phys 3

connective tissue components

-skeletal muscles are surrounded by a fibrous epimysium

-connective tissue called perimysium subdivides muscle into fascicles

-fascicle is subdivided into muscle fibers (my-fibers) surrounded by endomysium

skeletal muscles

muscles are attached to bones across joints

-attached to bone by tough tendons

-origin

• attached to stationary bone

-insertion

• attached to moving bone

when a muscle contracts, it shortens

-places tension on tendons connecting it to a bone

-insertion pulled towards origin

names are interchangeable

muscle cell= muscle fiber= myofiber

muscle fiber structure

-have many of the organelles found in other cells

-have plasma membranes called sarcolemma

-are multinucleated

-are striated… more soon

• I bands: light bands

• A bands: dark bands

• Z lines (discs): dark lines in the middle of the I bands

muscle fiber banding

each fiber (cell) has densely packed subunits called myofibrils that run length of muscle fiber

-stacked so that the dark and light bands align

-composed of thick and thin myofilaments

structure hierarchy

-muscle tissue

-fascicle

-myofiber or muscle fibers

-myofibrils

-myofilaments

-actin (thin)

-myosin (thick)

striations

produced by thick (myosin) and thin (actin) filaments

-I bands contain only thin filaments, primarily protein, actin

-A bands contain all thick filaments with some thin filament overlap; thick filament is protein, myosin

-H bands are center of the A band with no thin filament overlap

-Z discs (lines) are found in center of each I band

the sarcomere

-basic subunit of striated muscle contraction

-area from one Z disc to the next

-M lines are found in center of each A band and help anchor thick filaments (myosin)

-titin: protein that runs from Z disc to M line and allows elastic recoil

motor unit

-a single motor neuron and all the muscle fibers it innervates

-when somatic neuron activated, all muscle fibers in a motor unit are stimulated to contract

-graded contractions

• varied contraction strength due to the number and size of motor units being stimulated

control of motor units/ contraction strength

contraction strength comes from motor unit recruitment

-size principle: motor units recruited in size order

• smaller motor units will always be recruited before larger ones

-finer muscle control requires recruitment of many smaller motor units (fewer muscle fibers)

• eye muscles may have about 23 muscle fibers per motor unit

  • fine motor control= small motor units

• larger, stronger muscles have thousands of muscle fibers per motor unit

  • strength of contraction= larger motor units

  • Eg: quadriceps, gastrocnemius (1:1000)

control and strength are trade offs

neuromuscular junctions and motor end plates

-neuromuscular junction: site where a motor neuron stimulates a muscle fiber

-motor end plate: area of the muscle fiber sarcolemma where a somatic motor neuron stimulates it using the neurotransmitter, acetylcholine

transverse tubules

-narrow membranous tunnels formed from the sarcolemma (cell membrane)

-open to extracellular environment

-able to conduct action potentials from outside the sarcoplasmic reticulum

-closely situated next to terminal cisternae

sarcoplasmic reticulum

-modified endoplasmic reticulum

-stores Ca2+ when muscle at rest

• most stored in terminal cisternae

stimulating a muscle fiber- excitation contraction coupling

-acetylcholine released from somatic motor neuron- binds to nicotinic receptors

-excitatory end plate potentials (EPSP) are produced

-action potentials are generated (all or none event) and travel down sarcolemma and transverse tubules

-voltage gated calcium channels in transverse tubules open and cause neighboring calcium channels in sarcoplasmic reticulum to open

-calcium is released and can bind to troponin C

-tropomyosin-troponin complex changes and cross bridges attach to actin

sliding filament theory

when a muscle contracts, sarcomeres shorten

-A bands do not shorten

• move closer together

-I bands do shorten

• Z discs move closer together

-thin filaments do not

• thin filaments slide toward the H band

-H band shortens or disappears

summary of the sliding filament theory of contraction

1. a muscle fiber, together with all its myofibrils, shortens by movement of the insertion toward the origin of the muscle

2. shortening of the myofibrils is caused by shortening of the sarcomeres- the distance between Z lines (or discs) is reduced

3. shortening of the sarcomeres is accomplished by sliding of the myofilaments- the length of each filament remains the same during contraction

4. sliding of the filaments is produced by asynchronous power strokes of myosin cross bridges, which pull the thin filaments (actin) over the thick filaments (myosin)

5. the A bands remain the same length during contraction, but are pulled toward the origin of the muscle

6. adjacent A bands are pulled closer together as the I bands between them shorten

7. the H bands shorten during contraction as the thin filaments on the sides of the sarcomeres are pulled toward the middle

cross bridging and power stroke

thick: composed of the protein myosin

-two globular heads with actin binding sites and ATP binding sites

thin: composed of the protein actin

-have proteins called

• tropomyosin

• troponin

• prevent myosin binding at rest

action of sliding

1. sliding is produced by several cross bridges that form between myosin and actin

-the myosin head serves as a myosin ATPase enzyme, splitting ATP into ADP+Pi

-this allows the head to bind to actin when the muscle is stimulated

2. release of Pi upon binding cocks the myosin head, producing a power stroke that pulls the thin filament toward the center

3. after the power stroke, ADP is released and a new ATP binds

-a) this makes myosin release actin

-b)the new ATP is split

4. the myosin head straightens out and rebinds to actin farther back

5. continues until the sarcomere has shortened

role of calcium

muscle fiber is stimulated

-Ca2+ diffuses out of calcium-release channels

-EXCITATORY!

some attaches to troponin C (‘calcium’)

-causes conformational change in troponin and tropomyosin

-exposes myosin binding sites on actin

-allows cross bridge formation

end of a contraction

-Ca2+ is actively pumped back into sarcoplasmic reticulum

regulation of contraction

regulation of cross bridge attachment to actin due to

-tropomyosin

• switch for muscle contraction and relaxation

• physically blocks across bridges

• in relaxed muscle blocks binding sites on actin

-troponin complex

• troponin I inhibits binding of myosin

• troponin T binds to tropomyosin

• troponin C binds to calcium

muscle relaxation

-action potentials stop

-calcium release channels close

-Ca2+ -ATPase pumps move Ca2+ back into sarcoplasmic reticulum (active transport)

-no more Ca2+ is available to bind to troponin C

-tropomyosin moves to block myosin heads from binding to actin

muscle twitch and summation

twitch

-muscle is stimulated with a single electrical shock (above threshold)

• quickly contracts then relaxes

-increasing stimulus increases strength of twitch (up to a maximum)

summation

-additive response when a second twitch partially piggybacks the first after second shock applied before muscle relaxes

latent period and graded concentrations

latent period

-time between stimulus and contraction

-due to excitation-contraction coupling to the attachment of myosin cross bridges to actin

graded concentrations

-contraction strengths depends on number of motor units recruited

-stronger contractions result in recruitment of more fibers, until all fibers are contracting

tetanus

incomplete tetanus

-increasing frequency of electrical shocks decreases relaxation time between twitches

complete tetanus

-smooth, sustained contraction

-at a certain frequency, there is no relaxation

types of muscle contractions

-isometric

-isotonic concentric contraction

-isotonic eccentric contraction

isometric contraction

-same length

-static contractions

-tension developed but joint angles remain constant

-may be used to prevent a body segment from being moved by external forces

when muscles contract they generate forces

isotonic concentric contraction

-same tension

-muscle force> resistance

-moves the body segment

-muscle shortens

isotonic eccentric contraction

-same tension

-muscle force< resistance

-cannot move segment

-muscle lengthens

-controls movement like brakes on a car

series elastic component

-tendons are elastic, resistant distention, and snap back to resting length

-non-contractile parts of muscle and tendons must be pulled tight when muscles contract

-tendons absorb some of tension as muscles contract

force velocity curve

-exercises with high velocities, imply contraction with relatively low force

-light load moved much more quickly than heavy

-would have small strengthening effects since muscle forces are so low

force velocity relationship

-greater force, slower contraction

-defines dynamic properties of cross bridges which cycle during muscle contraction

• force generated by muscle depends on total number of cross-bridges attached

• takes time for cross bridges to attach…

• as velocity decreases, more cross-bridges have time to attach (and generate force), force increases

• as velocity increases, less time to attach, less force

length tension relationship

muscle strength is determined by

-number of fibers recruited to contract

-frequency of stimulation

-thickness of each muscle fiber

• thicker fibers= more myofibrils

-initial length of fiber at rest

• ideal length which can generate max force

-increasing sarcomere length decreases muscle tension

• fewer cross bridges can attach

• at certain point, no tension can be generated

-decreasing sarcomere length decreases muscle tension

• fiber gets shorter and thicker

• increased distance, no cross bridges attach

why did we learn how ATP is made

ATP is needed for:

-myosin ATPase (70%)

• breakdown of ATP on myosin head to allow for cross bridge formation between actin and myosin

-Ca2+ pump to actively return calcium to the sarcoplasmic reticulum (30%) in resting

where muscles get their energy

muscle cells utilize free fatty acids (FFAs), intramuscular triglycerides (IMTGs), intramuscular glycogen stores, and plasma glucose at all times

-the ratio of use of these energy sources changes with exercise

at rest and for mild exercise

-primarily from aerobic respiration of FFA

for moderate exercise

-primarily from glycogen stores, FFAs, and IMTGs (intramyocellular triacylglycerol) (equally mixed fuel source)

for heavy exercise

-primarily from glycogen stores in the working muscle

-as exercise intensity and duration increase, GLUT4 channels are translocated into the sarcolemma to allow more glucose into cells

phosphocreatine

-ATP may be used faster than created through cellular respiration

-so… ADP steals a Pi from phosphocreatine

1) rapid source of renewal of ATP

2) creatine is produced by liver and kidneys (or diet)

3) phosphocreatine stores replenished at rest

-creatine supplements can increase muscle phosphocreatine and aid short term high energy exercise

muscle fiber types

-skeletal muscle fibers divided by contraction speed

• slow twitch (type 1)

• fast twitch (type 2)

-differences due to different myosin ATPase isoenzymes that are slow or fast

slow twitch (type 1)

-slower contraction speed

-can sustain contractions for long periods without fatigue

-large capillary supply with more: mitochondria, respiratory enzymes, and myoglobin

-high oxidative capacity, called slow oxidative fibers

• due to high myoglobin content (red pigment), called red fibers

• found in postural muscles

fast twitch (type 2)

-faster contraction speed

-fatigue fast

-fewer capillaries mitochondria

-respiratory enzymes less myoglobin

-termed white fibers

-high glycogen stores (fast glycolytic fibers)

-typically found in high force producing muscle

intermediate (type 2A)

-fast twitch but with high oxidative capacity

-great aerobic ability

-resist fatigue

-high oxidative capacity, so called fast oxidative fibers

-people vary greatly in percentage of fast or slow twitch fibers in their muscles

• result of genetics and training

muscle fatigue

“reduced ability to generate force”

due to:

-accumulation of extracellular K+

• reducing membrane potential

-depletion of stored glycogen

-reduced sarcoplasmic reticulum calcium release

-lactic acid production and lower pH (note this is heavily debated)

• lactic acid exists in a dissociated state (lactate and H+ ions)

  • accumulation of H+ ions lowers pH and causes muscle cramps

-increased concentration of PO4 due to phosphocreatine breakdown (reduced cross bridge force)

-lack of ATP/ buildup of ADP

-fatigue of upper motor neurons (in the CNS), called central fatigue

adaptations to strength training

-hypertrophy

• type 2 muscle fibers become thicker due to increased amount of actin and myosin (more sarcomeres)

-thicker fibers can split into two fibers

• also increase in size

-requires muscle building and repair…

adaptation to endurance exercise

1. improved ability to obtain ATP from oxidative phosphorylation

2. increased size and number of mitochondria

3. less lactic acid produced per given amount of exercise

4. increased myoglobin content

5. increased intramuscular triglyceride content

6. increased lipoprotein lipase (enzyme needed to utilize lipids from blood)

7. increased proportion of energy derived from fat; less from carbohydrates

8. lower rate of glycogen depletion during exercise

9. improved efficiency in extracting oxygen from blood

10. decreased number of type IIX (fast glycolytic) fibers; increased number of type 2A (fast oxidative) fibers

muscular adaptations

-cytokines: signaling proteins that act as chemical messengers to control cell communication, inflammation, and immune defense

-myokines: cytokines that are releases by skeletal muscle

• irisin: secreted into circulation during aerobic exercise to promote browning of adipose tissue, raises BMR

• adipostatin: stimulates new adipocytes that increase insulin sensitivity

• myostatin: suppresses muscle growth

muscle damage and repair

satellite cells

-stem cells located near muscle fibers

-fuse to damaged muscle cells and repair them

-fuse to each other to form new muscle fibers

-requires titan, nebula, and obscurin

• proteins that are muscle fiber scaffolding

cytokines

-immune cells

-help repair muscle fibers

muscle sensory organs

sensory feedback needed to control skeletal muscle movements, comes from:

Golgi tendon organs

-respond to tension a muscle puts on a tendon

muscle spindle apparatus

-respond to muscle length

-muscles that require more control have more spindles

-stretching a muscle causes spindles to stretch

skeletal muscle reflexes

-skeletal muscles are usually referred to as voluntary and are controlled by descending motor pathways under conscious control

-they can also contract unconsciously in response to certain stimuli- a reflex

Golgi tendon organs

constantly monitor tension in tendons

-sensory neuron stimulates interneuron in spinal cord

-interneuron inhibits motor neuron

-tension in tendon is reduced

reciprocal innervation

-in knee jerk reflex, interneurons are also stimulated in the spinal cord to inhibit antagonistic muscles on that limb

-more complex reflexes require control of muscles on contralateral limb

• called double reciprocal innervation

• Ex: when limb is flexed, antagonistic extensor muscles are passively stretched

cardiac muscle

-striated

-myosin and actin filaments form sarcomeres

-contraction occurs by means of sliding thin filaments

-unlike skeletal muscle fibers, these fibers are short, branched, and connected via gap junctions called intercalated discs

• create electrical synapses that permit impulses to be conducted cell to cell

• faster AP transmission due to intercalated discs

myocardium

-a mass of cardiac muscle cells connected to each other via gap junctions

-action potentials that occur at any cell in a myocardium can stimulate all the cells in the myocardium

-it behaves as a single functional unit

-the atria of the heart= one myocardium

-the ventricles of the heart= another myocardium

calcium channels

-unlike skeletal muscle, voltage gated calcium channels are not directly connected to calcium channels in the sarcoplasmic reticulum

-instead, calcium acts as a second messenger to open sarcoplasmic reticulum channels

-called calcium induced calcium release

-excitation contraction coupling is slower

role of calcium in cardiac muscle

during AP, Na channels open which causes Ca channels to open in transverse tubules

1. Ca diffuse into cytoplasm

2. Ca channels in sarcoplasmic reticulum open; release calcium

3. Ca binds to troponin= contraction

4. Ca pump transports Ca to cisternae of sarcoplasmic reticulum, muscle relaxes

excitation-contraction coupling

depolarization of myocardial cells…

-Ca2+ stimulated Ca2+ release

-APs move along sarcolemma/ T tubules, open voltage gated Ca2+ channels

-Ca2+ (mostly from sarcoplasmic reticulum) binds to troponin to stimulate contraction

repolarization

-Ca2+ in cytoplasm reduced by active transport back into sarcoplasmic reticulum

-myocardium relaxes

smooth muscle

-found in blood vessel walls, bronchioles, digestive organs, urinary and reproductive tracts

• alternating contractions of the circular and longitudinal muscles produce peristaltic waves to propel contents of these organs

-characteristics

• no sarcomeres, but still contain large amounts of actin and myosin

• long actin filaments attached to dense bodies or regions of the plasma membrane

• myosin filaments are stacked vertically and can form cross bridges with actin its entire length

• arrangement allows contraction even when greatly stretched

smooth muscle units

single unit: multiple gap junctions that make neighboring cells behave as a unit

-most smooth muscles are single unit

-they display pacemaker activity moderated by stretch or autonomic innervation

-only a few cells in a single unit receive acetylcholine stimulation

-muscarinic ACh receptors respond by closing K+ channels

-display intrinsic or myogenic electrical activity and contraction in response to stretch without autonomic stimulation

multi unit smooth muscle

-multi unit: require individual nerve innervation (no pacemaker activity)

-few or no gap junctions

-arrector pili muscles in skin and ciliary muscles in eyes are multi unit

autonomic innervation of smooth muscle

-neurotransmitter is released along the length of an autonomic neuron from varicosities

-receptor proteins on the entire surface of smooth muscle cells

-a number of smooth muscle cells are stimulated at once

excitation contraction coupling in smooth muscle

-begins with a sharp rise in intracellular calcium concentrations

-calcium binds to calmodulin (no troponin in smooth muscle)

• activates myosin light chain kinase (MLCK)

-myosin light chain kinase phosphorylates myosin light chains

• this allows myosin to form cross bridges with actin to initiate contraction

-stimulation is graded. more stimulation allows more calcium to enter, which allows stronger contractions

-contractions are slow and sustained

• may enter a “latch state”

smooth muscle relaxation

-calcium is pumped out using calcium ATPase active transport pumps

-calmodulin dissociates from myosin light chain kinase

-phosphate groups are stripped from the myosin by myosin light chain phosphates (MLCP)

functions of the circulatory system

transportation: respiratory gases, nutrients, and wastes

regulation: hormonal (transports) and temperature

protection: clotting and immunity

major components of the circulatory system

1. cardiovascular system

-heart

• four chambered pump

• pushes blood through body

-blood vessels

• arteries, arterioles, capillaries, venules, and veins

• allows blood flow

2. lymphatic system

• lymphatic vessels, lymphoid tissues, lymphatic organs (spleen, thymus, tonsils, lymph nodes)

• transport interstitial fluid

blood

-average adult volume is about 5 liters

-arterial blood: leaving the heart; bright red, oxygenated except for blood going to the lungs (pulmonary artery)

-venous blood: entering the heart; dark red, deoxygenated except for blood coming from the lungs (pulmonary vein)

-made of 45% formed elements and 55% plasma

structure of heart

-heart has 4 chambers

• 2 atria receive blood from venous system

• 2 ventricles pump blood to arteries

• 2 sides of heart are 2 pumps separated by muscular septum

• fibrous skeleton

  • separates atria from ventricles

  • atria work as one unit, ventricles work as a separate unit

  • forms the annuli fibrosi rings, hold in heart valves

right atrium

receives deoxygenated blood from the body

left atrium

receives oxygenated blood from the lungs

right ventricle

pumps deoxygenated blood to the lungs

left ventricle

pumps oxygenated blood to the body

pulmonary circulations

between heart and lungs

-deoxygenated blood pumps to lungs via pulmonary arteries

-oxygenated blood returns to heart via pulmonary veins

system circulations

between heart and body tissues

-oxygenated blood pumps to body tissues via aorta

-deoxygenated blood returns to heart via superior and inferior vena cava

pulmonary and systemic circulations

resistance in systemic circuit> pulmonary

-amount of work is done by left ventricle pumping to systemic is 5-7x greater

• causing left ventricle to be more muscular (3-4x thicker)

**rate of blood flow through systemic= flow rate through pulmonary circulation

atrioventricular (av) valves

-located between the atria and the ventricles

-one way valves

-allow blood to flow from atria to ventricles

-tricuspid: between right atrium and ventricle

-bicuspid or mitral: between left atrium and ventricle

papillary muscles and chordae tendinae prevent the valves from everting

semilunar valves

-located between the ventricles and the arteries leaving the heart

-one way valves

-open during ventricular contraction

-pulmonary: between right ventricle and pulmonary trunk

-aortic: between left ventricle and aorta

opening and closing of valves occur as a result of pressure differences

heart sounds

produced by closing valves

-”lub”

• closing of AV valves

• occurs at ventricular systole

-”dub”

• closing of semilunar valves

• occurs at ventricular diastole

heart murmur

-abnormal heart sounds produced by abnormal blood flow through heart

• many caused by defective heart valves

EXAMPLE:

-mitral stenosis: mitral valve calcifies and impairs flow between left atrium and ventricle

• may result in pulmonary hypertension

cardiac cycle

-repeating pattern of heart contraction and relaxation

-systole: contraction of heart muscles

-diastole: relaxation of heart muscles

end-diastolic volume (EDV)

total volume of blood in ventricles at end of diastole

stroke volume (SV)

amount of blood ejected from ventricles during systole

end systolic volume (ESV)

amount of blood left in ventricle after systole

-1/3 of the end diastolic volume

pressure changes during the cardiac cycle

1. ventricles begin contraction, pressure rises, and AV valves close up (lub); isovolumetric contraction

2. pressure builds, semilunar valves open, and blood is ejected into arteries

3. pressure in ventricles falls; semilunar valves close (dub); isovolumetric relaxation

4. pressure in ventricles falls below that of atria, and AV valve opens. ventricles fill

5. atria contract, sending last of blood to ventricles

electrical activity of the heart

-cardiac muscle cells are interconnected by gap junctions called intercalated discs

-action potentials spread via intercalated discs (gap junctions). once stimulation is applied, impulse flows from cell to cell

-area of heart that contracts from one stimulation event is a myocardium or functional syncytium (remember 2 myocardia)

-atria and ventricles are separated electrically by the fibrous skeleton

sinoatrial node (SA)

-automaticity

• automatic nature of the heartbeat

-”pacemaker cells”

-located in right atrium

-1st/ primary

atrioventricular node (AV) and purkinje fibers

-secondary pacemakers of ectopic pacemakers

-slower rate than the “sinus rhythm”

-slight delay to allow atria to finish contracting

pacemaker cells (different from neurons)

diastolic depolarization

-spontaneous depolarization

-slow, leak channels

-between heartbeats

-triggered by hyper polarization

-at -40mV (cardiac threshold), voltage gated Ca2+ channels open, triggering action potential and contraction

-repolarization occurs with opening of voltage gated K+ channels (K+ flows out of cell)

overall pacemaker potential

pacemaker cells in the SA node depolarize spontaneously, but rate at which they do so can be modulated

sympathetic pacemaker potential

1. epinephrine and norepinephrine increase the production of cAMP, which keeps cardiac pacemaker channels open (sympathetic)

2. called HCN channels for two reasons

a) “H” means hyper polarization-activated

b) “CN” means cyclic nucleotide gated channels (these will also respond to B1 receptors activating cAMP as sympathetic response)

3. Na+ inflow will cause depolarization

parasympathetic pacemaker potential

1. parasympathetic neurons secrete acetylcholine, which opens K+ channels to slow the heart rate

2. movement of K+ out of the cell slows the time it takes to reach threshold and go through depolarization again

= slowing of the heart rate

**this is one of those (weird) time that ACh does not stimulate

conduction of impulses

-action potentials from the SA node spread rapidly

• intercalated discs/ gap junctions

• 0.8-1.0 meters/ second

-at the AV node, things slow down

• 0.03-0.05 meters/ second

• accounts for half of time delay between atrial and ventricular contraction

• allows ventricles to relax and fill with blood

-speed picks up in bundle of His, reaching 5 meters/ second in purkinje fibers

-ventricles contract 0.1-0.2 seconds after atria

myocardial contraction (when heart muscle contracts)

cardiac muscle cells depolarize causing mechanical contraction

-begins with myocardial action potential stimulated by SA node

• causes Ca2+ stimulated Ca2+ release

myocardial action potentials (cardiac cell AP)

-myocardial (cardiac) cells have a resting potential of -85mV

-depolarized to threshold (-40mV) by action potentials spreading from SA node

-voltage gated Na+ channels (fast inward Na+) open, and membrane potential plateaus at -15mV for 200-300 milliseconds

• due to balance between slow influx of Ca2+ and efflux (outward) of K+

-more K+ opened, depolarization occurs

-long plateau prevents summation and tetanus

Reminder!!

-myocardial (cardiac) cells will be stimulated by action potentials from pacemaker cells first (SA node)

-when myocardial cells are depolarized, we will see excitation contraction coupling (actual muscle contraction from Ca2+ stimulated Ca2+ release)

-take away: pacemaker spreads to myocardial resulting in contraction

correlation of myocardial action potential with myocardial cell contraction

-AP of cardiac cells is long

-atria and ventricles contract as single units but cannot sustain contraction (short period)

-long refractory periods before can contract again

electrocardiogram (ECG/ EKG)

-a recording of electrical activity of heart conducted through ions in body to surface

• P wave: atrial depolarization

• QRS wave: ventricular depolarization

• S-T segment: plateau phase

• T wave: ventricular repolarization

-the electrocardiograph records the electrical activity of the heart by picking up the movement of ions in body tissues in response to this activity

• does not record action potentials, but results from waves of depolarization

• does not record contraction or relaxation, but the electrical events leading to contraction and relaxation

• does not measure flow of blood through the heart

correlation of ECG with heart sounds

-1st heart sound (lub) comes immediately after QRS wave as AV valves close

-2nd heart sound (dub) comes at T waves begins and semilunar valves close

types of blood vessels

-arteries

-arterioles

-capillaries

-venules

-veins

tunics of blood vessels

blood vessel walls have 3 tunics

-tunica interna

-tunica media

-tunica externa

tunica interna

-inner layer

-composed of simple squamous endothelium on a basement membrane and elastic fibers

tunica media

-middle layer

-composed of smooth muscle tissue

tunica externa

-outer layer

-composed of connective tissue

arteries

-elastic arteries

-muscular arteries

-arterioles

elastic arteries

-closer to the heart

-allow stretch as blood is pumped into them and recoil when ventricles relax