muscle (skeletal, cardiac, and smooth) Flashcards
from largest to smallest, list the organization/components of skeletal muscle
- whole muscle
- fascicle
- muscle fiber
- myofibril
- sarcomere
- filaments (thick and thin)
- protein
what is the structure of thin filaments
intertwined chains/strands of ACTIN molecules
tropomyosin vs troponin
- tropomyosin covers the active sites/myosin binding sites on actin (looks like a strand)
- troponin is bound periodically to tropomysosin and contains 3 subunits
what are the 3 subunits of troponin
TnC= ca2+ binding
TnT=binds to tropomyosin
TnI= inhibitory role
what is the structure of thick filaments
composed of myosin….with myosin heavy chains and myosin light chains. also contains the “cross-bridge”. there is an ATP binding site and an actin binding site
what is an isoform
same protein but slightly different a.a and still has similar fn
what is a sarcomere
functional unit of contractile muscle that can shorten to generate force
what is a sarcomere composed of (3)
thick and thin filaments are z-discs
I-band
composed of only thin filaments…changes length during a contraction
A-band
composed of thick and thin filaments (overlapping)
H-zone
only thick filaments…changes length during a contraction bc the thin filaments move in towards the m-line
what are titin filaments for
they have rigid compenent that are anchored at z-discs and at the m-line on thick filamens. they STABILIZE thick filaments in the center of the sarcomere
do the lengths of thick and thin filaments vary from different muscle fibers
thick filaments DONT…always 1.6 microns in all mm fibers
thin filaments can vary in length
what is nebulin
it is a protein within thin filaments to determine the length of the thin filament…it spans the whole length of the thin filament and is anchored at the z-line along with the thin filament
describe the “pseudo crystalin” structure of a myofibril
- every thin filament surrounded by 3 thick filaments
- every thick filament surrounded by 6 think filaments
what is excitation-contraction coupling
mechanism by which AP (excitation) in sarcolemma (membrane) initiates a contraction
in excitation-contraction coupling there is a very large increase in what
rapid, large increase in the free Ca2+ within the muscle cell
what is the mechanism for excitation coupling
- a.p reaches the sarcolemma and enters the T-TUBULE
- this causes Ca2+ to be released from the LATERAL SACS of the sarcoplasmic reticulum out into the sarcoplasm
- Ca binds to TnC and removes the tropomyosin block on the actin active sites
- Ca2+ is removed from TnC (reblocking the actin active sites)
- Ca2+ is uptaken into the fenestrated collar of the sarcoplasmic reticulum= relaxation
uptake of Ca2+ into the fenestrated collar during muscle relaxation is what kind of transport
active transport…uses ATP via the Ca2+-ATPase pump in the s.r
free Ca2+ is stored where
lateral sacs of the sarcoplasmic reticulum
what does free Ca2+ bind to in order to be held in the lateral sacs
calsequestrin
what is the DHP receptor
receptor in the sarcolemma/t-tubule region of a muscle cell. contains 2 components:
- Ca2+ channel that is INACTIVE
- a voltage sensor that senses the a.p that reach the muscle cell
the DHP receptor voltage sensor contacts what other receptor
ryanodine receptor
what is the ryanodine receptor
a receptor located on the s.r membrane that is a Ca2+ channel that releases Ca from the lateral sac of the s.r
what is the latent period in skeletal muscle contraction
the time during which there is no change in muscle length….aka the mechanical event has not yet occurred (a.p is traveling along the sarcolemma–>t-tubule–>s.r–>Ca2+ released–>etc)
what is the sliding filament theory
muscle shortens by a relative sliding of thick and thin filaments, the filaments don’t change length. the thin filaments move inwards towards the m-line
what is the cross-bridge theory
thick and thin filaments are not connected at rest. cross bridges form when there is an increase in free Ca2+
what are the 4 stages of the cross bridge cycle
- (following an increase in Ca) ENERGIZED myosin binds to actin and (ADP and P are bound)
- power stroke in which ADP and P are released and the actin/thin filaments move inward
- ATP binds to UNENERGIZED myosin (at ATP binding site) and causes the cross-bridge to detach
- ATP hydrolysis occurs–> ADP + P to ENERGIZE myosin (no cross bridge exists still)
the amount of force generated is proportional to
the number of attached crossbridges
the rate of the cross-bridge cycle determines the rate of
muscle shortening/contraction
what is the source of energy for muscle contraction
ATP
the ATP inside the muscle cell does not change concentration during muscle contraction due to what
phosphocreatine (molecule in muscle cells) acts as a buffer. PCr and ADP combine to form ATP via the activity of creatine kinase
where is there the highest concentration of creatine kinase enzyme
at the m-line!
what are 3 sources of ATP in muscle cells
- phosphocreatine via creatine kinase
- oxidative phosphorylation (ETC)
- glycolysis
during muscle contraction/relaxation, what uses ATP
- the myosin ATPase during contraction
- the Ca2+-ATPase during relaxation…when Ca is uptaken into the fenestrated collar
what is the length-tension relationship
- reflects the arrangement AND the length of thick and thin filaments
- the greater the length of the muscle/muscle fiber/sarcomere, the greater amount of force that can be generated (up to a certain extent)
- the length of the sarcomere is depended upon the thin filament length which is different b/w different muscles due to the type of nebulin present
the amount of force generated is dependent on
the length of the muscle fiber/sarcomere…bell curve
what is a motor unit
a single motor neuron and all the muscle fibers it innervates
slow fibers vs fast fibers…. NMJ
smaller NMJs
slow fibers vs fast fibers….diameter
smaller in diameter
slow fibers vs fast fibers….isoforms
slow contain different sarcomere protein isoforms
slow fibers vs fast fibers….contraction velocity
contract more slowly
slow fibers vs fast fibers….fatigue
more fatigue resistant
slow fibers vs fast fibers….glycolysis
less glycolysis. fast fibers are more glycolysis
slow fibers vs fast fibers….oxidative phosphorylation
slow fibers have more oxidative phosphorylation and have more mitochondria
fast fibers= type II fibers…what are the two types of type II fibers
IIa (fast oxidative) and IIb (fast glycolytic)
type IIa vs type IIb…size
IIa is smaller
type IIa vs type IIb…oxidative metabolism
IIa depend more on
type IIa vs type IIb…fatigue
IIa less fatigable
type IIa vs type IIb…contraction velocity
IIa contract slower
type IIa vs type IIb…glycolytic metabolism
IIb depends more on
type IIa vs type IIb…efficiency
type IIb (although faster and generate more power) are less efficient than IIa
what skeletal fiber type is more efficient
type I…or slow fibers!
muscles for posture have what predominant fiber type
type 1
muscles for tasks that are rapid or require a lot of dexterity have what fiber type
type II
is there nebulin in the heart
no…varying lengths of thin filaments found here
what contractile proteins are found in cardiac sarcomeres and skeletal muscle sarcomeres
MHC-beta and TnC (which is in slow fibers but not fast)
what contractile proteins are unique to cardiac sarcomeres
MHC-alpha and an isoform of TnI
cardiac vs skeletal muscle cell size
cardiac=much smaller
how are cardiac cells connected
end to end via intercalated discs
what is the purpose of gap jns w/in the intercalated discs of cardiac cells
rapid and direct transmission of a.ps (electical synapses) b/w cardiac cells
does skeletal muscle contain gap jns
no
what is the significance of the LONG REFRACTORY PERIOD in cardiac muscle ventricular cells
makes sure that the cells can’t be stimulated at a high fq…this is a protective mechanism so that the ventricles can relax and allow for diastole/heart to fill with blood. prevents heart from undergoing tetanic contraction
when does the ap in cardiac muscle end compared to its contractions
a.p lasts until the contraction is 50% relaxed
during the phase 0 of a cardiac a.p what occurs
rapid depolarization, increase Na conductance as Na comes into the cell
during phase 1 of a cardiac a.p what occurs
movement of Na has slowed due to electrical gradient, K flows out. so gNa decreases and gK increases
during phase 2 of a cardiac a.p what occurs
plateau phase. gK decreases and leaves cell, but gCa increases and comes into cell. 2 cations being exchanged so you see a plateau phase
during phase 3 of a cardiac a.p what occurs
gK increase and gCa decreases…see a rapid repolarization phase
during phase 4 of a cardiac a.p what occurs
no net current flow….steady m.p at resting potential
what are the 2 sources of Ca for the heart
- Ca can enter the cell from interstitial space via channels in the sarcolemma during the plateau phase (phase 2)
- the Ca from the interstitial space triggers Ca release from the s.r
what is calcium-induced calcium release
Ca coming in from the interstitial space triggers the release of Ca from the s.r which can bind to TnC causing muscle activation
mechanisms for Ca removal in cardiac muscle
- S.r is the primary mechanism (Ca-atpase pump)
- pump in the sarcolemma…a Ca-ATPase pump that moves Ca out of the cell
- Na/Ca exchanger
what does the Na/Ca exchanger do
moves Na into the cell and Ca out.
where does the Na/Ca exchanger get energy from
not ATP directly. uses the Na [ ] gradient…thus is secondary active transport. the Na/K, ATPase pump maintains the Na [ ] gradient
the amount of Ca2+ that is removed by the Ca/ATPase exchanger (sarcolemma) and the Na/Ca exchanger, equals what
the Ca that moved in during the plateau phase of the cardiac a.p
what component of smooth muscle is homologous to z-lines of striated muscle
dense bodies that thin filaments attach to
is there troponin in smooth muscle
no
where is smooth muscle innervation from
autonomic n.s= involuntary
compare the cell lengths of smooth vs striated muscle
greater range of cell lengths in smooth to accomodate changes in volume of organs
rate of ATP splitting in smooth vs striated
smooth is 10-100 times slower…no fatigue…force is the same as striated though …so greater economy
excitation coupling in smooth muscle
- increase in Ca
- Ca binds to calmodulin
- Ca-calmodulin binds to myosin light chain KINASE to create an ACTIVE MLCK enzyme
- active MLCK phosphorylates relaxed myosin…myosin attaches to actin
- phosphatase (always active) removes the P from myosin to relax it
what causes the myosin to detach from the actin
ATP causes dissociation of myosin from actin
what is the purpose of the phosphatase
to prevent reattachment of myosin to actin
how does smooth muscle maintain force with very little ATP consumption
myosin can remain attached to actin even when dephosphorylated to maintain the contraction without using ATP= high economy
what are the 2 sources of Ca for smooth muscle contraction
- s.r
2. extracellular fluid via channels in membrane
what initiates an a.p in smooth muscle
Ca2+ in the rising phase! rather than Na in striated muscle
what are the 4 things that can activate smooth muscle
- cells that spontaneously generat a.ps…pacemaker potential
- ANS ending release n.t in vicinity of smooth muscle cells. NO NMJ IN SMOOTH MUSCLE
- hormones act as above
- local factors (pH, O2 level, etc)
what are the 3 mechanisms of Ca removal in smooth muscle
- Ca pump in sarcolemma
- Na/Ca exchanger
- s.r
what is single unit smooth muscle
muscle fns as single unit. uses electrical synapses (through gap jns). is spontaneously active (by pacemaker cells). stretch activated. innervation is by pacemaker cells)
examples of single unit smooth muscle
uterus, intestines, small b.v
what is multi unit smooth muscle
cells activated independently, not spontaneously activated, gap jns are rare
examples of multi unit smooth muscle
large arteries, large airways
