1. elongated
2. multiple peripheral nuclei
3. voluntar
4. striation

1. branching cell
2. single central nucleus
3. involuntary
4. striation

1. spindle-shaped cell
2. single central nucleus
3. lack visible striation
4. involuntary

1. motor neuron + fibers
2. innervates numerous muscle fibers
3. fibers contract simaltaneous
4. ^contraction ^more motor units

1. prevent fatigue
2. only at submax contracttions
3. alternate motor units

1. length of muscle
2. multi mitochon/nuclei
3. many myofibrils

1. extend across mus fiber
2. thick(1.6) & thin(1.0) filaments
3. A band, Z line, sarcomere, M line, cross bridges

stacked thick fil + thin fil 

thin fil overlap both ends of thick fil

Z line

(myofibril)

cytoskeleton protein

connects thin fil w/ adjoining sarcomeres

sarcomere

(myofibril)

between z lines

smallest contractile unit of muscle

contain: Aband, M line, H zone

M line

(myofibril)

proteins holding thick fil vertically

middle of Aband

cross bridges

(myofibril)

extend between thick & thin fil

6 thin surrouned 1 thick fil

myosin heads

1. myosin
2. club shaped subunit
3. tails intertwined
4. globular heads (cross bridges)
5. head has actin bind site
6. & myosin ATPase site

1. actin=spherical
2. double helix strands
3. myosin binding site
4. tropomyosin
5. troponin

tropomyosin

(thin)

1. threadlike protein along actin spiral
2. covers myosin binding sited on actin
3. blocks for at rest

troponin

(thin)

3 proteins

1. attach to actin strand
2. binds to tropomyosin
3. calcium binding reversibly

ends up moving tropomyosin, expose myosin-binding sites

membrane surface

dips into fiber

modifed ER

surround myofibril

encircles each A band

1. Ach released by terminal button
2. Ach binds receptors on motor end plate
3. =end plate potential=AP
4. AP down Ttubes
5. sarco retic release Ca
6. Ca bind to troponin
7. troponin moves tropomyosin
8. cross bridge cycling
9. Ca taken up by SR (no more AP)
10. tropomyosin returns to block

1. binding of myosin to actin
2. power stroke
3. rigor
4. unbinding myosin & actin
5. coking myosin head

(cross bridge cycle)

myosin binds to actin

1. myosin energized (ADP&Pi in ATPase(myosin head))
2. myosin binds to actin monomer
3. need Ca

(cross bridge cycle)

Power stroke

1. Pi & ADP release from ATPase
2. myosin pivot to middle sarcomere
3. pulls thin fil w/
4. myosin = low energy state

(cross bridge cycle)

rigor

think of rigor mortis 

1. low energy form
2. myosin/actin tightly bound

(cross bridge cycle)

unbinding of myosin & actin

1. new ATP in ATPase
2. decrease affinity myosin/actin
3. releases

(cross bridge cycle)

cocking of myosin head

1. ATP split by hydrolsis
2. into ADP & Pi
3. enter Ca, start over

between initation of stim

& start of contraction

between contraction and peak tension

continue til all Ca gone

many rapid stimuli prevents musc relax

contraction max strength

asynchronous not possible

1. creatine phosphate 
2. glycolysis/kreb's cycle/oxidative phosphorylation
3. anaerobic pathways

creatine phosphate

(ATP source)

1. energy reserves
2. 5x more than ATP
3. creatine phosphate+ADP=ATP+creatine
4. 1min or less

glycolosis 

kreb's cycle & oxidative phosphorylation

(ATP source)

mitochondria need O2

makes 38 atp(2, 36)

glyco give pyruvate (acetyl) to krebs
pyruvate takes O2

=H2O & CO2 & 36 atp

anerobic pathway

(ATP source)

1. atp rapidly
2. 2 atp/glucose
3. rapid depletes
4. lactid acid
5. fatigue
6. short time

no longer respond to stimulation

lactic acid

depletion of energy

neuromuscular fatigue:

motor neuron no make Ach

central fatigue (psychological)

1. creatine phosphate resynthesized
2. lactic acid metabolized
3. replenish glycogen

slow oxidative (type I) fibers

fast oxidative (type IIa) fibers

fast glycolytic (type IIb) fibers

most muscles have all

motor unit=1 type

IIa & IIb interconvert

(IIa)

high: oxygen, mitochondria dens, capillary dens, myoglobin#, resist fatigue

low: glycolytic, contraction, ATPase activity, fiber diameter, motor unit size, force-generate capacity

(IIa)

high: oxygen, mitochondria dens, capillary dens, myoglobin#

medium: resist fatigue, glycolytic, contraction, ATPase activity, fiber diameter, motor unit size, force-generate capacity

low: 

(IIb)

low: oxygen, mitochondria dens, capillary dens, myoglobin#, resist fatigue

high: glycolytic, contraction, ATPase activity, fiber diameter, motor unit size, force-generate capacity

hyptrophy

hyperplasia (rare)

increase muscle diameter

increase muscle fibers 

1. spinal reflex
2. primary motor cortex cerebral cortex
3. cortical/subcortical
   (basal nuclei/cerebellum/thalamus) via brainstem 

1. hollow organs/tubes
2. contractions=mvmnt
3. spindle shaped=1 nucleus
4. smaller than skeletal
5. dont extend full length
6. arranged in sheets

myosin=longer than skeletal

actin=(NO troponin) & 10-15 to 1

(anchored to dense bodies)

medium filaments =support

myofibrils

z lines (but has dense bodies, anchored to membrane)

 Ttubes

(underdeveloped SR)

1. Ca enters thru membrane (concentration grad ECF-ICF)
2. SR releases Ca
3. Ca=enzyme calmodulin
4. calmodulin=myosin light chain kinase
5. MLCK = myosin (splits phosphate off ATP
6. myosin binds actin (cross bridge cycle)
7. Ca removed (active trans)=calmodulin/MLCK inactive
8. phosphatase=remove phosphate
9. myosin no bind actin=relax

multiunit smooth muscle

(rare)

1. different units (seperate stim)
2. stimulated by autonomic (neurogenic)
3. found: large blood cells, large airways to lungs, eye musc (distance), iris, goosebumps

single unit smooth muscle

(common)

1. muscle fibers make single unit
2. contract together
3. AP anywhere transfered throughout (via gap junctions)
4. autonomic
5. myogenic activity

myogenic activity

(single unit smooth muscle)

pacemaker activity

slow wave potential

pacemaker activtiy

(single unit smooth muscle)

1. membrane depolarizes byself (change in channel permeability
2. AP fired=spreads to rest of smooth muscle cells via gap junct
3. lymph vessel

slow wave potential

(single unit smooth muscle) 

1. alternate hyper/depo larizing
2. Na causes cyclical changes (active transport back and forth membrane)
3. threshold not garentee
4. if it reached, burst in AP's
5. intestines

contraction strength factors

(smooth muscle)

modified cytosolic Ca

1. both branches autonomic NS
2. hormones
3. metabolites
4. mechanical stretch
5. drugs

muscle=maintain tension w/o fatigue

accomadate volume w/ little change

contraction strength

(single unit smooth muscle)

1. fiber tension modified by cytosolic Ca concentration
2. ^cyosolic Ca=^cycling cross bridge
3. maintain low cyosCa= low lvls contraction (muscle tone)

contraction strength

(multi unit smooth muscle)

1. functional unit recruiter (=skeletal muscle)
2. cytosolic Ca concentration varies

striated

lots of mitochondria

gap junctions

autonomic

fibers joined in branching network

Ca enter cytosol from ECF & SR

some like pacemaker activity

AP's long duration

circulatory system

heart, blood, blood vessels

pulmonary: heart-lungs

systemic: heart-body

heart as a dual pump

pulm(all blood goes thru lungs)

low press/resist

syst(not all blood visits body parts)

high press/resist

atrium-receives

ventricle-pumps out

veins-return blood

vena cavae-systemic to heart

pulmonary veins- lungs to heart

arteries-push blood

aorta-heart to systemic

pulmonary artery- heart to lungs

four 1 way valves

pressure difference

2 AV valves

1 aortic valve- Lventricle/aorta

1 pulmonary valve- Rventricle/pulmonary valve

1. musc fibers interlaced/spirally around circumference of heart
2. ventricular contraction= diameter decrease, apex goes up, 

1. cells joined end to end
2. gap junctions
3. no AP's go between atria/ventricle
4. desmosomes (hold cells together under stress)

autorhythmic cells

(1%)

1. decrease passive leak out of K
2. increase Na leak in
3. voltage reached=Ca Ttype channels open
4. reach threshold voltage
5. Ca Ltype channels open
6. depolarization=AP
7. membrane repolarizes (K leaves)

contractile cell

(99%)

1. AP through gap junct
2. Na opens=depolarization
3. Na close @ +30mv
4. depol=Ca move in slowly (plateau)
5. depol=K inactive (plateau)
6. repolarization= Ca closes, K open

1. AP via gap junc, Ca enter via ECF
2. AP moves down Ttubes
3. =SR release Ca
4. Ca=plateau=prolonged contraction
5. Ca binds to troponin
6. troponin moves tropomyosin
7. =cross bridge cycle
8. Ca removed by active trans
9. muscle relax
10. long refractory of cardiac AP & muscle contractions stop tetanus of cardiac muscle=death

electrical activity of entire heart

(intrinsic conduction)

1. SA node: R atrial, 70-80 AP/min, initiates AP
2. (AP spread via gapjunc)
3. AV node: base R atrium, 40-60
4. bundle of his -> bundle branches, 20-40
5. purkinje fibers:terminal fibers

electrocardiograms represents

(ECG)

1. record electical activity reaching body surface (not actual heart EA)
2. record overall spread of EA throughout heart (not AP in heart)
3. compare electrodes on 2 diff body surfaces (not AP)

electrocardiograms trace

(ECG)

1. Pwave: atrial depolatization
2. PRsegment: AV nodal delay
3. QRScomplex: ventricular depol (atrial repol)
4. ST segment: ventricles contracting & emptying
5. Twave: ventricular repolar
6. TP interval: ventricles relaxing (passively filling)

1. volume blood pumped by each ventricle/minute
2. HR*stroke volume

parasympathetic

-vagus nerve (no effect on vents)

slow depolarization in SA node

increase AV node delay

Na, Ca, K more neg

sympathetic

-atria

increase depol in SA node

reduce AV node delay

speed up bundle his & purkinje

bind epi to beta 1 on pacemaker cells increase Na & Ca

epi bind on beta1 on contractile cells

increase contractile strength

1. increase Ca
2. increase rate of myosin ATPase

causes vasodilation

swelling