physio exam 2 muscles Flashcards
skeletal muscle structure
striated, series of alternating light and dark bands with multiple nuclei
large
muscle fiber
multiple nuclei
cell formed by fusion of undifferentiated, mono nucleated myoblasts into single multinucleate cell
formation of muscle cell/fiber
development
fusion of multiple, undifferentiated mono nucleated myoblast cells into single multinucleated cell
muscle fiber damage
repair by undifferentiated satellite cells
become active in response to injury and undergo mitotic proliferation.
daughter cells differentiate into myoblasts that can fuse to form new fibers or fuse with injured ones to reinforce
regulated by hormones
satellite cells
undifferentiated
repair muscle cells
activated by injury and undergo mitotic proliferation
daughter cells differentiate into myoblasts and fuse to form new muscle cells or fuse with injured sites to reinforce
regulated by hormones
hypertrophy
satellite cell mediated
muscle
skeletal muscle fibers bond together by connective tissue and attached to bones by tendons
tendons
bundles of connective tissue consisting of collagen fibers
attach muscles to bones
striated muscles
result of arrangement of cytosolic proteins organized into thick and thin filaments
filaments arranged into cylindrical bundles = myofibrils
most of the cytoplasm of a muscle fiber is full of myofibrils
thick filaments
composed of myosin
myosin - 2 heavy chains and 4 light chains
2 globular heads and an intertwined heavy chain tail forming cross bridges to thin filament and exert contraction forces
myosin
make up thick filament
has 2 heavy chains and 4 light chains
2 globular heads and a tail (intertwined heavy chains)
each globular head has 2 binding sites - thin filament attachment and ATP binding (enzyme myosin-ATPase)
myofibril
filaments arranged into bundles of myofibrils
most of cytoplasm of a fiber is filled w myofibrils
linked to tendons
myosin-ATPase
binds to globular head of myosin in thick filaments
hydrolyzes sound ATP to harness energy for contraction
thin filaments
composed of actin, nebulin, troponin and tropomyosin
actin
makes thin filament
globular protein w monomer
polymerizes w other actins to form polymer of helical chains
each actin has binding site for myosin
sarcomere structure
a repeating unit of thick and thin filament pattern
each sarcomere contains 2 sets of thin filaments,
each
how skeletal muscle fibers are classified
- their maximal velocities of shortening (fast or slow twitch)
- major pathway they use to form ATP (oxidative or glycolytic)
2a. enzymatic machinery for synthesizing ATP
fast and slow twitch fibers
contain myosin that differ in maximal rates at which they use ATP
myosin subtype in each fiber determines the maximal rate of cross-bridge cycling and thus maximal shortening velocity
slow twitch fibers
type 1 fibers
contain myosin with low ATPase activity
type 1 fibers
slow twitch fibers
contain myosin with LOW ATPase activity
fast twitch fibers
type 2 fibers
myosin with high ATPase activity
type 2 fibers
fast twitch
contain myosin with high ATPase activity
main myosin subtypes are 2A and 2X (faster)
oxidative fibers
red muscle fibers
- red bc Mb
numerous mitochondria and have high capacity for oxidative phosphorylation
ATP produced is dependent on blood flow to deliver O2
these fibers are surrounded by blood vessels
contain myoglobin Mb - increases rate
myoglobin
in oxidative fibers = red muscle fibers
increases rate of oxygen diffusion into the fiber and provides small store of O2
gives fiber a dark red color
red muscle fibers
oxidative fibers has red color bc of high Mb conc.
lots of mitochondria =
high capacity for oxidative phospho.
surrounded by blood vessels
rely on blood flow to carry O2
Mb is O2 binding protein that increases rate of O2 diffusion into muscle fiber and gives red color
glycolytic fibers
white muscle fiber
FEW mitochondria
HIGH glycogen
HIGH glycolytic enzymes
LOW O2 use
LOW surrounding blood vessels
Little Mb
3 principal type sof skeletal muscle fibers
- Slow oxidative fibers (type 1)
- fast oxidative glycolytic fibers (2A)
- Fast glycolytic fibers (2X)
slow oxidative fibers
type 1
low myosin-ATPase activity with high oxidative capacity
- generate least isometric tension
fast oxidative glycolytic fibers
type 2A
high myosin ATPase activity with high oxidative capacity and IM glycolytic capacity
fast glycolytic fibers
type 2X
combine high myosin-ATPase activity with high glycolytic capacity
- generate greatest tension
high myosin-ATPase activity with High glycolytic capacity
fast glycolytic fibers -2X
low myosin ATPase activity with high oxidative capacity
slow oxidative fibers
- generate least tension
high myosin ATPase activity and high oxidative capacity and IM glycolytic activity
fast oxidative glycolytic fibers
- generate greatest isometric tension
isometric tension
slow oxidative – least tension
fast glycolytic - greatest tension
due to DIFFS in fiber DIAMETER
slow fibers have smaller diameters than fast fibers
cross-bridges in force
during contraction
slow oxidative = smallest proportion of cross bridges
greatest in fast-glycolytic
differences of muscle fibers
- fast and slow twitch - max velocities of shortening/contraction
- pathway to form ATP (mitochondria)
- rate ATP consumed
- cross bridge cycling
- myosin ATP activity
- isometric tension
- resist fatigue
capacity to resist fatigue
fast glycolytic 2X - fatigue rapidly
slow oxidative 1 resistant to fatigue and maintain contractile activity for long periods with little loss of tension
fibers resistant to fatigue
type 1 slow oxidative
can maintain contractile activity for long periods with little loss of tension
rapid fatigue
2X fast glycolytic fibers
differences in maximal shortening velocity/contraction due to…
diff myosin enzymes with high/low ATP activity, giving rise to fast or slow twitch fibers
characteristics of type 1 slow oxidative fibers
oxidative phosphorylatioon prods ATP
lots of mitochondria
lots of capillaries
high Mb = red muscle
slow rate of fatigue
slow contraction velocity
small fiber diameter
low myosin ATPase activity
characteristics of fast-oxidative glycolytic fibers - 2A
oxidative phosphorylation in primary source ATP
many capillaries
high Mb = red muscle
fast contraction velocity
large fiber diameter
IM
2X characteristics of fast glycolytic fibers
glycolysis is main source ATP
few mitochondria
few capillaries
low Mb = white muscle
fastest contraction velocity
fast fatigue rate
high glycogen content
high myosin-ATPase activity
large fiber diameter
total tension of muscle depends on
- amount of fiber developed by each fiber
- # fibers contracting at a timealso controls shortening velocity
- # of fibers contracting at a time depends on # of fibers in each motor unit (size) and # of active motor units
factors determining muscle tension
- AP freq.
- Fiber length
- fiber diameter
- Fiber type
- fatigue
# of active fibers
force of single fiber
depends on fiber diameter
greater diameter = greater force
fast glycolytic have largest diameter
fast glycolytic motor units
have more muscle fibers and larger diameters so produces MORE force
recruitment
process of increasing the # of ACTIVE motor units in muscle
- activate excitatory synaptic inputs to more motor neurons
more active motor neurons, more motors units recruited and greater muscle tension
- depends on motor neuron size
factors for recruitment
for motor units
1. motor neuron size = diameter of neuronal cell body/axon
same # of Na enter cell at excitatory synapse - greater depolarization in small neuron
given same synaptic input, small neurons recruited 1st and generate APs 1st
large neurons recruited as synaptic input increases
- smallest motor neurons innervate slow oxidative motor units = recruited 1st
how motor neuron size affects recruitment of motor units
given same synaptic input/Na enter cell at excitatory synapse -
small neuron undergoes greater depolarization and generates AP 1st so recruited 1st (slow oxidative motor units)
as input increases w strong contraction, large neurons recruited (fast glycolytic units)
neurons innervating different motor units
smallest motor neurons innervate slow oxidative motor units
(recruited 1st)
strong contraction - fast glycolytic 2X motor units - fatigue rapidly
neural control of whole muscle tension involves…
- freq of APs in motor units (to vary tension)
- recruitment of motor units
motor neuron activity
occurs in bursts of APs which prod titanic contractions of motor units rather than single twitches
(tension of single fiber increases from twitch to titanic contraction)
low intensity exercise
increase # of mitochondria in muscle fibers and
shift myosin composition of fast fibers from 2X to 2A
increase # capillaries around fibers
increased ability to sustain muscle contraction the oxidative metabolism
w/ minimal fatigue
improve delivery O2
high intensity exercise
fast twitch fibers recruited
fibers increase in diameter (hypertrophy) due to satellite cell activation and increased synthesis of actin and myosin filaments which form more myofibrils
myosin of fast fibers shifts from 2A to faster 2X
glycolytic activity increased by increasing synthesis of glycolytic enzymes
rapid fatigue
gain strength without hypertrophy
increased synchronization in motor-unit recruitment
enhanced ability to recruit fast glycolytic 2X motor neurons
reduced inhibitory afferent input from tendon sensory receptors
effects of exercise on fibers
does not change proportions of fast and slow fibers in a muscle
DOS change proportion of 2A and fast glycolytic 2X fibers in a muscle
possible influences on muscles
contractile activity, pattern APs, intracellular Ca+, tension, growth factor 1, anabolic steroids androgens
myostatin
regulatory protein produced by skeletal muscles that binds to same muscle cells receptors exerting NEGATIVE feedback effect to prevent hypertrophy
aging
decrease in fiber diameter
decreases capacity to generate tension
soreness
structural damage to muscle cells activates inflammation
histamine released and activates endings of pain neurons in muscle
results from lengthening muscle fiber which damages more than shortening or isometric contraction
isometric contraction
no change in muscle length
but contractions/force
stabilizes
lever action of muscles and bones
contracting muscles exert pulling force on bones thru connecting tendons
contracting muscle exerts pulling force and muscle shortens
flexion
bending limb at a joint
laws of chem and physics EX
lever system of muscles, bones, joints
mechanical disadvantage offset by increased maneuverability
disadvantage = tension exerted my muscle is greater than load supporting
lever sys amplifies velocity of muscle shortening
tension produced by whole-muscle contraction depends on
amount of tension each fiber develops and the number of active fibers in the muscle.
order of recruitment
- slow oxidative motor units
- fast oxidative glycolytic motor units
- fast glycolytic during strong contractions
Increasing motor-unit recruitment increases the velocity at which a muscle will move a given load.
why increase recruitment
Increasing motor-unit recruitment increases the velocity at which a muscle will move a given load.
poliomyelitis
viral disease
destroy motor neurons
paralysis
respiratory failure
muscle cramps
Involuntary tetanic contraction of skeletal muscles
APs fire at abnormally high rates bc electrolyte imbalances in ECF or chem.
spicy food reduces muscle cramps by stimulating sensory receptors they activate neural pathways that reduce excessive firing go alpha motor neurons that cause cramps
Involuntary tetanic contraction of skeletal muscles
muscle cramps
electrolyte imbalance of ECF or chem.
hypocalcemia tetany
involuntary titanic contraction of muscles when extracellular ca2+ conc. decreases 40% below normal.
changes the plasma membrane
low HYPOCALCEMIA extracellular Ca2+ increases the opening of Na+ channels in excitable membranes = membrane depolarization and spontaneous firing of APs
cause increased muscle contraction ~ cramping
muscular dystrophy
genetic degeneration of muscle fibers - death from respiratory/cardiac fail
defect or absence of proteins that make up costumers in striated muscles
costameres
clusters of structural and regulatory proteins that link he Z disks of outermost myofibrils to sarcolemma and ECM
- absent in muscular dystrophy
proteins of costameres fxns
- some absent in muscular dystrophy
transmit force from sarcomeres to ECM and muscle fibers
stabilize sarcolemma
Duchenne muscular dystrophy
sex linked rec. mutation on X chromosome codes for protein dystrophin
dystrophin forms link ~ contractile filament actins and proteins embedded in overlying sarcolemma so when absent, muscle fibers subject to repeated contraction may rupture
dystrophin
large costamere protein related to muscular dystrophy
forms link ~ contractile filament actins na proteins embedded in overlying sarcolemma
in absence, fibers subjected to deformation during contraction subject to rupture
myasthenia gravis
neuromuscular
worsens with muscle usage
CAUSE - destruction of nicotinic ACh receptor proteins of motor end plate, mediated by antibodies of own immune sys
release of ACh from axon terms is norm but magnitude of end plate potential is reduced bc decreased availability of receptors
myasthenia gravis cause
autoimmune
destruction of nicotinic ACh receptor proteins of motor end plate by antibodies of own immune system
myasthenia gravis treatment
autoimmune -
Acetylcholinesterase AChE inhibitors -pyridostigmine
compensate for reduction in ACh receptors by prolonging time ACh is at synapse
suppress immune sys with glucocorticoids
remove thymus to reduce production of antibodies
plasmapheresis replaces plasma with offending antibodies
smooth muscle
LACK cross striated banding patterns found in skeletal/cardiac fibers
nerves to them are part of AUTONOMIC NS, not somatic
NOT under direct voluntary control
- uses cross bridge movements ~ actin and myosin filaments to generate force
Ca ions control cross bridge activity
muscle is smaller and spindle shaped
mono nucleated and can divide thru lifetime
regulated by paracrine
smooth vs skeletal muscles
SMOOTH:
spindle shaped, smaller
mono nucleated
divide thru lifetime
lack cross-striated banding
autonomic NS
involuntary
SKELETAL - larger
multinucleate, limited ability to divide once differentiated
somatic
BOTH - thick myosin containing filaments and thin actin containing filaments (tropomyosin)
smooth muscle filaments
thick myosin-containing filaments and thin actin-containing filaments. NOT organized into MYOFIBRILS as in striated muscles
tropomyosin present in the thin filaments, protein troponin is absent.
protein caldesmon associates w/ the thin filaments;
The thin filaments are anchored either to the plasma membrane or to cytoplasmic structures - dense bodies, which are functionally ~ to the Z lines in skeletal muscle fibers.
smooth muscle myosin and actin
less than in striated muscles
actin conc is MORE
smooth muscle isometric tension
varies w/ fiber length
tension highest at IM lengths
adaptive ability of smooth muscle
since smooth muscles surround organs that can change in volume and therefore change length of smooth muscle walls,
muscle fibers retain ability to develop tension
smooth muscle property surrounding organs
skeletal muscle - optimal length for force generation is narrow. When stretched/contracted too much, the thick thin filaments within the muscle fibers might lose their overlap, reducing the force-generating capacity of the muscle.
smooth muscles - a broader range of lengths for force generation. advantageous
if skeletal muscle fibers were subjected to more distortions they might be stretched beyond their optimal length, leading to a reduction in force generation.
overview of smooth muscle contraction and control
changes in cytosolic Ca2+ conc control the contractile activity in smooth muscle fibers
different bc smooth lacks Ca2+ binding protein of troponin so instead, cross bridge cycling controlled by Ca regulated enzyme that phosphorylates myosin
cross bridge activation of smooth muscles
smooth muscle lacks Ca2+ binding protein troponin
so tropomyosin is blocks cross bridge access to actin
thin filament is NOT main regulator of cross bridge cycling
controlled by Ca2+ regulated ENZYME THAT PHOSPHORYLATES MYOSIN
only phosphorylated form of smooth muscle myosin can bind actin and undergo cross bridge cycling
steps of cross bridge activation in smooth muscle
- increase in cytosolic ca2+. Ca2+ binds calmodulin protein in cytosol of cells (similar to troponin)
- Ca2+–calmodulin complex binds another cytosolic protein, myosin light chain kinase, activating enzyme
- active myosin light chain kinase uses ATP to phosphorylate myosin light chains in globular head of myosin
- phosphorylation of myosin drives cross bridge away from thick filament backbone, allowing it to bind actin
- cross bridges of thru repeated cycle of force generation as long as myosin light chains are phosphorylated
calmodulin
Ca2+ binding protein in cytosol that’s similar to troponin and as a complex with Ca2+, binds myosin light chain kinase to activate the enzyme and allow cross bridging
mediating CBC in smooth vs skeletal muscles
Ca2+ mediated changes in THICK filament for smooth muscles
Ca2+ mediated changes in THIN filament of skeletal muscles
myosin of smooth muscles
Myosin has LOW ATPase activity
rate of ATP hydrolysis determines rate of CBC and shortening velocity, smooth muscle shortening is slower and less fatigue
ATP hydrolysis determines
CBC and shortening velocity
smooth muscle shortening is SLOWER (myosin has LOW ATPase activity)
SLOW energy use = LOW fatigue
functions of ATP in smooth muscle
- hydrolyzing ATP to phosphorylate myosin light chain starts cross bridge cycling
- after CBC, 1 ATP per cycle is hydrolyzed to provide energy for force generation
to relax a contracted smooth muscle
myosin dephosphorylated so cant bind actin
dephospo mediated by myosin light chain phosphatase enzyme
when cytosolic ca2+ conc. increases, rate of myosin phosphorylation by activated kinase exceeds rate of dephospho by phosphatase and phosphorylated myosin increases = bind actin = increase tension
when Ca2+ conc decreases, rate phosphorylation falls below rate of dephosphorylation and relaxation
latch state
when stimulation persists and cytosolic Ca2+ conc is elevated,
rate of ATP hydrolysis DECLINES even tho isometric tension maintained (without movement)
dissociated of cross Bridges from actin occurs at slow rate
= ability to maintain tension for long time with low rate of ATP consumption
- sphincter muscles of GI tract
sources of increasing cytosolic Ca2+
- sarcoplasmic reticulum
- extracellular ca2+ entering thru plasma membrane Ca2+ channels
sarcoplasmic reticulum on cytoplasmic Ca2+ conc
no t-tubules
APs in plasma memb coupled to release of sarco reticulum Ca2+
OR secondary messengers released from plasma membrane can trigger release of Ca2+ from sarco reticulum
What about extracellular Ca2+ in excitation–contraction coupling?
voltage-sensitive Ca2+ channels in the plasma membranes
ECF Ca2+ is»_space; cytosol
so, opening of Ca2+ channels in plasma membrane results in increased flow of Ca2+ into cell.
removal of Ca for relaxation
removed from cytosol
ACTIVE transport of Ca2+ back into the sarcoplasmic reticulum and out across the plasma membrane.
degree of Ca activation ~ diff muscle types
skeletal muscle - single AP releases sufficient Ca2+ to saturate all troponin sites on the thin filaments,
SMOOTH - only a portion of cross-bridges are activated in response to most stimuli.
tension generated by a smooth muscle cell can be graded by varying cytosolic Ca2+ conc. The greater the increase in Ca2+ concentration, the greater the number of cross-bridges activated and the greater the tension.
smooth muscle tone
cytosolic Ca2+ conc is sufficient to maintain low basal CBC activity in absence of external stimuli
Inputs Influencing Smooth Muscle Contractile Activity
electrical activity in plasma membrane,
NTs released by autonomic neurons
hormones
stretch
- influ contractile activity by alter cytosolic ca2 conc
membrane activation for smooth muscle contraction
in smooth muscles in which APs occur, Ca ions, NOT than sodiumNa ions, carry a positive charge into the cell so depolarization of the membrane opens voltage-gated Ca2+ channels, producing Ca2+-mediated rather than Na+-mediated action potentials.
smooth muscle cytosolic Ca2+ conc can be increased (or decreased) by graded depolarizations (or hyper- polarizations) in membrane potential, which increase or decrease the number of open Ca2+ channels.
pacemaker potential
membrane potential change occurring during the spontaneous depolarization to threshold
smooth muscle gradually depolarize until threshold and prod AP
depolarize and then depolarize so seq. of APs prod rhythmic state of contractile activity
slow waves
periodic fluctuations from membrane potential drifts up and down due to regular variation in ion flux across the membrane
1. excitatory input, slow waves depolarized above threshold and APs lead to contraction
nerves and hormones on contraction
NT release by autonomic neurons
smooth muscle cells do NOT have a specialized motor end-plate region
varicosities of autonomic neurons contain NTs in vesicles that are released when AP passes
varicosity
axon of a postganglionic autonomic neuron enters smooth muscle cells, divides into many branches, each branch containing a series of swollen regions that contains many vesicles filled with neurotransmitters, some of which are released when an action potential passes the varicosity
response from chemicals
type of response (excitatory or inhibitory) depends not on the chemical messenger, but on the RECEPTORS the chemical messenger binds to in membrane and on intracellular signaling those receptors activate.
local factors on smooth muscles
altering smooth muscle contraction in response to changes in the muscle’s immediate internal environment, which can lead to regulation that is independent of long-distance signals
relaxation
nitric oxide NO - paracine, relaxation
Nitric oxide NO
paracrine compounds for smooth muscle relaxation
NO is released from some axon terminals (paracrine) influences cells very near release sites
stretching
Stretching opens mechanically gated ion chan- nels, leading to membrane depolarization. The resulting contrac- tion opposes the forces acting to stretch the muscle.
types of smooth muscle
smooth muscle cells form layers of muscle tissue within an organ
1. single unit smooth muscles
2. multiunit smooth muscles
single unit smooth muscles
undergo synchronous activity, both electrical and mechanical
each muscle cell is linked to adjacent fibers by GAP JUNCTIONS allow APs occurring in 1 cell to propagate to others by local currents.
some are pacemaker cells that spont gen. APs and conducted by gap junctions to rest
- stretching
EX of single unit smooth muscles
GI tract, uterus
contractile response can often be induced by stretching
multi unit smooth muscle
NO/FEW GAP JUNCTIONS
cells respond independently. muscle tissue behaves as multiple units
richly innervated by branches of the autonomic NS
contractile response of muscle tissue depends on the # of muscle cells activated and freq of nerve stimulation
cardiac muscle
striated muscle with regularly repeating sarcomeres composed of myosin-containing thick filaments interdigitating w thin filaments that contain actin
Troponin and tropomyosin present in thin filament
Cellular membranes include a T-tubule system and assoc. Ca2+-loaded sarcoplasmic reticulum
mono nucleated
Adjacent cells are joined end to end at structures called intercalated disks (contain desmosomes)
intercalated disks
adj. cells of cardiac muscle are joined end to end here
contain desmosomes that hold cells together and myofibrils attach
also contain GAP JUNCTIONS
arranged in LAYERS
surround heart
Excitation–Contraction Coupling
in Cardiac Muscle
contraction in resp to Memb AP that propagates thru T-tubules
depolarization due to influx of Ca2+ thru voltage gated Ca2 channels = L-type Ca2 channels (modified DHP receptor)
entering Ca2 depolarizes plasma web and cause small inc in cytosolic Ca2+ conc and triggers release of larger Ca2 amount from sarcoplasmic reticulum
L-type Ca2 channels
long lasting channels special for cardiac muscle
allow depolarization
modified DHP dihydropyridine receptors that act as voltage sensor
cardiac muscle contraction
- plasma membrane depolarized by influx of Na entry
- APs begin
- depolarization triggers L-type Ca2 channels in t-tubulin for propagation of AP
- triggers amount of Ca2 to enter cytosol and contribute to depolarization
Ca2 binds and open ryanodine receptor ca2 channels in sarcoplasmic reticulum membrane - Ca2 flow into cytosol, increase Ca2 conc
- binding ca2 to troponin exposes CBC binding sites on thin filaments
- CBC causes force gen. and sliding of filaments
- Ca2 ATPase pump return Ca2 to sarcoplasmic retic
- Ca2+ ATPase pumps and Na/Ca exchangers remove ca2 from cell
- membrane potential depolarized when K+ exits to end AP
special effects of Ca2+ in cardiac muscle
small increase in cytosolic Ca2+ conc serves as a trigger for the release of larger amount of Ca2+ from the sarcoplasmic reticulum. BC ryanodine receptors in the sarcoplasmic reticulum terminal cisternae are Ca2+ channels opened by the binding of trigger Ca2+ in the cytosol.
calcium induced calcium release
Once cytosolic Ca2+ is increased, thin filament activation, cross-bridge cycling, and force generation occur
most of the Ca2+ that initiates cardiac muscle contraction comes from the sarcoplasmic reticulum,
calcium induced calcium released
membrane depolarization by small increase in cytosolic Ca2+ conc serves as a trigger for the release of larger amount of Ca2+ from the sarcoplasmic reticulum. BC ryanodine receptors in the sarcoplasmic reticulum terminal cisternae are Ca2+ channels opened by the binding of trigger Ca2+ in the cytosol.
calcium induced calcium release
important notes ab Ca2 in cardiac muscle
most of the Ca2+ that initiates cardiac contraction comes from sarcoplasmic reticulum
calcium induced calcium released
L-type ca2 channels
- dependent on the movement of extracellular Ca2+ into the cytosol.
Cardiac muscle contractions are thus graded ~ to smooth muscle
cardiac muscle contraction ENDS
when cytosolic Ca2+ conc is restored to its OG low resting value by active Ca2+- ATPase pumps in the sarcoplasmic reticulum and sarcolemma and Na+/Ca2+ counter transporters in the sarcolemma.
l-type ca2+ channels of cardiac muscle
prolong duration
cardiac muscle CANNOT undergo titanic contractions
- APs and twitch are prolonged due to lasting Ca2 current
plasma membrane remains refractory as long as depolarized, not possible to intit mult APs dur single twitch
critical for heart function as oscillating pump
What initiates action potentials in cardiac muscle?
cardiac muscle cells exhibit pacemaker potentials that gen spont APs
cardiac cells linked via GAP junctions, when AP is init by pacemaker cell, it propagates rapidly
features of cardiac muscle
striated
myofibrils w repeating sarcomeres
troponin in thin filaments
t-tubules conduct/prop. APs
sarcoplasmic reticulum terminal cistern store Ca2+
cells layers and connected by gap junctions at intercalated disks
contraction involves L-type ca2 channels that trigger ryanodine receptors to open nd release more ca2 from sarco reticulum
NO tetany
