronary

3 types of circulatory systems

pulmonary veins

brings blood from the lungs to the left heart

bicuspid

valve separating the left atrium and ventricle, prevents backflow into the left atrium