Group 8/12/19 Flashcards
Learning issues and look-ups
Here are our learning issues for Wednesday:
Physiology of muscle skeletal tissue contraction (Costanzo and Pawlina and Guyton Hall)
Histology of skeletal muscle (Pawlina)
structure of skeletal muscle
muscle cells arranged in parallel fascicles and are vertically oriented
types of myofilaments
thin and thick filaments
thin filaments structure
composed primary of actin protein
F-actin is the thin filament
G-actin is globular actin that gives rise to F-actin
other important proteins: tropomyosin and troponin
thick filaments structure
mainly has protein myosin 2
name for muscle cytoplasm
sarcoplasm
striated muscle structure
cells have cross-striations
skeletal muscle location and function
location: attached to bone
function: moves axial and appendicular skeleton, maintains body position and posture, eye movement
name for the muscle cells in skeletal muscles
a multinucleated syncytium
muscle fiber development
small, individual muscle cells called myoblasts fuse during development
plasma membrane of skeletal muscle fiber and parts
sarcolemma: plasma membrane, external lamina, and surrounding reticular lamina
endomysium
surrounds individual muscle fibers
perimysium
surrounds a group of fibers to form a bundle or fascicle
fascicle
functional units of muscle fibers that work together to perform a specific function
epimysium
sheath of dense connective tissue that surrounds a collection of fascicles that envelopes the muscle
also called deep investing fascia
metabolic profile of the muscle
indicates the capacity for ATP production by oxidative phosphorylation or glycolysis
metabolic activity is a characteristic of skeletal muscle
markers of muscles that use lots of oxidative metabolism
large amount of myoglobin, mitochondria
myoglobin structure and function
oxygen-binding protein that has Fe2+
stores oxygen in muscle fibers for their metabolism
traumatic injuries of skeletal muscles effect
cause breakdown (rhabdomyolysis), release myoglobin into circulation
myoglobin removed by kidneys; if too much, can cause acute renal failure
detection of myoglobin in blood can indicate muscle injury
types of skeletal muscle fibers*
type 1 (slow oxidative), type 2a (fast oxidative glycolytic), and type 2b (fast glycolytic) based on their enzymatic activity
type 1 fibers: structure, function*
“slow oxidative fibers”
structure: look red, lots of mitochondria, myoglobin, more blood vessels, smaller
function: slow-twitch, fatigue-resistant motor units, endurance athletes
type 2a fibers: structure, function*
“fast oxidative glycolytic fibers”
structure: many mitochondria and myoglobin, and glycogen
function: fast-twitch, fatigue-resistant motor units, anaerobic glycolysis, sprinters
type 2b fibers: structure, function*
“fast glycolytic fibers”
structure: light pink, less myoglobin and mitochondria, lots of glycogen
function: fast-twitch, fatigue-prone motor units, fatigue rapidly because of lactic acid, rapid contraction and fnie movements
enzymatic activity compared between types of skeletal muscle fibers
type 1 fibers have slowest myosin ATPase reaction velocity
type 2a fibers have high reaction velocity
type 2b fibers have highest reaction velocity
what is the structural and functional subunit of the muscle fiber?
myofibril
parts and subparts of the skeletal muscle
skeletal muscle has muscle fascicles
muscle fascicles have muscle fibers
muscle fibers have myofibrils
myofibrils have myofilaments (thick and thin)
functional unit of the myofibril
sarcomere
sarcoplasmic reticulum structure and function
structure: smooth-surfaced endoplasmic reticulum (sER) that surrounds the myofilament bundles
function: stores and releases Ca2+ or excitation-contraction coupling
A band vs. I band identification*
A band contains all thick filaments and overlaps with some thin filaments (darker)
I band contains only thin filaments (lighter)
Z line, M line, and H band identification*
Z line are darkest lines that separate edges of sarcomere
H band only contains thick filaments, within the A band
M line in the middle of the H band
important regulatory proteins in striated muscle, and their location
tropomyosin and troponin, intertwined with actin strands
what are the proteins that mask the myosin-binding sites at muscle rest?
tropomyosin and its regulatory protein, the troponin complex
cytoskeletal proteins in myofibrils
dystrophin, titin, nebulin and alpha-actin
dystrophin
an actin-binding protein that anchors the myofibrillar array to the cell membrane
absence of this protein associated with progressive muscular weakness (ie Duchenne muscular dystrophy)
titin
in thick filaments, centers them to the sarcomere. Extends from M line to Z discs
prevents excessive stretching of the sarcomere
nebulin
in thin filaments, extends from either ends of thin filaments, the Z lines
transverse (T) tubules structure and function
structure: part of sarcolemmal membrane that goes into muscle fiber
function: carry depolarization
steps of excitation-contraction coupling*
- Action potential opens up presynaptic voltage-gated Ca2+ channels, including ACh release
- Postsynaptic ACh binding leads to muscle cell depolarization at motor end plate
- Depolarization travels over entire muscle cell and deep into muscle via T tubules
- Membrane depolarization induces conformational change in voltage-sensitive dihydropyridine receptor (DHPR) and its mechanically coupled ryanodine receptor (RR), so Ca2+ is released from SR into cytoplasm
- Tropomyosin is blocking myosin-binding sites on the actin filament. Released Ca2+ binds to troponin C (TnC), shifting tropomyosin to expose the myosin-binding sites
- Myosin head binds strongly to actin, forms a crossbdrige. P is then released, to cause power stroke.
- During power stroke, force is produced as myosin pulls on thin filament. Muscle shortening occurs, and ADP is released at end of power stroke
- Binding of new ATP molecule causes detachment of myosin head from actin filament. Ca2+ is resequestered.
- ATP hydrolysis into ADP and P results in myosin head returning to high-energy position (cocked). The myosin head can bind to a new site on actin to form a crossbridge if Ca2+ remains available.
relaxation stage of excitation-contraction coupling*
ATPase of the SR membrane, called SERCA, reaccumulates Ca2+ into the SR
Not enough Ca2+ for the binding to troponin C
Tropomyosin returns to original position, blocks the myosin-binding site
parts of the troponin complex, and their functions
three globular subunits: troponin-C (TnC) binds to Ca2+, troponin-T (TnT) binds to tropomyosin, and troponin-I (TnI) binds to actin and prevents actin-myosin interaction
tropomodulin
actin-binding protein
regulates the length of the actin filament in the sarcomere
accessory proteins functions and examples
function: they maintain the precise alignment of thin and thick filaments within the sarcomere, so that muscle contraction is efficient and fast
examples: titin, alpha-actinin, desmin, M line proteins, myosin-binding protein C, dystrophin
what happens to the sarcomere when the muscle contracts?*
sarcomere and I band shorten, H band narrows
A band remains the same length (HIZ shrinkage, A band Always same length)
neuromuscular junction
contact made by the terminal branches of the axon of the motor neuron with the muscle fiber, occurs at the motor end plate
name for the neurotransmitter in the synaptic vesicles at motor end plate of neuromuscular junction
acetylcholine (ACh)
function of ACh in muscle contraction
ACh will be released into the synaptic cleft, and initiates depolarization of the plasma membrane
where does ACh bind?
binds to cholinergic receptors on plasma membrane bordering cleft
binds to nicotinic ACh receptors (nAChR) on sarcolemma of striated muscle
what type of channel is nAChR?
transmitter-gated Na+ channel
what happens when ACh binds to nAChR?
ACh binds, this opens Na+ channels, Na+ goes into the striated muscle cell, causes membrane depolarization
what happens to ACh after it causes a depolarization?
enzyme called acetylcholinesterase (AChE) breaks down the ACh so it won’t cause repeated stimulation
motor unit
a single motor neuron with the specific muscle fibers that it innervates. Less fibers per motor neuron for muscles responsible for fine movements.
tissue atrophy
muscle cell may undergo regressive changes if the nerve supply to it is disrupted. Causes the muscle to thin.
what types of cells do muscles develop from, where does this occur?
multipotential myogenic stem cells -> myoblasts
originate in the embryo from unsegmented paraxial mesoderm
what activates muscle-specific gene expressions and differentiation of skeletal muscle lineages?
MyoD transcription factor with other myogenic regulatory factors (MRFs)
myostatin
a growth factor protein that has inhibitory effect on muscle growth and differentiation
what are the two types of myoblasts in developing muscles?
early and late myoblasts
what do early myoblasts develop into?
these form primary myotubes, which go between the tendons of developing muscle. They differentiate into mature skeletal muscle fibers
what do the late myoblasts develop into?
form secondary myotubes, and have direct contact with nerve terminals
satellite cells: where they come from and what is their role
multipotential myogenic stem cells generate these late in fetal development
these are undifferentiated cells that have the ability to undergo myogenic differentiated. Play a role in the muscle’s ability to regenerate
characteristic transcription factor of satellite cells
Pax7
what happens to satellite cells when the muscle is injured?
after muscle tissue injury, satellite cells become activated and become myogenic precursors of muscle cells. Then they re-enter the muscle development cycle, and co-express Pax7 with MyoD, key for myogenic differentiation. Gives rise to new myoblasts -> fuse with external lamina -> myotubes -> new fiber
healing of external lamina of muscle
when external lamina of muscle is disrupted, fibroblasts repair the injured site, and form scar tissue
muscular dystrophies
progressive degeneration of skeletal muscle fibers, places demand on satellite cells to replace degenerated fibers, so the satellite pool becomes exhausted. Leads to loss of muscle function.
three sources of energy for muscle contraction
muscle fibers have ATP that they use for contraction, but it is used very fast. Other energy sources are:
- phosphocreatine
- glycogen
- oxidative metabolism (biggest source)
isometric vs isotonic contractions
isometric contractions do not shorten muscles
isotonic contractions shorter muscle while tension on the muscle remains the same
force summation
summation means the adding together of individual twitch contractions to increase the intensity of overall muscle contraction
summation that occurs by increasing the number of motor units contracting simultaneously
multiple fiber summation
summation that occurs by increasing the frequency of contraction
frequency summation, leads to tetanization
tetanization
in frequency summation, individual twitch contractions happen with increasing frequency, so eventually they’re overlapping so much that it seems like one big smooth muscle contraction. Reaches a maximum, sustained due to the Ca ions in the sarcoplasmic reticulum.
staircase effect (treppe)
when a muscle begins to contract after a long period of rest, its initial strength of contraction may be about half compared to its strength many twitches later
muscle tone
even when muscles are at rest, some tautness usually remains. Results from a low rate of nerve impulses
muscle fatigue
directly proportional to the rate of depletion of muscle glycogen. Muscle is not able to continue to supply the same work output.
