which muscles are striated

which are under voluntary control?

striated: skeletal muscle & cardiac muscle

voluntary control: skeletal muscle

what are the levels of organization of skeletal muscle?

muscle: made of parallel muscle fibers conected by CT

Muscle Fibers: single skeletal muscle cell (myocyte)

Myofibril: contractile parts of muscle fibers.  made of repeating sarcomeres

Myofillaments: has contractile proteins.  (thick myosin, thin actin)

Sarcomere: functional unit of skeletal muscle.  give a striated look.  (not in smooth)

define

Z line

A band

I bands

M line

H zone

Z line: start and stop of a sarcomere

A band: overlapping of thick and thin filaments

I band: thin filaments only

M line: midline of a sarcomere

H zone: thick only

<thick filaments>

Titin:

Myomesin:

Creatine Kinase:

C-protein:

MLCK:

Myosin

Titin: stretches from M line to Z line, controls length, and elasticity

Myomesin: in M line, keeps titan, and myosin's 3D look

CK: in M line.  enzyme that transfers p from cretin phosphate to ADP

C-Protein: maintains width of thick filaments

MLCK: binds to thick filament, phosphorylates light chain of myosin.  sensitizes myosin to Ca activation.

Thin Filaments

Actin:

Tropomyosin:

Troponin:

Actin: sphere shaped protein, has binding site for myosin.  makes double helix shape

Tropomyosin: threadike, blocks actin active site (mom)

Troponin: protein bound to tropomyosin, made of Tn-I, Tn-C, Tn-T

In troponin how does

Tn-C and Tn-I work?

when Ca binds to Tn-c, initiates conformational change that displaces Tn-I, so myosin can have axcess to actin binding site.

there are 6 thin filaments aroud each thick

there are 3 thick around each thin.

Z line shortens

H band shortens

I band shortens

what are the steps in cross bridge cycling?

1.) myosin head activated by ATP, so now myosin head has ADP+P, but myosin can't bind to actin b/c tropomyosin

2.) Cross Bridge formation.  Ca binds to troponin, tropomyosin moves, now myosin head binds to actin active site

3.) power stroke: ADP+P released from myosin, thin filament slides across thick filament

4.) cross bridge detachment: ATP binds t myosin, myosin separated from actin, cross bridge breaks.  hydrolysis of ATP to ADP+P returns myosin to active position.

(-) if the is not enough ATP, myosin can't release from actin, eg Rigor Mortis

A.) cross bridge breaking, hydrolysis of ATP activates myosin.

B.) Ca-ATPase pumps cytosol ATP into SR.  less Ca = muscle relax.

End Plate Potentials

(EPP)

• only at motor end plates
• triggered by influx of Na, efflux of K due to nicotinic ACH receptor binding (not membrane voltage)
• Graded potential, so can decay and sumate.

Excitation Contraction Coupling

1

2

3

4

5

6

7

1 AP generated

2 AP goes down T tubule to center of muscle

3 AP activates VG Ca channels which release Ca from SR

4 Ca binds to troponin, so tropomyosin moves

5 myosin heads bend pulling actin to center of sarcomere

6 AP terminates, VG Ca channelse close, SR stops sending out Ca, so Ca actively pumped back in (was always pumping) by Ca-ATPase

7 tropomyosin covers action again

slow oxidative fibers

type I

low intensity, long duration. 

many mitochondria, high capilary density

low fatigue,

effective use of glucose, high production of ATP

takes a long time

gets ATP from oxidative phosphorylation

high myoglobin (red)

low glycogen

small fiber diamater

small motor unit size

fast Oxidative-Glycolytic Fibers

Type IIa

contract faster than the slow,

maintain longer than fast-glycolytic

medium oxidative capacity, moderate fatigue

many mitochondria

gets ATP from oxidative phosphorylation

high myoglobin (red)

Fast Glycolytic Fibers

Type IIb

low oxidative capacity,

few mitochondria,

low capilary density

high fatigue

gets ATP from glycolysis

low myoglobin (white)

high glycogen content

large fiber diameter

large motor unit size

Isotonic contraction

(dynamic contraction)

muscle tension is constant, muscle shortens

isometric contraction

(static)

muscle prevented from shortening.

tension rises, muscle length constant

muscle tension = load

load pulls muscle longer

eccentric contraction

muscle tension is less than the load

adding sarcomeres at end of myofibril (lengthening)

adding myofibrils (hypertrophy)

adding cells (hyperplasia)

muscle fiber # stays constant*

distinguish between

disuse atrophy

denervation atrophy

disuse: don't use, lose muscle strength

denervation: death of inervating neuron

triggered by damage to sarcolema

1 Ca spills into muscle from interstitial fluid

2 ca activates proteases that digest proteins

3 this releases proteases and cytokines that stimulates immune system

4 inflamitory process happens

1 activation of satalite cells

2 satalite cells move to injury to become myoblasts

3 myoblasts become myotubes

4 myotubes synthesize muscle proteins for repair

muscle damage during exercise

high intensity exercise

low intensity exercise

high intensity: muscle injury early.  disruption of sarcolema raising cytosolic Ca

low intensity: long duration exercise, muscle injury later, inhibition of Ca reuptake my SR

post exercise soreness

when does Delayed Onset Muscle Soreness happen?

Muscle changes

cause of delayed soreness

DOMS: 24-48 h due to eccentric fast twitch injury.

muscle changes: osmotic changes, damage to sarcolema/contractile proteins, efflux of enzymes like CK/myoglobin, altered SR function

Causes: acute inflammation, and cell swelling due to raise in Ca

distinguish between

active (exploring) electrodes

pasive (indifferent) electrodes

unipolar leads

bipolar leads

active: an electrode that records a voltage, electrical lead

Pasive: a reference electrode at 0 mv

unipolar lead: combo of active + pasive.  measures voltage only at active

bipolar leads: combo of two actives.  measures charge difference

Lead I: RA(-) LA(+)

 what axes/planes do the leads monitor?

limb leads (standard/augmented)

precordial leads

limb leads: frontal (vertical) plane

precordial leads: transverse (horizontal) plane

what is

AVR

AVL

AVF

Augmented limb leads

AVR: Right arm

AVL: Left Arn

AVF: left leg

can determine atrial/ventricular heart rate

regularity of rhythem

conduction times

direction of depolarization of cardia structures

size of chambers

SA node

Location:

Function:

location:between superior vena cava & RA

Function: primary pacemaker of the heart.  fires fastest

secondary pacemakers

AV node bundles of His

Bundle Branches

Purkinji fiber network

tract conecting right to left atrium

coordinates R and L Atrium.

AV node

Where:

Function:

Where: in RA, bottom left side

Function: slow conduction of pacemaker from SA.

Bundle of His

Where:

Function:

AKA AV bundle

Where: medial of heart, next to AV node

Function: conducts pace from AV in RA to the ventricles.

Purkinji Fibers

whre

function

where: bottom of both ventricles

Function: fast conduction, spreads impulse through L&RV

distinguish between

intervals

segments

interval: period of time that includes waves

Segments: period of time between waves (normally isolelectric)

P-R interval

where?

What it tells?

where: measured from start of P to start of Q

what: time for atrial depolarization, and delay through AV node. 

normal: 0.12-0.20s

Q-T interval

where?

What it tells us?

where: start of Q to end of T

What: time for ventricular depolarization and repolarization.  verry dependent on Heart Rate

S-T segment

Where?

What it tells us?

where: end os S to start of T

What: time between finishing ventricular depolarization and repolarization.

left axes deviation

right axes deviation

Left axes deviation: mean QRS axes is more negative than 0

Right axes deviation: mean QRS axes is more posative than 90

left ventricular hypertrophy

pregnancy

obesity

infarct in right ventricle

right ventricular hypertrophy (enlargement)

infarct in left ventricle (death)

first degree AV block

prolonged PR interval

slow conduction through AV node or bundle of His

1 P for every QRS

asymptomatic

partial dissociation of atria and ventricles

not every P wave is folowed by a QRS

but a pattern exists (eg) 2 P then a QRS

complete dissociation of atrium and ventricles

P and QRS act completely independently of 1 another

Complete heart block

distinguish between

isometric contraction

isotonic contraction

isometric: force is generated without a change in fiber length. no volume change, pressure change, (isovolumetric)

Isotonic: a decrease in fiber length, but no force is generated, volume change, no pressure change

isometric contraction, then a isotonic contraction.

pressure builds up, then valve opens releasing liquid.

distinguish between

systole

Diastole

Systole: contraction of the heart

Diastole: period between contractions including rest

cardiac cycle 2

ventricular systole stage 1

2 isovolumetric contraction phase.  ventricles contract after depolarization, both sets of valves closed

pressure rises, volume constant

cardiac cycle 3

ventricular systole stage 2

ventricular ejection stage

when pressure in ventricles is more than diastole pressure, valves open, blood is ejected

cardiac cycle 4

ventricular diastole stage 1

isovolumetric relaxaton phase

both valves closed

ventricular pressure declines, no chance in volume

cardiac cycle 1

Ventricular diastole stage 2

ventricular filling

blood flows from atria to ventricle

Rapid filling: atria pressure is more than ventricle pressure, so pasive fillinf from atria to ventricle occurs

Reduced filling: slower blood flow as both pressures get closer

Atrial contraction: (atrial systole) active, fills te remaining 20% of ventricle.  powered by atrial contraction

compare cardiac cycle left and right

afterload:

contraction

outfloe valve

afterload: right is lower than left

contraction: left earlier than right

outfloe valve: right opens before left, right closes after left

closing of atrioventricular valves (mitral/tricuspid) at the start of systole.  mitral valve (left) closes before tricuspid (right) only hear 1 sound.

valves close when ventricle P> Atrial P

happns durring diastole.  closure of semilunar valves.  (aortic & pulmonic)

valves close when artery P >Ventricle P.

Aortic (A2) closes before pulmonic (P2).  both audible. "physiological split"

Extra systolic heart sounds

sound:

causes:

sound: click

caused by: aortic/pulmonic narrowing, or dilation

clicks late in systole are due to popinh inside out of mitral/tricuspid valve.

Extra Diastolic heart sounds

sound 3

3:common in children, bad for adults.  during rapid ventricular filling, due to turbulent blood oscilation in ventricles.  in adults, S3 is due to increased ventricular volume b/c congestive heart failure or mitral/tricuspid heart "regurgitation"

Extra diastolic heart sounds

sound 4

late in diastole

due to atrial contraction into a stiff ventricle.  stiffened ventricle can be caused by hypertrophy (enlargement) or ischemia (lack of blood suply?)

cause turbulent bloodflow 

high pitched whistle murmur

turbulent backflow because valve not completely closed

low pitched gurgling murmur

systolic murmur

when

why

during or after S1

-AOrtic/Pulmonic valve stenosis (thinner valve), so turbulent flow

-mitral/tricuspid valve insufficiency.  blood backflow from a leaky valve

-interventricular septal disease: unsealed opening between ventricles

murmurs

continuous

to & fro

continuous: occurs throught systole and diastole.  due to patent ductus arteriosis (mixing of blood within atriums, Oxygenated and unoxygenated)

to & fro: during parts of systole and diastole.  when an outflow valve is stenosed and insufficient.

Flow

increases with more:

decreases with more:

Increase: with bigger Δ P, and bigger radius of pipe

Decreases: with more resistance, longer length

Ohm's law

Flow =

Flow = ΔP/Resistance

(pressure = force/area)

Distinguish between

Hydrostatic Pressure:

Dynamic/Kinetic pressure:

Transmural Pressure

Driving Pressure:

Hydrostatic: F_g of the liquid

Dynamic/Kinetic: F_movement against mass

Transmural: P_{inside (r1)}-P_{outside (r2)}

Driving Pressure: Hydrostatic+dynamic

Vascular resistance

Series:

Parallel:

Series: R_total= R₁+R₂+R₃ (adding more raises R_t)

Parallel: conductance = g = 1/R_t. 

1/R_t=1/R₁+1/R₂+1/R₃. not much resistance in capillaries b/c there are many capillarys

Poiseuille's law

F=ΔP/Resistance

this tells us that

blood flow: vessel radius^x

blood flow: blood viscosity

Blood flow is directly praportional to vessel radius⁴

Blood flow is inversely praportional to blood viscosity

Viscosity

where in the vessel does blood move fastest?

frictionness of the liquid

viscosity = sheer stress/sheer rate (P/V)

blood moves fastest in the center of the vessel, slowest at walls

laminer flow

turbulent flow

laminer flow: organized consentric circular flow.  silent

Turbulent: disorderly flow.  happens when driving pressure increases, crit velocity reached

Reynold's #

contributers:

affinity of a liquid to do turbulent flow

higher the number, easier for turbulent flow to occur.

contributers: Diameter, velocity, density, viscosity

laplace relationship

Wall Tension =

wall tension = [transmural pressure XRadius]

                                  Wall thickness

increased tension results in aneurysm

as wall tension raises, more energy needed to maintain.  (eg) enlarged heart has more wall tension, so takes more energy to beat.

Types of Smooth muscle contractions

Basal Tone:

Phase contraction:

Tonic contraction:

Basal Tone: low lvl contraction in absence of extrinsic factors

Phase Contraction: brief stimulus results in rapid contraction and rapid relaxation. present in Gi & bladder

Tonic Contraction: continuous force as Ca falls (but still above basal lvl).  present in lungs, blood vessels, GI sphyncter

how is smooth muscle "special"?

lacks

has

lacks: striation, T tubules, sarcomeres, troponin, less SR, Has: Myosin thick, actin thin, regulation of cross bridges is by the thick filament

1 increased cytosolic Ca

2 Ca binds to calmodulin (protein) in cytosol

3 Ca-Calmodulin activates MLCK enzyme

4 MLCK uses ATP to phosphoryate myosin cross bridge

5 phosphorylated myosin binds to actin

6 cross bridge cycling produces shortening

7 power stroke, release of AP+P

8 cross bridge detachment, release ATP

occurs in smooth muscle

influx of extracelular Ca into smooth muscle cells causes release of more Ca from SR

small amount of Ca outside an resuly in lots of Ca inside

excitation contraction coupling of smooth muscles

Resting Membrane Potential:

AP:

RMP: variable (-65 to 45) dependent on Na/K

AP: Ca influx dependent.  single unit cells fire AP, most multy unit cells don't fire AP

1 decreased cytosolic Ca B/c returned to SR by ATP pump, extrusion of Ca by Na/Ca pump

2 MLCK returns to inactive form

3 myosin phosphitase removes P from myosin

4 cross bridge reatachment inhibited

smooth muscle drugs

Ca antagonists

K chanel openers

Nitric oxide/cyclic GMP stimulators

Ca Antagonists: block Ca channels, so less Ca influx/Ca induced Ca release

K chanel openers: cause hyperpolarization of smooth muscle cells (relax of smooth muscle, vasodilation of peripheral vascular smooth muscle)

Nitric oxide/cyclic GMP stimulators: cause raise in cGMP in cytosol to relax smooth muscles.  also lowers BP.

Types of cardiac cells

Contractile

Conductile

Pacemaker (nodal)

Contractile: ventricular and atrial, contracts (pumps)  Fast AP, majority

Conductile: Purkinje, rapidly spreads electrical signal.  fast AP.  can weakly contract

Pacemaker: SA/AV node.  slow AP

Excitation Contractile Coupling

in Cardiac Cells

1 AP causes depolarization of cell membrane

2 L-type Ca channels open (during plateau of AP)

3 Ca enters cell

4 Ca induced Ca release from SR

5 cytosolic Ca lvls increase

6 Ca binds to troponin

7 crossbridge cycling (same as skeletal muscle)

8 contraction

(most Ca is from SR)

repolarize when K is pumped out of the cell

(unsure)