Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
54 Cards in this Set
- Front
- Back
|
sarcomere
|
Z line to Z line in the myofibril (made up of thin & thick filaments, titin & nebulin)
|
|
|
Z line
|
two Z lines per sarcomere
attachment site for thin/actin filaments |
|
|
M line
|
middle! attachment site of thick filaments, devides A band in
|
|
|
A band
|
entire thick/myosin filament, plus part of thin filaments-includes zone of overlap and M line
|
|
|
I band
|
only thin/actin filaments (and titin), Z line runs through middle of I band, each half of I band belongs to a different sarcomere (shortens during contraction)
|
|
|
H zone
|
Central region of A band with only thick/myosin filaments (shortens during contraction)
|
|
|
myofibril
|
the contractile structures of a muscle fiber. Composed of troponin, tropomyosin, myosin, actin, titin, & nebulin.
|
|
|
Fascicles
|
group/bundle of muscle fibers/cells which contain nuclei, sarcolemma/T-tubules, sarcoplasmmitochondria, glycogen granules, sarcoplasmic reticulum and myofibrils.
|
|
|
sarcoplasm
|
cytoplasm. contains sarcoplasmic reticulum, myofibrils, mitochondria, glycogen granules
|
|
|
sarcolemma
|
cell membrane (T-tubules continuation of sarcolemma –functionally linked to SR)
|
|
|
sarcoplasmic reticulum
|
modified endoplasmic reticulum with longitudinal tubules that store and releases Ca+ into T tubules
|
|
|
T-tubules
|
(transverse tubules) continuation of sarcolemma, brings a.p. into interior of muscle fiber. Terminal cisternae flank T-tubules and together are called a triad
|
|
|
terminal cisternae
|
enlarged regions at the ends of the longitudinal tubules of the sarcoplasmic reticulum that concentrate and sequester Ca+
|
|
|
Contractile proteins
|
myosin/thick and actin/thin
|
|
|
Regulatory proteins
|
Troponin & Tropomyosin
|
|
|
Accessory proteins
|
Titin and Nebulin
|
|
|
thick filaments
|
250 myosin molecules to one thick filament- rode tail and tadpole heads hinge region.
|
|
|
thin filaments
|
made up of actin. F-actin chain contains G-actin molecules that each have a myosin-binding site
|
|
|
Sliding Filament Theory
|
Myosin and actin filaments are a fixed length and slide past each other to create contractions. The sarcomere shortens during contraction. H-zone and I-band shorten. A-band remains constant. HI-A.
|
|
|
Titin
|
in middle of myosin (attached at Z disk and spans to M line), provides elasticity and stabilizes myosin
|
|
|
Nebulin
|
in middle of actin, helps align actin (attaches to Z disk but doesn't not extend to M line)
|
|
|
troponin
|
A Ca+ binding complex of 3 proteins. Controls the position of Tropomyosin. Ca+ binds to troponin C. Ca+ and Troponin C complex pulls tropomyosin away from actin’s myosin binding sites. Allows myosin to form strong crossbridges with actin and carry out power strokes.
|
|
|
tropomyosin
|
elongated protein polymer that partially covers actin’s myosin-binding sites at rest
|
|
|
motor end plate
|
region of sarcolemma with junctional folds and receptors. Specialized postsynaptic region of a muscle fiber
|
|
|
motor units
|
a motor neuron and the muscle fibers it innervates
|
|
|
neuromuscular junction
|
the synapse of a somatic motor neuron and a skeletal muscle fiber. Neuron releases Ach to Nm type receptors that allow Na+ to move into the cell depolarizing it.
|
|
|
Excitation- contraction coupling mechanism in skeletal muscle
|
Somatic motor neuron releases Ach acetylcholine at NMJ to Nm type receptors on muscle fiber motor end plate. This allows channels for Na+ (and K+) to move into the cell depolarizing the membrane creating an end-plate potential which initiates a muscle action potential. This a.p. is conducted down T-tubules by the opening of voltage gated Na+ channels. This a.p. alters conformation of DHP (dihydropyridine L-type calcium channels) receptor. This conformation change opens the RyR Ca+ release channels in the sarcoplasmic reticulum. Ca+ enters cytoplasm. (Latent period). Ca+ binds to troponin, troponin Ca+ complex pulls tropomyosin revealing the myosin binding site on actin. Crossbridge formation/contraction phase. Myosin (which has a hydrolyzed ATP ie ADP and Pi bond to it) releases Pi (inorganic phosphate) and this release of Pi allows the myosin head to swivel. The head swings toward the M line bring the actin filament with it. This is the power stroke which creates a contraction. Myosin releases ADP at the end of the power stroke which creates a tighter bond between actin and myosin (rigger state). Then the cycle can restart with ATP (from mitochondria) binding to myosin (decreasing the actin-binding affinity of myosin) so it releases from actin. APT is hydrolyzed by myosin into ADP and Pi which provides energy for the myosin head to rotate and reattach to actin at a 90 degree angle weakly (because tropomyosin is blocking actin binding site-resting muscle fibers). Creatine phosphate (PCr or phosphocreatine) provides a phosphate and works with ADP to recreate ATP quickly is muscle cells.
Relaxation phase: At the synapse Acetylocholinesterase breaks down ACh (limits the duration of the contraction). Ca+ channels close and sarcoplasmic Ca+-ATPase pumps Ca+ back into SR. (relaxation requires ATP also!) Decrease in free cytosolic Ca+ causes Ca+ to unbind from troponin. Tropomyosin re-covers binding site. When myosin heads release, elastic elements (titin?) pull filaments back to their relaxed position. Na+ K+ ATPase restores ions that cross cell membrane during a.p. to their original compartments. Relaxed state: myosin head is cocked and weakly bound. |
|
|
latency period
|
the short delay between the muscle action potential and beginning of muscle tension development
-time required for calcium release and binding to troponin |
|
|
single twitch
|
single contraction-relaxation cycle. Muscle relaxes completely between stimuli.
|
|
|
summation
|
stimuli closer together do not allow muscle to relax fully. Repeated stimulation before relaxation phase.
|
|
|
treppe
|
staircase effect of summation leading to tetanus. Repeated stimulation after relaxation phase
|
|
|
incomplete tetanus
|
muscle never relaxes completely. Stimuli are far enough apart to allow muscle to relax slightly between stimuli.
|
|
|
Complete tetanus
|
relaxation phase is eliminated. Muscle reaches steady tension. If muscle fatigues, tension decreases rapidly
|
|
|
Length-tension relationship
|
Tension directly proportional to the number of cross bridges
Too much or too little overlap of resting muscle results in decreased tension Gama motors neurons maintains muscle tone (optimal resting length) |
|
|
fast twitch
|
glycolytic fibers, anaerobic glycolysis-2 ATP, can’t be sustained, generates lactate, develops tension faster, splits ATP more rapidly, pumps Ca+ into SR more rapidly, fast-ballistic movement
|
|
|
slow twitch
|
Relies primarily on oxidative phosphorylation, aerobic metabolism-needs oxygen. Goes through TCA cycle generates 36 ATP. Endurance.
|
|
|
contraction (force)
|
contraction-creation of tension in a muscle
contraction force- increased by recruitment of additional motor units by the nervous system |
|
|
relaxation
|
release of tension
|
|
|
muscle fatigue
|
a reversible condition in which a muscle is no longer able to generate or sustain expected power output. Possible causes of muscle fatigue: 1. Decline in ATP levels (because depletion of glucose), 2. Buildup of lactic acid/Pi, 3. Decrease in Ca+ release
|
|
|
creatine phosphate
|
(PCr or phosphocreatine) provides a phosphate and works with ADP to recreate ATP quickly is muscle cells.
|
|
|
isotonic contractions
|
create force and move a load. Tension rises, length changes (shortens) concentric action=shortening action, eccentric action=lengthening action
|
|
|
isometric contractions
|
create force without moving a load, sarcomeres shorten while elastic elements stretch, resulting in little change in overall length. Tension rises, length stays same, creates force without moving a load.
|
|
|
Central fatigue
|
subjective feeling of fatigue during exercise. fatigue originating from the CNS-somatic motor neuron, psychological effects/protective reflexes
|
|
|
Peripheral fatigue
|
physiological. Depletion theories-PCr, ATP, glycogen. Accumulation theories-H+, Pi, Lactate, & decreases in neurotransmitter release causes decrease receptor activation, change in muscle membrane potential, Ca+ leak (out of cell?), decrease Ca+ release, decrease Ca+ troponin interaction.
|
|
|
Motor unit recruitment
|
Asynchronous recruitment of motor units helps avoid fatigue-different motor units take turns maintain tension.
|
|
|
arrangement of myosin and actin in smooth muscle
|
actin is plentiful with less myosin, myosin filaments are longer and have hinged myosin heads along the entire length of the filament, no troponin. actin and myosin are loosely arranged around the periphery of the cell, crisscrossed, held in place by dense bodies of protein (where they cross). Actin attaches to the dense bodies and each myosin molecule is surrounded by actin filaments. This arrangement of fibers causes cell of become globular when contracting
how it is different from the skeletal muscle |
|
|
Smooth muscle morphology (form structure)
|
no striations/sarcomeres, actin is plentiful with less myosin, myosin filaments are longer, no troponin, involuntary movement controlled by autonomic nervous system, smaller cells-spindle shaped, 1 nuclei, MLCK.? Contraction initiated by electrical and/or chemical signals, extensive cytoskeleton formed by intermediate filaments that connect dense bodies. SR amount varies and is less organized, no T-tubules but have caveolae, no specialized receptor regions, Ca+ from extracellular fluid and Sarcoplasmic Reticulum, Ca+ initiates a cascade ending with phosphorylation of myosin light chain and activation of myosin ATPase
|
|
|
phasic smooth muscle
|
periodic contraction/relaxation. contraction and relaxation come in phases. ex: walls of intestine
|
|
|
Tonic Smooth muscle
|
continuous contractions. Contraction maintained over time. ex: blood vessels, sphincters/esophagus, bladder.
|
|
|
Excitation-contraction coupling in smooth muscle
|
Ca+ comes from the extracellular fluid (through membrane channels whose opening is regulated by membrane stretch-activated Ca+ channels, depolarization –voltage gated Ca+ channels, or chemical signals-neurotransmitters, hormones, or paracrines) AND the sarcoplasmic reticulum. SR Ca+ releases is mediated by an IP3-activated receptor-channel (which opens in response to single transduction pathways that produce IP3). ↑ cyctolic Ca+, Ca+ binds to Calmodulin (CaM) a binding protein in cytosol, Ca+-CaM complex activates myosin light chain kinase (MLCK). MLCK enhances myosin ATPase activity by phosphorylating light protein chains near the myosin head activating myosin heads. When myosin ATPase activity is high, actin binding and crossbridge formation occurs and increases tension in the muscle
|
|
|
Relaxation of smooth muscle
|
Ca+ -ATPase pumps Ca+ back into SR. Additionally some Ca+ is pumped out of the cell by the Ca+-Na+ antiport exchanger & Ca+ ATPase. ↓ in free cytosolic Ca+ causes Ca+ to unbind from calmodulin, this inactivates MLCK. Myosin phosphate removes phosphate (dephosphorylation) from myosin decreasing myosin ATPase activity, less myosin ATPase=less muscle tension
|
|
|
latched state
|
Why smooth muscles can never undergo fatigue. Dephosphorylated myosin may remain attached to actin for a long time. Sustained contraction without ATP- less fatigue
|
|
|
Slow wave potentials
|
unstable membrane potential in smooth muscle. cyclic depolarization and repolarization of membrane potentials
|
|
|
pacemaker potentials
|
unstable membrane potential in smooth muscle. regular depolarization that always reaches threshold and fires action potential
|
