exam 3

compare and contrast the three types of muscle

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skeletal: voluntary, long cylindrical tubes or striations with a. lot of nuclei

* movement
* maintain posture
* stabilize joints
* heat production
* metabolism

cardiac: involuntary: striations, 1-2 nuclei, no neuromuscular junction

* cardiac output- pumping blood

smooth: involuntary, 1 nuclei, no striations

* vascular tone- radius
* gastrointestinal motility
* arrestor pili and pupil

what embryonic layer does skeletal muscle come from

mesoderm

steps of muscle development from embryonic layer

myoblasts group together and fuse to from myotube (not a lot of contractile proteins, nuclei are in the center)

more myoblasts douse together in the myotube so the myotube grows

nervous sytem must join a junction with myotube in order to trigger the myotube to produce contractile proteins

once contractile proteins are made in large quantities myotubule is matured into myofiber

list the structural organizational levels of muscle

muscle- organ

fascial

muscle fiber- cell

myofibril

sarcomere- smallest functional unit

myofilaments

muscle - organ

surrounded by epimysium – dense irregular connective tissue

distinguishes one muscle form another

fuses with connective tissue of tendon or if no tendon is present it will fuse with periosteum of bone (in some cases perichondrium of cartilage)

surrounds all of contents of muscle

tendon

dense irregular used to attach one end of muscle to bone

associated with epimysium

aponeurosis

dense connective tissue

found in abdomen and end of back

sheet like layer of connective tissue where muscle can connect with one end and aponeurosis and connect to bone

fasicle

bundles all contents together

portion of muscle

surrounded by perimysium- dense irregular connective- wholes the myofibers together

muscle fiber

surrounded by endomyisum- loose areolar- outside basement membrane

nucleus

sarcolemma

sarcoplasma

sarcoplasmic reticulum

myofibril

organized into sarcomeres

complex organelle dcomposed of bundles of myofilaments

started muscle

every myofibril is made of multiple sarcomeres

sarcomere

ne sarcomere runs from one z disc to anothersmallest functional unit of strained muscle

thick and thin filaments

thick filaments found between two thin filaments

thin filaments attached to Z disc

thick filaments are independent of thin

one sarcomere runs from one z disc to another

dark vs light band

light= I (isotropic- light can pass through) not lots of protein: no thick filaments – due to this less protein

dark= a (anisotropic) abundance of protein

light and dark band reflect contractile protein

what part of sarcomere is part of dark bands

myosin and actin (thick and thin filaments)

H zone

In middle of a band: H zone- region of lighter shaded areas- less protein

bisecting H zone is

M line- dark line in middle of H zone- lots of structural proteins- hold the thick filaments together and anchor it to center of sarcomere

what is the proportion of thick:thin band

1:6

describe thick filaments

o   Myosin- complex protein – DIMER

Made of two subunits made of myosin proteins

o   Globular heads not in the H zone

o   Where the two subunits interact= tail

Fixes into thick filament- attaches to proteins in M line

o   There’s a hinge point: conformational shape change occurs here

Allows for myosin to have large conformational shape change- essential for muscle contraction to take place

o   Globular head: two important components- actin binding site and ATPase (enzyme)

  ATPase activity- breaking down ATP

describe thin filament

o   3 proteins: actin, troponin, tropomyosin

o   Actin subunits containing myosin binding site

o   Myosin binding sites aren’t exposed usually because of the tropomyosin (regulatory protein) covers up these binding sites

o   Troponin- complex of 3 proteins- this tugs on tropomyosin to pull it back to expose myosin binding site during contraction- regulates position of tropomyosin

what are the 3 components of troponin

* Troponin T- were troponin and tropomyosin are bound
* Troponin C- where Ca2+
* Troponin I- where actin is connected

sarcoplasmic reticulum

·       where muscle stores, releases and sequesters Ca2+

runs entire length of myofiber and surrounds each myofibril

o   calcium activates which can break down proteins and destroy muscle

o   terminal cisternae of SR against T tubule\`

T-tubule

Transvere

running one side of myofiber to other

part of sarcolemma

adjacent to SR

cistern of SR

region of SR that stores and releases C2+

triad of SR

cistern, tubule, cisterne

tubule

* (part of organelle- connect to cisternae) of SR where Ca2+ reuptake occurs- primary active transport- calcium pumps from sarcoplasm into SR

H zone vs A zone

·       A band has thick and thin filaments H zone only has thick filaments

o   H zone is light zone (I zone) in center of sarcomere – in middle of A band

cardiac muscle

·       specialized striated muscle

o   Only in walls of heart

o   Striated for all same reasons skeletal muscle is striated

o   Contraction mechanisms are identical to skeletal

o   Branched

o   Very small- only 1-2 maybe 4 nuclei

neural control of cardiac muscle

§  Autonomic nervous system: either speeds up or slows down

§  Parasympathetic- decrease HR

§  Sympathetic- increase HR

§  Never tells it when to beat- has automaticity

§  No neuromuscular junction- no neural influence

what is the junction between two cardiomyocytes

o   intercalated discs- lots of structural proteins

§  Desmosomes (stress junctions) and gap junctions (communication junctions)

cardiac muscle functional structures

§  Sarcomere

§  Intercalated discs w gap junctions

§  Mitochondria

§  SR/caveolae

sliding filament theory

* during contraction thin filaments slide past thick so actin and myosin overlap to a greater degree
* shortening Z disc length
* actin move towards each other
* thick filaments DONT REALLY move
* myosin pulls on thin filaments moving them towards center

what is the name of the process that causes the filaments slide

cross bridge cycling

cross bridge cycling steps

o   myosin binding to actin and globular head changes shape causing inorganic phosphate to fall off causing big shape change

o   myosin goes from cocked to uncocked shape

o   this changing causing the thing filaments to move towards center of sarcomere – POWER STROKE

o   when power stroke occurs its associated with ADP falling off myosin

o   then ATP joins and binds to the ATPase in myosin head this weakens bond between myosin and actin (myosin goes into low-E configuration)

o   can then break down ATP in form of heat and reset myosin molecule (myosin now in high E position)

o   can now reform new cross bridge

true or false: myosin all act in unison

false- they all have their own base w

what will happen to a muscle fiber if it doesn’t have ATP

·       it will be rigid – stuck in place- rigormortis – when u die all muscles will be contracted at one- bc no ATP to break actin-myosin bond

How do we regulate cross bridge cycling?

·       Regulate shape of troponin through Ca2+ and regulate position of tropomyosin

why is too much Ca2+ bad for the body

it can cause the cell to breakdown from the inside

action potential critical points

o   -90= resting -55= threshold 0= +30= where depolarization peaks

describe action potential

\-if more Na+ enters than K+ leaves the membrane potential will rise towards threshold

* depolarization- becoming more positive: lots of Na+ diffusing across membrane into cell

o   After it reaches +30 it will rapidly fall below the resting membrane potential: REPOLARIZATION

o   Being below resting membrane potential= hyperpolarization

o   After it repolarization it slowly rises back to resting

o   Potassium will leave cell taking positive charges with it to repolarize causing membrane potential to become negative again

o   During hyperpolarization use sodium potassium pump to reestablish the Na+ and K+ gradient – get back to resting membrane potential

sodium voltage gated channel

changes in voltages in voltage triggers it to allow Na+ to enter

o   2 gates: CAN NEVER BE CLOSED AT SAME TIME – need both open tho to allow sodium to cross membrane into cell

o   Both will become open when voltage reaches -55

* State 2

o   Once he hit +30 other side of gate will close

* State 3

o   When membrane potential hyperpolarizes- channel resets

* State 1

o   Cant have another action potential until rest occurs

potassium gated channel

only one fate

when at rest it is closed

it only opens when depolarization occurs- +30mv

causes cell to become more negative bc K+ leaves

hyper polarization classes K+ gate: going past -90mv

propagation

·       series of sodium voltage gated channels length of membrane 

o   If we open up one sodium voltage gated channel we open up all: like dominos 

o   When sodium rushes it in changes resting membrane potential trigger next one to open

o   This will also trigger opening of K+ voltage gated channel 

o   Potassium channels will be triggered along membrane (also like dominos)

excitation contraction coupling

* action potential in neuron propagates down the membrane of a neuron till it reaches the axon terminal
* at the end of the Na+ channels on the terminal is the axon terminal which has Ca2+ voltage gated channels
* AP propagating to the axon terminal causes release of Ca2+ into neuron
* this causes exocytosis of ACh which is housed in vesicles in axon terminal
* on sarcolemma ACH receptors- ACH diffuses across synaptic cleft to bind to receptors
* Act bound to receptor causes conformational change of integral proteins and allow Na+ to rush in (limited K+ leaves)
* this causes a local AP in the sarcolemma
* local action potential will propagate to the rest of the sarcolemma and eventually down the T-tubules
* set of proteins that connect SR to t-tubule called coupling proteins (Ca2+ channels)
* Ca2+ will diffuse into cytosol to bind to troponin C and expose myosin binding site to form cross bridge

how does the production of contractions stop

depolarization in neruon- stop producing action potential in neuron stop releasing ACH

stop releasing ACH stop action potential in sarcolemma from happening

no more AP down T tubule

no more coupling proteins opened

no more Ca2+ released from SR into cytosol

Ca2+ is also being up-taken via active transport to move from cytosol back into SI

less Ca2+ in cytosol less Ca2+ bound to troponin- less pull on tropomyosin- actin-myosin binding sites are no longer exposed- no more cross bridges

3 phases of a twitch

\-  Latent period: no force/tension is generated- initiating the cross bridge cycling- doing what we need to, to begin cross bridge cycling

\-  Contraction period: actively cross bridge cycling, more Ca2+ binding to troponin to expose more actin-myosin binding cite to produce more cross bridges- tension will peak 

\- Relaxation period: removing Ca2+, more being uptake by SR, less Ca2+ in the cytosol, fewer cross bridges- less force

gastrocnemulus vs soleus vs eye muscle

o   Gastrocnemius- locomotor

o   Soleus- always contracting 

\-Slowest: both in the latent and relaxation phase

o   Eye muscle- extraocular muscle- always twitching

 -Fastest: both in the latent and relaxation phase

What is the trigger for power stroke during cross bridge cycling

* Pi unbinding and leaving 
* Pi unbinding causes the major shape change of myosin 
* After the power stroke ADP leaves 
* Then ATP will rebind 

What is the term for the ability of a muscle to extend or stretch

extensibility

What shortens during muscle contraction

I band

Name and describe factors that influence the force of a skeletal muscle contraction

* Stimulation frequency- number of action potentials before muscle can relax - more calcium in cytosol to bind to more actin- more cross bridges- more cross bridges= more force
* Motor unit recruitment- strength of action potential /stimuli increase and more motor units are recruited = more force 
* Size principle: small motor units are recruited first (small amount of muscle fibers) then intermediate then large (1000 of muscle fibers)
* Length tension relationship- 80-120% of length 

What control is smooth muscle under 

autonomic nervous system

stimulation frequency

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o   Superimposing stimulus on top of first twitch u generate more tension

\-there is more Ca2+ released during the second due to more action potentials and not all the Ca2+ being completely taken back up from the first

\-more calcium leads to more cross bridges 

\-wave summation

The unfused tetanus- increased stimulus frequency causes more intracellular Ca2+

Fused tetanus - maximizing calcium released and therefore maximizing number of cross bridges formed - no stair stepper

motor neuron recruitment

o   increase stimulus increase number of motor units excited therefore increase number of muscle fibers activated and increased strength of muscle contraction 

o   all or none

o   threshold stimulus 

o   fine delicate task only activate few motor units 

o   more effort/more force recruit more motor units- activate more myofibers to generate the force needed

o   there comes a point where more stimulus doesn’t yield more force 

o   as you learn how to do a task more you better learn how to recruit number of motor units to perform the task

what is a motor unit

o   one motor neuron and multiple muscle fibers but no overlap in motor unit

o   motor units are independent and distinct- discrete

size principle

·       you recruit small motor units before you recruit medium size motor and you recruit medium b4 you recruit large motor units (part of neural recruitment)

o   small: one neuron 10/15/20 fibers

o   medium: one neuron and 100-200 fibers

o   large: one neuron 1000 fibers

different motor units have different compositions:

o   small always made of neuron and slow twitch muscle fibers

o   medium- vary- some have neuron and slow and some neuron and fast – depends on muscle and genes

o   large- neuron and fast twitch 

length tension relationship: ideal range

·       number cross bridges formed determines amount of tension produced

o   tension development reflects number of cross bridge interactions between thick and thin filaments

o   100= resting – baseline for sarcomere

o   80=shortening sarcomere by 20% 

o   120= lengthening sarcomere by 20% 

o   What must be true in order to hit max cross bridges: max ca2+ and overlap of thick and thin filaments 

o   Maximize number of cross by mazing overlap of myosin globular heads with actin  

o   80-120% is optimal ideal sarcomere length- near max if not max tension due to number of cross bridges

stretching: length tension relationship

increase length by 40% force will decrease bc there is less overlap between myosin and actin- less cross bridges formed 

shortening: length tension relationship

\
o 60-80 really fast

when it shortens fluid inside cell has to go somewhere- fluid goes sideways so you increase radius of muscle- some of fluid causes displacement of thin filaments which increase distance between thin and thick filament making it more difficult to form a cross bridge

as sarcomere shortens there is also interference between the thin filaments

can only shorten so much bc eventually Z discs will push against thick filaments

smooth muscle neural control

§  automatic nervous system: parasympathetic and sympathetic

·       in veins sympathetic excites 

·       in GI parasympathetic excites 

§  NO NEUROMUSCULAR GAP JUNCTION 

§  If you stretch smooth muscle it will automatically contract 

But if you stretch and hold it, it will rest to that length after some time 

two types of contraction in smooth muscle

\-  Phasic contraction- single unit- GI tract- smooth muscle connected by gap junctions so they act as a unit

\- Tonic contraction- multi unit- arteries and veins- each one on its own- no gap junction 

smooth muscle functional structures

o   Intermediate filaments- form lattice work, come together to form dense bodies contractile proteins associated 

o   Caveolae- concentrate Ca2+ in extracellular fluid- invaginations in plasma membrane 

\- Gated channels to allow Ca2+ diffuse across membrane: Poorly mature sarcolemma 

o   Thick filaments 

o   Thin filaments- no troponin or tropomyosin

o   Ration 1:13 to thin filaments 

o   No sarcomeres 

o   During contraction due to arrangement of thick and thin and intermediated filaments– there’s a twist in the muscle 

o   SR is small doesn’t store a lot of Ca

EC coupling in smooth muscle

o   When Ca diffuses into cytosol through caveolae it will bind to cytosolic protein= calmodulin 

\- Ca alters shape of the protein 

o   Calmodulin is a kinase- breaks down ATP and phosphorylate myosin light chain kinase- activates it

o   myosin light chain kinase will break down another ATP to phosphorylate myosin – this activates myosin 

o   smooth muscle myosin doesn’t have enzyme- needs the myosin light chain kinase to phosphorylate ATP to then cause the myosin to change shape 

o   cross bridge cycle

o   if you phosphorylate myosin it will continue to cycle 

o   need to dephosphorylate to stop 

·       influx of calcium causes shape change in myosin – activate myosin 

·       decrease Ca2+ decrease phosphorylation of myosin – decrease cross bridges- relaxation 

·       very slow 

·       can remain bound to actin in fixed position and not change shape for some time

example of where tonic contraction is important

·       maintain some state of contraction

·       important in veins and arteries: maintains BP: energy efficient 

when is there an action potential in smooth muscle

when you stretch smooth muscle

muscle tone

small numerous tautness/tension in muscle due to weak involuntary contractions

sustained partial contraction

red vs white fiber

red fiber: slow rate, fatigue resistance

white: fast rate, fatigue easily

treppe

stair case effect due to increase strength due to increase in Ca2+

why do athletes warm up

causes treppe

increased warmth due to activity causes an increase in the efficiency of muscle enzyme systems.

isotonic

changes in length and moves load

muscle tension remains relatively constant

what characteristic distinguishes muscle tissue

ability to transform chemical energy into mechanical

contractures

due to total lack of ATP

O2 deficient

difference between amount of oxygen needed and the amount used

which muscle type can regenerate

smooth

alimentary canal

buccal cavity, esophagus, stomach, small intestine, large intestine

accessory organs

·       aid alimentary canal in functions 

o   tongue, salivary glands, pancreas, liver, gallbladder

6 functions of GI tract

· 6 main functions 

o   Ingestion- mouth 

o   Propulsion- swallowing, peristalsis (esophagus, stomach, small and large intestine)

o   Mechanical breakdown- chewing, churning, segmentation 

o   Chemical digestion- enzymes break down food we have ingested- stomach and small intestine 

o   Absorption- transport nutrients from ( )– mainly in small intestine, small amount in oral cavity, small amount in large intestine

o   Defecation- elimination of solid material 

abdominopelvic cavity is a ( ) membrane and found only in the ( ) portion of the cavity

serous membrane

only in ventral portion

name the two parts to the serous membrane

o   Parietal peritoneum (area not in contact w organ)

o   Visceral peritoneum (in contact w organ)

what is the function of the peritoneum

o   allow organs of canal to change size and change size as FOOD MOVES THROUGH CANAL 

o   As organs change size and shape it puts pressure on other organs in the area 

o   Peritoneum reduces friction – lubrication due to fluid 

dorsal mesentery

two layers of peritoneum fused together

usually parietal layer

forms stronger tissue

acts like a ligament to hold organs in place

two types of smooth muscle units

single and multi unit

single unit smooth muscle

·       commonly called visceral muscle 

o   contract rhythmically as a unit

o   electrically coupled via gap junction 

o   may exhibit spontaneous action potentials 

o   arranged in opposing sheets and exhibit stress-relaxation response 

* peristalsis

describe process of peristalsis

o   alternating contractions and relaxations of smooth muscles that mix and squeeze substances through lumen of hollow organs 

o   two layers: inner circular layer- smooth muscle cells orientated around diameter around lumen of tube– when it contracts we decrease layer of lumen 

o   all cells connected via gap junction 

o   cells of circular layer are separate from longitudinal layer

o   longitudinal layer cells run length ways- all cells here are connected via gap junctions- cells contract as unit 

o   when longitudinal layer contracts organ dilates and contracts – lumen will increase and length of organ decreases

o   longitudinal and circular layer never contracted at the same time 

o   when circular layer contracts organ elongates 

o   alternating allows food to move 

o   causes food to mix with enzymes- also increases likelihood of food coming in contact with lumen which will absorb nutrients 

multi unit smooth muscle

o   rare gap junctions 

o   each act as own entity 

o   infrequent spontaneous depolarizations 

o   structurally independent muscle fibers 

o   rich nerve supply may form motor units 

o   graded contraction 

o   lungs

o   arteries

o   arrector pili 

o   internal eye muscles 

stress relaxation response

·       smooth muscle responds to stretch only briefly then will adapt to its new length

o   bladder or stomach- single unit

o   smooth muscle will rest to new length to release tension

o   enables organs to temporarily store contents

hyperplasia

·       certain smooth muscle can divide via mitosis and increase their numbers 

o   arteries: atherosclerosis: inflammatory state causes cells to divide and increase thickness of blood vessels 

o   shown by estrogens effect on uterus- at puberty (ovulation) and during pregnancy 

o   as uterus gets larger cells multiple to allow uterus to get larger 

o   irreversible

cardiac muscle development

§  Cardiomyocyte- only in walls of heart

§  Single or denucleated 

§  Branched

§  Striated like skeletal 

§  Myoblasts don’t give rise to cardiac muscle- it’s a similar myoblast like cell 

true or false myoblasts give rise to all muscle cell types

false only skeletal muscle

cardiac muscle contraction

§  automaticity- spontaneous 

§  depolarization- releases Ca2+- actin myosin control 

§  automaticity- can spontaneously depolarize and then contract- can generate its own 

§  how you stimulate membrane is different from skeletal 

§  heart goes on own- tells it how fast : DIFFERENT FROM SMOOTH OR SKELETAL- they tell when 

syncytium- single cell function as 1: gap junctions

cardiac muscle neural control

§  autonomic nervous system: parasympathetic- relax sympathetic- stimulate car

§  no neuromuscular junction 

cardiac muscle functional structure

§  intercalated disks- gap junctions and desmosomes

§  myofibrils arranged into sarcomere: actin and myosin

§  SR not as well developed so it doesn’t contribute all of Ca2+

§  Has caveolae – get Ca2+ from ECM

§  Mitochondria

o   CANT OPERATE AEORBICALLY

which is more forceful: eccentric or concentric

eccentric

isometric contraction

no shortening of the muscle but tension increases

name the four regions within the alimentary canal

mucosa

submucosa

mesclarias externa

serosa

describe the 4 parts of the alimentary canal

mucosa-

* epithelial layer: stratified squamous/simple columnar/pseudostratified columnar
* followed by lamnia propria (provides nutrietns for epithelial layer, like basement membrane)- loose areolar
* muscualris mucosa- able to contract and cause wrinking serve to help increase surface area fro absoprtion

submucosa- loose areolar connective muscularis externa- longitudinal and circular layers- peristalsis

serosa- serous membrane - epithelium (mesothelium) then connective tissue (loose areolar)

* parietal and visceral

\*\*adventitia - dense irregualr - in esophagus

what type of epithelial cells is the mucosa layer

depends on the organ

·       stomach has simple columnar but small intestine pseudostratified 

·       can be ciliated in some areas 

·       rectum and anal reverts back to stratified squamous 

intrinsic nerve plexus

\-Myenteric nerve plexus

\- Submucosal nerve plexus

\-Myenteric nerve plexus

regulates contraction and relaxation of smooth muscle in musclarias externa- peristalsis, churning in stomach 

·       Controls GI tract motility 

\- Submucosal nerve plexus

 affects gland secretions, regulates muscularis mucosa 

·       Glands and smooth muscle in mucosa 

what processes take place in the mouth

ingestion, mechanical breakdown, limited amount of digestion due to enzymes, propulsion (swallowing), tiny but of absorption, vomiting counts as elimination