1.  determines what type of muscle fiber the bundle will be

2. Stimulates the muscle bundle. 

3. Releases Acetylcholine for muscle contractions

1. are inside muscle fibers

2. Thick and thin filaments

1. Stand for transverse tubules

2. wrap around and go inside the muscle bundle

3. They help with conduction of the action potential so that it activates all the muscle fibers in the muscle bundle. 

1. Stimulated by the T-tubule

2. Releases Ca2+ for muscle contraction

1. Gets released from SR

2. binds to troponin to move tropomyosin out of the way

3. Then myosin can attach to the actin filament

1. Surgical procedure that switches the alpha motor neuron to different muscle bundles

2. Type I AMN will make that muscle bundle Type I, Type IIb AMN will make that muscle bundle Type IIb. 

Type I: SLOW

Type IIa: FAST

Type IIb: FAST

Type I: SMALL

Type IIa: LARGE

Type IIb: LARGE

Type I: HIGH

Type IIa: RELATIVELY HIGH

Type IIb: LOW

Type I: HIGH

Type IIa: RELATIVELY HIGH

Type IIb: LOW

Type I: HIGH

Type IIa: RELATIVELY HIGH

Type IIb: LOW

Type I: LOW

Type IIa: HIGH

Type IIb: HIGH

Type I: HIGH

Type IIa: RELATIVELY HIGH

Type IIb: LOW

Type I: HIGH

Type IIa: MEDIUM

Type IIb: LOW

Type I: LOW

Type IIa: HIGH

Type IIb: HIGH

Type I: DARK

Type IIa: DARK

Type IIb: NO STAIN

Type I: NO STAIN

Type IIa: DARK

Type IIb: DARK

Insulin dependent

autoimmune disorder

antibodies destroy beta cells that make insulin

Non-insulin dependent

Makes some insulin but not enough to bring BG levels down in a timely manner

Polyurea- frequent urination

polydipsia- drinking a lot, always thirsty

polyphagia- eating a lot, always hungry

When the liver makes ketone bodies from fatty acids. 

Patient's breath and sweat smells like acetone.

protective mechanism because the brain thinks there is no glucose

changes amino acids to glucose via gluconeogenesis

Neuropathy (myelin sheaths destroyed on nociceptors)

Nephropathy (kidney failure)

Retinopathy (blindness)

Heart disease

pancreas is making defective beta cells

Insulin resistance

the beta cells are being "worn out" trying to make so much insulin to break down the calories of saturated fats

and transfatty acids act like saturated fat by packing in the phospholipid bilayer to tight that it alters the shape of the insulin receptor

decrease heart disease by elevating HDL

upregulate the insulin receptors because glu will decrease, ins will decrease, and insR will increase

potential complication for treatment of diabeties

Hyperinsulinemia occurs due to too much insulin to control the hyperglycemia

causes dyslipidemia (elevates livers production of LDL cholesterol)

Leads to HTN because the kidneys reabsorb more sodium and BP increases

endurance

slow contractility

small fiber diameter

high mitochondrial density

high capillary density

high myoglobin content

low glycolytic enzymes

high oxidative enzymes

high fat

low glycogen

speed and strength

fast contractility

large fiber diameter

relatively high mitochondrial density

relatively high capillary density

relatively high myoglobin content

high glycolytic enzymes

relatively high oxidative enzymes

medium fat

high glycogen

Speed and strength

fast cotractility 

large fiber diameter

low mitochondrial density

low capillary density

low myoglobin content

high oxidative enzymes

low fat

high glycogen

Lots of type I fibers

Cardiac can share an action potential, skeletal does not

different NT's: cardiac uses epinephrine or noepinephrine

skeletal uses acetylcholine

different nervouse system branches

cardiac= autonomic

skeletal = somatic

mitochondrial density is higher in cardiac muscles

isovolumic contraction period

rapid ejection period

slow ejection period

isovolumic relaxation period

slow filling period

increase the end diastolinc volume (EDV)

and lower the end systolic volume (ESV)

both can be done by exercising, increases HR, increases concratility, increases SV

Goal is to increase tensions and force

Body recruits type I fibers first, then type IIa, then type IIb 

Related to the size of the AMN, type I has small AMN amd type II has large AMN

This principle does not apply to speed, with speed body can go straight to type II fibers

SV/EDV

how much blood was pumped out of the heart divided by how much blood was in the heart before it contracted. 

action potential SA node phases 

P wave

phase 0 = the increase when sodium is leaking into the SA node

phase 3 = the decrease when K+ is leaving

phase 4 = the lowest point when the cells are reestablishing their gradient

Action potential phases for the ventricle

QRST 

Phase 0 = Na is rushing in fast so line goes straight up

phase 1 = initially K+ starts to leave which changes the mV direction

phase 2 = plateus because Ca2+ is coming in and K+ is coming out around equal rates

phase 3 = K+ leaves the cell because Ca and Na are coming in and the like charges repel 

phase 4 = Ca comes back into the cell to reset the whole process

Endocardium is first to depolarize and last to repolarize

epicardium is last to depolarize and first to repolarize

Epinephrine binds to the beta receptor

Activates G protein

Activates Adenylate cyclase

ATP make cAMP

cAMP activates protein kinase and lets Ca into receptors

NE binds to the alpha receptor

G protein activated

phospholipase C activated

PLC changes PID to IP3

IP3 stimulates the SR to release Ca2+ 

Ca brings cell to threshold faster and muscle fibers contract

ACH binds to the ACH receptor

inhibits either adenolyne cyclase or PLC

which decreases Ca2+

and decreases contracility

(also increases K+ permeabiilty)

VO2 = CO x (A-V O2 difference)

A = O2 leaving the heart

V = O2 returning to the heart

Skeletal: 3 fold increase in amount of O2 used

Cardiac: 10% increase in the amount of O2 used

the narrowing of the coronal and peripheral arteries

reversible

starts with an injury to the vessel wall, usually from high BP

HTN causes an injury to the endothelial cells

platelets bind to the site of injury

PDGF (platelet derived growth factor) causes growth

but also regrows the smooth muscle cells and makes artery narrow

bulge collects fats and cholesterol

the hardening of the arteries with calcium

this is irreversible

a piece can break off and cause a stroke if stuck in the brain or a heart attack if stuck in the heart

converts inactive phosphorylase kinase b to active phosphorylase kinase a, which converts inactive glycogen phosphorylase b to active glycogen phosphorylase a, which allows glycogen to undergo glycogenolysis and breaks down glycogen. 

OR

converts active glycogen synthase to inactive glycogen synthase (which prevents glycogen from being fomed)

NE binds to alpha receptor

G-protein ativated

PLC activated

PIP turned into IP3

stimulates SR to release Ca2+

Ca2+ binds to calmodulin

calmodulin makes inactive protein kinase b into active protein kinase a

internal = glycogen

external = blood glucose

EPI binds to the beta receptor

activates G protein

activates Adenolate cyclase

ATP makes cAMP 

cAMP initiates the PK lipolysis pathway

cAMP converts inactive cAMP dependent protein kinase to active cAMP dependent protein kinase, which converts inactive hormone sensitive lipase to active hormone sensitive lipase, which breaks off FA chains of a triglycerol. 

OR

Active cAMP dependent protein kinase can convert active ACC to inactive ACC and stop the production of FA chains. 

Glucose-FA Cycle 

purpose and pathway

PURPOSE: when elevated use of fat inhibits the use of blood glucose

PATHWAY:

FA levels are high so Acetyl CoA increases

PDH is inhibited and increases PYR

PYR will redirect to OAA production more than Acetyl CoA

More OAA will make more citrate

citrate will back up in the krebs cycle and leave the mitochondria

Citrate inhibits PFK in the cytoplasm

inhibited PFK will back up G6P

G6P accumulation will inhibit hexokinase

no hexokinase will allow glucose to leave cell

BG levels will increase

Glucose Fatty Acid Reversal 

purpose and pathway

PURPOSE: elevated use of glucose will inhibit the use of fat

PATHWAY: Citrate will start to accumulate in krebs cycle

citrate will leave mitochondria due to concentration gradient

in the cytosol citrate will split by citrate lyase

either into OAA or to acetyl coA 

The acetyl coa will convert to malonyl coa via ACC

malonyl coa will make FA starting point and can inhibit the carnitine shuttle so fat cannot get into mitochondria

it increases glucose uptake

increases FA and glycogen synthesis

makes citrate come out into the cytoplasm

insulin binds to it's R and stimulates ACC

promotes the citrate lyase and increases malonyl coa

inhibits the carnitine shuttle 

promotes the reversal cycle

Catecholamines include EPI and NE

they inhibit ACC

which inhibits malonyl coa formation

inhibits the citrate lyase and keeps citrate intact

citrate inhibits PFK

increases G6P

inhibits hexokinase

BG levels rise

stimulated by ADP

it is the rate limiting enzyme for glycolysis

can override vasoconstriction

O2 consumption: decreases PO2, increases PCO2, and decreases pH

O2 deficit = happens because it took time for the O2 to get there

O2 dept = O2 is gradually decreasing

work to increase stimulation for hypertrophy

and prevents fatigue of muscle 

creatinine is made from creatine

creatinine is expelled form urine and could disrupt diagnostic method for kidney problems

brain

spinal cord

peripheral nerves

NMJ

contration (CONTRACTILE FATIGUE)

the muscle accumulates protons from the lactic acid

positive charge repels the Ca2+ from the SR 

no more force retention and muscle fatigues

BG  and insulin decrease

catecholamines, glucagon, and corticol increase

when BG decreases, PEPCK increases because it is the rate limiting enzyme for gluconeogenesis

There is a tear in the Z-line or myofibril

neutrophils open up the endothelial cells

monocytes turn into macrophages and clean up the cellular debri in the area

macrophages release bradykinin and PGE to sensitize nociceptors

mRNA assembly genes released from the nucleus to increase the size and number of the mitochondria

mRNA enzymes released and make more ATP to increase energy and mitochondria splits

increase size and number of mitochondria

increase mitochondrial enzymes

increase capillary density

increase ability to metabolize fat

increase in number of insulin receptors

increase in number of Glut 4

increased insulin sensitivity

Current (I) = Voltage (V) / Resistance (R)

Internal resistance = membrane resistance / surface area

type II has larger SA to smaller IR, so higher I

Type II requires more current to stimulate thatn type I which supports the recruitment pattern

increase LV volume

increase LV mass

increase in SV

increase in HDL

decrease in beta receptor density

lower HR at rest and during exercise

Respiratory exchange ratio = 1.0 means burning carbs

RER = 0.7 burning fats

VCO2/VO2 = RER

0.9 would be closer to carbs/glucose

0.8 would be closer to fats

sychronization of motor units

decrease in golgi tendon organs which monitors muscle tension

increase in glycogen content

increase in glycogen phosphorylase

increase in PFK

increase in pyruvate kinase

regenerate muscle fibers

increase cell # and size

one satellite cell can regnerate multiple muscle fibers

gets to injury by chemotaxis

increase myofibril content

Type I has more than Type II

Type I is retained with age

protects organs

level system

movement/motility

storage for minerals

red and white blood cell production

increases calcitonin:

decreases Ca2+ reabsorption in kidneys

increases osteoblast activity in bones

decreases vit D:

increases osteoblast activity in bones

decreases Ca2+ absorption in small intestine

increase PTH:

increases Ca2+ reabsorption in kidneys

increase osteoclast activity in bones

increase vit D:

increase osteoclast activity in bones

increase Ca2+ absorption in small intestine

bone loss 3% per decade 

starts at 45 years old

bone loss 3% per decade

starting at 35 years old

bone loss 9% per decade

at menopause age 45-50

bone loss 3% per decade

10-15 years later

low Ca2+ intake

smoking

heredity

race/ethnicity

not enough high impact activities

Pizoelectric effect

in dry bone there is a neg potential which causes osteoblasts to store Ca2+

streaming potential in wet bone in body pushes fluid through organic matrix which makes pos and neg potentials line up and makes compression and increases the stress to push more fluid and creates electric potential and stimulates osteoblasts depositing Ca2+

measures the mass and volume of bones

DEXA = dual energy X-ray absorbtometry

may take a year to see difference

1% increase is alot

bone studies have high drop out rate. 

when the aorta is attached to the right ventricle and the pulmonary trunk attached to the left ventricle

lungs keep circulating same blood and body keeps circulating same blood-- two closed systems

baby will die

Can happen in skeletal muscle but not in cardiac muscle 

because cardiac muscle action potentials have a longer refractory period per one electrical event and has a greater AP duration than a skeletal musce that can just keep firing. 

Also because heart has beta receptors which bring Ca in straight from the extracellular space

Age

Family History

Inactivity

Pre-diabetes

dyslipidiemia

obesity

hypertension

smoking

The increase in cholesterol is also in the phosolipid bilayer of cells

oxidized LDL free radical (can be prevented with vitamin E) destroys the membrane 

rigidity increases and cells can get pulled off the endothelium resulting in injury to the vessel lining

Epi binding to beta receptor 

or

glucagon binding to glucagon receptor

has the same reaction as glucagon

helps to increase proteins during starvation

but most people don't get to this point because they stop exercising when they start to feel a little hypoglycemic

Pyr--->LA 

LDH5

NADH+H--->NAD+

LA-----Pyr

LDH1

NAD+---->NADH+H

Where is the calcium in bones stored?

How is it removed?

the hydroxyapatite matrix stores the Ca2+

osteoclasts release acid to break down hydroxyapatite and release Ca2+ for the body to use