lecture 10 Flashcards
3 types of muscular tissue and their functions
skeletal - contracts to move bones and stabilize body
cardiac - contacts to move blood blood through heart
smooth - contracts to regulate passage of substances through the body
myology
study of muscular tissue
4 properties of muscular tissue
- electrically excitable
- contractile
- extensible
- elastic
electrically excitable - property
muscle can produce electric signals called muscle action potentials
contractile - property
muscle action potentials stimulate contraction
contraction generates tension on bones which causes movement
extensible - property
tissue can be stretched without tearing
elastic - property
resting length is restored after stretching
difference between extensible and elastic properties (dont mix them up)
elastic - resting length RESTORED after stretching
extensible - can BE STRETCHED
cells of skeletal muscle tissue
myocytes
what do myocytes contain?
myofibrils
muscle (organ) is made up of (3)
muscle fibres
connective tissue
nerve and blood supply
fascia
connective tissue layers that surround muscles
fascia functions
group muscles with similar function
provide passage for nerves and vessels
3 layers of the fascia (superficial to deep)
epimysium
perimysium
endomysium
epimysium (what is it and what is it made of)
most superficial layer of fascia
dense irregular CT that wraps muscles
perimysium (what is it + made of)
intermediate layer of fascia
dense irregular CT that wraps fascicles
fascicles
bundles of muscle fibres (Cells)
endomysium (what is it + made of)
deepest layer of fascia
mostly reticular fibres that wrap individual muscle fibres
layers of muscle (superficial to deep) (7)
epimysium wraps:
muscle
perimysium wraps:
fascicles
endomysium wraps:
muscle fibres which contain:
myofibrils
fascia form:
tendons
tendons
connect muscle to bone via a rope like structure
made of epimysium (dense irregular CT)
aponeuroses
special type of tendon that forms a sheet
(eg. epicranial apoenurosis, connects bellies of occipitofrontalis)
why must muscle be extremely vascularized?
muscles preform aerobic cellular respiration which makes ATP
aerobic = required oxygen continuously
myoblasts
immature muscle cells in the womb, as they mature, they fuse and create multinucleate cells
plasma membrane of myocytes
sarcolemma
T tubules
invaginations of the sarcolemma
cytoplasm of myocytes (and what it is rich in)
sarcoplasm
rich in glycogen
myoglobin
only found in muscle cells
binds O2 at heme
receive O2 from in and outside the cell
myofibrils
long threads of contractile protein filaments called myofilaments
what gives muscle striated appearance?
pattern of overlapping filaments
sarcoplasmic reticulum
specialized SER in muscle cells
stores/releases calcium
folded around each myofibril
triad
where a terminal cisternae meets a T tubule
terminal cisternae
release Ca2+ to each t tubule
muscle hypertrophy
increase in sarcoplasmic volume
each fibre increases volume of cellular contents, mainly myofibrils, mitochondria, and SR
each myofilament is made of contractile units called:
sarcomeres
sarcomere
consists of overlapping thick and thin filaments
all zones and lines of a sarcomere (listed) (5)
I band
Z disc
H zone
A band
M line
A band
where tick and thin filaments overlap, and everything in between
covers most of the sarcomere
H zone
regions BETWEEN the zones of overlap of thick and thin filaments
goes from ends of thin filaments and crosses M line
I band
regions between zones of overlap and Z discs
spans over 2 sarcomeres
M line
Mid line of the sarcomere
Z disc
jagged lines that divide sarcomeres
three types of proteins involved in muscle contraction
contractile proteins
regulatory proteins
structural proteins
contractile proteins (2)
work to shorten the sarcomere
myosin - thick filaments
actin - thin filaments
myosin (4)
- a motor protein - contractile
- makes up thick filaments in sarcomere - 300 each ish
- has heads that extend and contact thin filaments
- converts chemical potential energy in ATP to mechanical energy
myosin head binding sites
top - actin binding site
side - ATP binding site
actin (3)
- cytoskeletal protein - contractile
- helical thin filaments
- have myosin binding sites
regulatory proteins
associate with thick and thin filaments to control contraction
troponin - binds Ca2+, moves tropomyosin to reveal myosin binding sites on thin filament
tropomyosin - blocks myosin binding sites on thin filaments
troponin
regulatory protein - binds Ca2+, moves tropomyosin to reveal myosin binding sites on thin filament
tropomyosin
regulatory protein - blocks myosin binding sites on thin filaments
structural proteins
stabilize / connect sarcomere to other structures
there are dozens, but know 2
titin - large elastic protein, spans M line to Z disc, stabilizes position of thick filaments
dystrophin - connect thin filaments to integral membrane proteins in the sarcolemma, transmits tension of sarcomere to tendons
titin
structural protein - spans Z disc to M line, stabilizes thick filaments
dystrophin
structural proteins - connects thin filaments to integral membrane proteins in sarcolemma, which attach to ECM components that attach to the fascia transmitting tension to tendons
how does dystrophin transmit tension of sarcomeres to tendons?
tension is transmitted from thin filaments to transmembrane proteins (via dystrophin) attached to components of ECM. This is then attached to fascia which form tendons
contraction cycle steps (4)
assume Ca is already binded to troponin
- myosin binds and hydrolyzes ATP
- myosin binds thin filaments, forms cross bridge
- myosin pulls thin filaments, power stroke
- myosin releases thin filaments
contraction cycle step 1 in detail
myosin binds and hydrolyzes ATP
myosin head hydrolyzes (makes ATP go to ADP and a P) ATP and becomes energized
contraction cycle step 2 in detail
myosin binds to thin filaments, forms cross bridge
myosin head will bind to actin, provided the myosin binding site is free (troponin has moved tropomyosin). cross bridge will form between myosin head and myosin binding site on actin
contraction cycle step 3 in detail
myosin pulls thin filaments, power stroke
myosin head pivots, pulling thin filament past the thick one to the centre of the sarcomere, also called a power stroke (think of rowing an ore)
contraction cycle step 4 in detail
myosin releases thin filament
a new ATP will bind to the myosin head, which will detach the cross bridge between myosin head and actins myosin binding site
role of Ca2+ in muscle contraction
change the conformation of troponin, which will let troponin move tropomyosin off of the myosin binding sites on actin
what happens to the H zone as the sarcomere shortens
it disappears
what happens to the I band as the sarcomere shortens
it narrows
how to sarcomeres move bones?
they shorten and pull on adjacent sarcomeres, they keep transmitting tension until the whole muscle fibre shortens
4 steps of how sarcomeres move bones
- sarcomere shortens
- pulls connective tissue
- pulls on tendons
- moves bones
length tension relationship
there is an optimal amount of filament overlap at rest
if overlap is too much, myosin cannot generate a lot of tension
- no room for sliding of thin filaments
if not enough, myosin cant generate much tension
- too few cross bridges
where is Ca2+ for muscle contraction stored
SER (sarcoplasmic) and mitochondria
NMJ (neuromuscular junction)
where neurons and muscles meet, where somatic muscle neuron releases chemical signals (eg, acetylcholine)
acetylcholine
released by neurotransmitters at NMJ, will bind to ligand gated ion channel and cause slight depolarization
ligand gated ion channel
acetylcholine will bind to this and there will be slight depolarization in the cell, causing the voltage gated sodium channels to open
ratio of sodium potassium pump
3:2
3 Na+ out / 2K+ in
the inside of the cell is more ______ than the outside
negative
depolarization
when the cell has a less negative charge than resting
repolarization
the restoration of a negative membrane potential after depolarization
what causes changes in membrane potential during action potentials?
plasma membrane transporters
- voltage gated ion channels
- signal that opens them is a change in membrane potential
- they facilitate diffusion and let ions flow down their gradients
voltage gated sodium channels (VGSCs)
allow Na+ to enter the cell
- only open when a change in membrane potential occurs
(in this case by the ligand gated channels)
how does acetylcholine binding to a ligand gated ion channel cause depolarization?
acetylcholine binds to a ligand gated channel which allows sodium into the cell. this causes a very slight depolarization which opens the Voltage gated sodium channels and will fully depolarize the cell
when does repolarization occur?
when the voltage gated potassium channels open and the sodium ones close
voltage gated potassium channels (VGKCs)
responsible for repolarization
- slower to open than VGNCs
- once open K+ flows rapidly out
- close as membrane repolarizes
how to action potentials stimulate muscle contraction
excitation-contraction coupling
excitation contraction coupling
- span of events that release calcium from the Sarcoplasmic reticulum to carry out contraction
- when action potential is done, Ca2+ ATPases pump it back to the SER or out of the cell and muscles relax
steps of excitation contraction coupling (3)
- action potential travels along sarcolemma
- triggers change in VGCCs that causes release of Ca2+ into the sarcoplasm
- Ca2+ carries out its processes with troponin and such
VGCCs (how much does it increase ca conc)
- has a plug in the sarcolemma, when moved Ca2+ rushed out of the SR into the cell
- increase intracellular Ca concentration by 10x
acetylcholinesterase
enzyme that degrades acetylcholine
what happens when there is no Ca2+ in the sarcoplasm?
muscles are relaxed
all 9 steps of muscle contraction
(all steps, excitation contraction coupling as well)
- nerve action potential in somatic motor neuron triggers release of acetylcholine
- ACh binds receptors, triggering muscle action potential
- acetycholinesterase destroys ACh to prevent more action potentials unless there is more ACh
- MAP travels along sarcolemma, triggers change in VGCCs, releases Ca2+ into sarcoplasm
- Ca2+ binds troponin, moving tropomyosin off myosin binding sites on actin
- myosin heads bind actin (cross bridge), power stroke, release
- VGCCs close, Ca2+ ATPase pumps Ca2+ into SR or out of cell (active transport)
- tropomyosin moves back onto actin, blocking myosin binding sites
- muscle relaxes
action potential to contraction ratio
1:1
more frequent action potentials =
more tension
motor unit
1 somatic motor neuron + all of the skeletal muscle fibres it synapses with (~150)
large muscles have many
motor units
twitch contraction
contraction generates in all skeletal muscle fibres of one motor unit due to one action potential
3 phases of twitch contractions
latent period
contraction period
relaxation period
latent period of twitch contraction
2 msecs
delay between stimulus and muscle action
period in which action potential is moving through the sarcolemma and calcium is being released from the SR
contraction period of twitch contraction
10-100msecs
cross bridges form and sarcomeres shorten
maximum tension develops in this period
relaxation period of twitch contraction
Calcium pumped back into SR
myosin detaches from actin
tension decreases
refractory period
a muscle cannot respond to 2 stimuli at once
temporarily unresponsive to new signals
muscle tone functions to ____
prevent fatigue, make movements smooth rather than jerky
what is muscle tone?
some skeletal muscles produce tension to stabilize positions, but not enough to move bones (eg, postural muscles in the neck)
which motor units work first in contraction of bigger muscles like the biceps brachii?
weaker, than stronger
muscle tone produces ____
small involuntary contractions of alternating motor units that lead to slight stiffness of the muscle
2 types of contractions (+ subtypes)
isotonic
- concentric
- eccentric
isometric
isotonic contractions
concentric
eccentric
concentric contractions
isotonic contraction
occur when the muscle shortens to decrease the angle around a joint
(biceps curls)
eccentric contractions
isotonic contraction
occurs when muscle resists a load as it lengthens
(the negative of preacher curls)
isometric contraction
tension generated is not enough to move the load, but functions to stabilize many joints
(static plate hold)
what do muscles require ATP for other than contraction?
membrane transport, protein synthesis
3 ways muscles generate ATP
- consuming creatine phosphate
- aerobic respiration
- anaerobic glycolysis
consuming creatine phosphate (way to make ATP) (what is the catalyst)
unused ATP is dephosphorylated to make creatine phosphate. muscles can rapidly dephosphorylate creatine phosphate to regenerate ATP. both to and from transfers are catalyzed by creatine kinase
creatine consumption - analogy
storing money in a bank account when not needed, can withdraw quickly at any time
creatine kinase
catalyst that catalyzes the forward and backward reactions of creatine + phosphate = creatine phosphate to either store (forward) or make (backward) ATP
aerobic respiration simple steps (3)
- glycolysis
- products transported to mitochondria
- many reactions occur to make lots of ATP
aerobic respiration full process
- glucose broken into 2 pyruvate, generates 2 net ATP and NADH (loaded w/electrons)
- pyruvate sent to mitochondria if O2 is present
- converts carbons to CO2 - exhaled, electrons from bonds go to electron transport chain
- flow of e- down the chain = free energy = harnessed to make 30-32 ATP
number of ATP produced per glucose
2
number of ATP produced per glucose with oxygen
30-32
anaerobic glycolysis
happens when O2 is absent and muscles cant respire products of glycolysis. pyruvate will consume electrons from NADH and become lactic acid. this acts as a place for e- to go since there is no terminal receptor, O2. NADH becomes NAD+, and glycolysis can continue
how does pyruvate fermenting to lactic acid facilitate ATP synthesis?
pyruvate accepts electrons from NADH and turns it into NAD+, and that will be used to preform glycolysis again
aerobic respiration chemical reaction
glucose + O2 –> CO2 + H2O + ATP (30-32)
glycolysis chemical reaction (no O2)
glucose + 2NAD+ –> 2pyruvate + 2NADH + 2ATP
mitochondrial reactions in aerobic respiration
krebs cycle mainly
why do muscles needs O2 after exercise? (3)
- replenish myoglobin
- convert lactic acid back to glucose in the liver
- replenish creatine phosphate
oxygen debt
muscles in need of O2 AFTER exercise
3 types of muscle fibres
(not skeletal, cardiac , etc)
slow oxidative fibres
fast oxidative-glycolytic fibres
fast glycolytic fibres
slow oxidative fibres
dark red
- slow contraction (100-200msecs)
- do not fatigue easily - function in postural muscles/endurance
- oxidative - aerobic respiration as main metabolic mode
fast oxidative-glycolytic fibres
rosey colour - largest
- fast contraction (<100msecs)
- not as resistant to fatigue, reaches max tension fast
- used in moderate exercise
- oxidative - aerobic respiration as main
- glycolytic - can use anaerobic glycolysis
- large glycogen stores
fast glycolytic fibres
white in colour
- reach max tension quick but fatigue easily
- function during quick intense movements
- large glycogen stores
- uses anaerobic glycolysis when O2 is limited
what gives muscle cells their colour? which muscle cells have which colour?
myoglobin and capillaries - dark red or rosey
few of those and few mitochondria - white
slow oxidative fibres - dark red
fast oxidative-glycolytic fibres - rosey
fast glycolytic fibres - white
cardiac muscle tissue features (there are fucking lots)
- found in heart
- striated
- intercalated discs
- has desmosomes and gap junctions
- no epimysium
- single nucleus per fibre
- have more/larger mitochondria than other muscle cells
- longer lasting contractions (10-15x) due to calcium proteins closing slowly
- autorhythmic - no acetylcholine required
- mainly uses aerobic respiration, anaerobic for short periods
smooth muscle tissue
- NOT arranged in sarcomere
- intermediate filaments assist in contraction
- not regularly arranged - hence non striated
- single nucleus
- no t tubules
- caveolae - collect Ca2+ rich interstitial fluid
caveolae
shallow invaginations of the sarcolemma in smooth muscle cells that collect calcium rich interstitial fluid
how does smooth muscle contract?
thin filaments are attached to dense bodies, so when they contract, the cell shortens and twists
why does smooth muscle contract slower than any other type?
they have a smaller SR and no T tubules = delay in calcium reaching troponin
what contributes to smooth muscle tone?
calcium leaves smooth muscle slowly
types of smooth muscle tissue (2)
viceral
multi unit
viceral smooth muscle
- autorhythmic
- gap junstions
- found in walls of hollow organs and blood vessels
- single unit
multi unit smooth muscle
- each fibre has its own autonomic motor neuron
- found in walls of large arteries, arrector pili, around pupil of eye
unique smooth muscel stress-relaxation response and why its important
when stretched, smooth muscle initially contracts, and tension decreases over time
important in hollow organs and vessels so contents remain under constant pressure
Ca 2+ ATPases
pump Ca2+ back into the SR or out of the cell once it is no longer needed for muscle contraction
