chapter 10- muscle system Flashcards
the term skeletal muscle fiber refers to what?
a cell, an individual cell of skeletal muscle
the C.T. layer that’s composed of collagen & elastin and functions to bundle the skeletal muscle into fascicles is what?
perimysium
during development, hundreds of what cells are fused to form a single skeletal muscle cell, the ones that didn’t fuse initially are retained as what cells?
myoblasts & satellite
tubes of sarcolemma that fold into the cell and wrap around the myofibrils are the what?
transverse tubules/T tubules
what is the function of myoglobin?
store oxygen inside the skeletal muscle cell
the primary function of the sarcoplasmic reticulum in a skeletal muscle cell is to contain what?
calcium
the smallest functional unit of myofibril is the what?
sarcomere
the whole width of the thick filaments is the what, it has the m-line in the middle of it?
A-band
nebulin functions to attach individual what proteins together into a long filamentous shape?
actin
what functions to cover the active sites of each G actin to prevent myosin binding?
tropomyosin
what is the stretch protein that holds thick filaments in place and aids the elastic recoil of a muscle after stretching?
titin
when muscle contracts, the zones of overlap increase in width and the what move closer together?
Z-lines/Z-discs
the binding of acetylcholine to its receptors on the motor end plate causes what to happen?
sodium channels open, sodium enters the cell
when an action potential reaches the triad, calcium is released from the sarcoplasmic reticulum to where it then binds to?
troponin
a cross bridge consists of an actin active site bound to a what?
myosin head
what enzyme uses the bond energy of ATP to break the cross bridge after a power stroke to reset for the next cross bridge and power stroke?
myosin ATPase
why does rigor mortis occur?
no ATP produced, no energy to actively transport calcium out of sarcoplasm, calcium bound to troponin allows myosin heads to bind to actin active sites creating cross bridges, no ATP to detach cross bridges & rest myosin heads, muscle can’t relax
what is the condition where a bacterial toxin causes spastic paralysis of the muscles?
tetanus
a twitch has 3 phases: the latent period, the contraction phase, and the other phase?
relaxation phase
the wave summation where rapid cycles of contraction and relaxation produce maximum tension called what and this is how cardiac muscle functions?
incomplete tetanus
all the cells controlled by a single motor neuron is a called what?
motor unit
during recruitment, which motor units are activated first?
slower, weaker ones
isometric contractions produce tension but do they also produce movement?
no (isotonic produce movement)
what phosphate is the more stable storage form of phosphate bond energy found in muscle cells?
creatine
muscle cells store glucose in the form of what?
glycogen
when there’s not adequate oxygen delivery to meet the need for ATP production, muscle cells ferment and product the waste product?
lactic acid
which cell type will be able to produce more power strokes per second: fast glycolytic fibers or slow oxidative fibers? which will be able to perform contractions for longer without fatigue?
fast glycolytic fibers = more power strokes, slow oxidative fibers = less fatigue
which activity would achieve more capillaries, mitochondria, and myoglobin in your muscles: weightlifting or jogging?
jogging
what metabolism does cardiac muscle use to make ATP?
aerobic respiration only
intercalated discs are composed of what for cell-to-cell communication and desmosomes to link myofibrils from one cell to next?
gap junctions
the what nervous system controls the contraction of smooth muscle?
autonomic
myosin light chain kinase is found in what kind of muscle tissue?
smooth muscle tissue
as we age, what happens with regard to the elasticity of the muscles?
fibrosis occurs: stretchy muscle tissue gets replaced with stiff collagen
skeletal muscle (muscle tissue type)
voluntary striated muscle
cardiac muscle(muscle tissue type)
involuntary striated muscle
smooth muscle (muscle tissue type)
involuntary nonstriated muscle
specialized cells (characteristics of all muscle tissues)
elongated, high density of myofilaments
myofilaments (specialized cells)
cytoplasmic filaments of actin & myosin
excitability/irritability (characteristics of all muscle tissues)
receive & respond to stimulus
contractility (characteristics of all muscle tissues)
shorten and produce force upon stimulation
extensibility (characteristics of all muscle tissues)
can be stretched
elasticity (characteristics of all muscle tissues)
recoil after stretch
skeletal muscle tissue
-forms skeletal muscles (44% of body mass)
-an organ: composed of skeletal muscle cells (fibers), C.T., nerves & blood vessels
functions of skeletal muscles:
- produce skeletal movement
- maintain posture & upright position
- stabilize joints
- guard entrances & exits
- support soft tissues
- generate heat (maintain body temp.)
skeletal muscle anatomy
-each muscle innervated by one nerve: must branch & contact each skeletal muscle fiber
-one artery, branches into extensive capillaries around each fiber to supply oxygen & remove wastes
epimysium (C.T. sheath that hold muscle together)
covers muscle, separates muscle from other tissues, composed of collagen, connects to deep fascia
perimysium (C.T. sheath that hold muscle together)
composed of collagen & elastin, has associated blood vessels & nerves, bundles muscle fibers into groups called *fascicles (perimysium covers it)
endomysium (C.T. sheath that hold muscle together)
composed of reticular fibers, contain capillaries, nerve fibers & satellite cells, surrounds individual muscle fibers
tendon (fibers from epimysium, perimysium & endomysium come together at the ends of skeletal muscle to create attachment)
cord-like
aponeurosis (fibers from epimysium, perimysium & endomysium come together at the ends of skeletal muscle to create attachment)
sheet-like
skeletal muscle fibers (cells)
-huge cells: 30cm long
-multinucleate
-formed by fusion of 100s of myoblasts
-nuclei of each retained to provide enough mRNA for protein synthesis in large fiber
-filled with myofibrils extending whole length of cell
satellite cells
-unfused myoblasts in adults
-capable of division & fusion to fiber for repair but can’t generate new fibers
sarcolemma
-cell membrane of skeletal muscle fibers
-maintains separation of electrical charges resulting in a *transmembrane potential
transmembrane potential
-Na+ pumped out of a cell creating positive charge on outside of membrane
-negative charge from proteins on inside gives muscle fibers a resting potential of -85mV
-if permeability of membrane is altered, Na+ will flow in causing change in membrane potential
*change in potential will signal the muscle to contract
transverse tubules (T tubules)
tubes of the sarcolemma, reach deep inside the cell to transmit changes in transmembrane potential to structures inside the cell
sarcoplasm
-cytoplasm of skeletal muscle fibers
-rich in glycosomes (glycogen granules) & myoglobin (binds oxygen)
myofibrils
consists of bundles of myofilaments made of actin & myosin proteins (80% of cell volume)
what kind of filaments does actin make?
thin filaments
what kind of filaments does myosin make?
thick filaments
what happens when thick & thin filaments interact?
contraction of the muscle occurs
sarcoplasmic reticulum (SR)
-contained in the sarcoplasm
-store calcium
-all calcium is actively pumped from sarcoplasm SR (has 1000x more Ca2+ than sarcoplasm)
triad
-located near ends of a sarcomere
-T-tubule wrapped around a myofibril sandwiched between 2 terminal cisternae of SR
sarcomere
smallest functional unit of a myofibril: least amount of myofilaments necessary to produce contraction
skeletal muscle is surrounded by and contain what?
epimysium & muscle fascicles
muscle fascicles are surrounded by and contain what?
-perimysium & muscle fibers
-each myofibril = ~10thousand sarcomeres
muscle fibers are surrounded by and contain what?
-endomysium & myofibrils
-each fiber = ~1thousand myofibrils
myofibrils are surrounded by and contain what?
-sarcoplasmic reticulum & sarcomeres (Z line to Z line)
-each fascicle = ~100muscle fibers
sarcomere contains what?
-thin & thick filaments
-I bands, A bands, Z lines, M line, titin
-each muscle = ~100fascicles
sarcomere structure
-resting length 1.6-2.6
-composed of: thick (myosin) & thin(actin) filaments, stabilizing & regulatory proteins
-organization of the proteins in sarcomere causes striated appearance of the muscle fiber
stabilizing proteins
hold thick & thin filaments in place
regulatory proteins
control interactions of thick & thin filaments
A-band
whole width of thick filament, looks dark microscopically
M-line
center of each thick filaments, middle of A-band: attaches neighboring thick filaments
H-zone
light region either side of M line, contains thick filaments only
zone of overlap
ends of A-bands, place where thin filaments intercalate between thick filaments (triads encircle zones of overlap)
I-band
area that contains thin filaments outside zone of overlap (not width of thin filaments)
Z-line/disc
center of I band, constructed of actinins, function to other thin filaments & neighboring sarcomeres, titin proteins bind thick filaments to Z-line, Z-lines mark ends of each sarcomere
thin filaments
-5 to 6nm diameter
-made of 4 proteins: actin, nebulin, tropomyosin & troponin
-the end of each filament is bound to thin filaments in neighboring sarcomeres by actinin in the Z-line
actin + nebulin
F-actin (filamentous) consists of rows of G-actin (globular), held together with nebulin; each G-actin has an active site that can bind to myosin
tropomyosin
covers the active sites on G actin to prevent myosin binding
troponin
holds tropomyosin on the actin, has receptor for Ca2+, when Ca2+ binds the troponin-tropomyosin complex it releases actin also allowing it to bind to myosin
crossbridge formation
actin + myosin bonding -> crossbridge formation = contraction
thick filaments
-10 to12 nm diameter
-composed of bundled myosin molecules
-each myosin has 3 parts: tail, head & hinge
-contains core of titin
-each is surrounded by hexagonal arrangement of thin filaments with which it interacts
head of thick filaments
hangs off tail by hinge, will ind actin at active site, no heads in H-zone
hinge of thick filaments
flexible region, allows movement for contraction
tail of thick filaments
tails bundled together to make length of thick filament, all point toward M-line
sliding filament theory
-contraction of skeletal muscle is due to thick & thin filaments sliding past each other, not compression of the filaments
-sliding causes shortening of every sarcomere in every myofibril in every fiber
-overall = shortening of whole skeletal muscle
evidence of sliding filament theory:
- H-zones & I-bands decrease width during contraction
- Zones of overlap increase width
- Z-lines move closer together
- A-band remains constant
excitation
excitation of muscle fiber is controlled by nervous system at neuromuscular junction using neurotransmitter
neuromuscular junction
where a nerve terminal interfaces with a muscle fiber at the motor end plate, one junction per fiber (control of fiber from one neuron)
synaptic terminal
expanded end of axon, contains vesicles of neurotransmitter -> acetylcholine (Ach)
motor end plate
specialized sarcolemma that contains Ach receptors & enzymes acetylcholinesterase (AchE)
synaptic cleft
space between synaptic terminal & motor end plate where neurotransmitter is released
1-2 events of excitation:
- arrival of an action potential (electrical message) at the synaptic terminal
- release of Ach: vesicles containing Ach fuse with neuronal membrane & exocytose their contents into synaptic cleft
event 3 of excitation:
- Ach binding at the motor end plate: binding of Ach to receptors increases the membrane permeability to sodium ions, which then rush into the cell through sodium channels triggering a change in the transmembrane potential
events 4-5 of excitation:
- appearance of an action potential in the sarcolemma: action potential spreads across the surface of the sarcolemma, while this occurs AchE removes Ach, and the sodium channels close
- return to initial state: resting transmembrane potential restored
excitation-contraction coupling
action potential on the sarcolemma is coupled to contraction events via triads
excitation-contraction coupling events:
- action potential on T tubules reaches a triad and causes release of calcium ions from the cistern of the SR into the sarcoplasm around zones of overlap of sarcomeres
- calcium binds to troponin on the thin filaments
- troponin pulls tropomyosin off the active sites of the actin so that cross-bridge can from
contraction events 1-2:
- actin, free of tropomyosin bonds to myosin via its active sites
- cross-bridges are formed (actin active sites bound to myosin heads)
contraction event 3:
- myosin heads have been pre-primed for movement via ATP energy before cross-bridge formation & are pointed away from the M-line, upon actin binding the myosin heads pivot toward the M-line in an event called the power stroke which pulls the thick filament along the thin filament
contraction event 4:
- myosin ATPase uses ATP to break the cross bridges releasing the myosin head from the actin active sites, resetting the myosin head pointed away
contraction events 5:
- myosin head is now primed to interact with a new active site on actin, myosin can carry out 5 power strokes per second while calcium & ATP are available, each power stroke shortens the sarcomere by 1%
relaxation events 1-3:
- Ca2+ reabsorbed by sarcoplasmic reticulum
- Ca2+ ions detach from troponin
- troponin, without Ca2+, pivots tropomyosin back onto active sites on actin no cross-bridges can form
relaxation event 4:
-sarcomeres stretch back out:
1. gravity
2. opposing muscle contractions
3. elastic recoil of titin protein
-muscle returns to resting length
rigor mortis
death, ATP used up, SR can’t absorb Ca2+, Ca2+ bind troponin, tropomyosin frees actin, cross-bridges form, no ATP to detach myosin head=fixed cross bridge (until necrosis releases lysosomal enzymes which digest cross bridges)
botulism/botox
bacteria clostridium botulinum (grows in improperly canned foods) produces botulinum toxin: toxin prevents release of Ach at neuromuscular junction, results in flaccid paralysis
tetanus
clostridium tetani (grows in soil) produces tetanus toxin: toxin causes over stimulation of motor neurons, results in spastic paralysis
myasthenia gravis
autoimmune disease, causes loss of Ach receptors, muscle become non-responsive
muscle tension
force exerted by contracting muscle, force is applied to a load
load
weight of object being acted upon
what does contracting tension depend on?
-for a single muscle fiber contraction is “all or none”
1. resting length of fiber
2. frequency of stimuluation
resting length
greatest tension produced at optimal rating length, enough overlap that myosin can bind actin, not so much that thick filaments crash into Z-lines
twitch (frequency of stimuluation)
-single contraction due to single stimulus, 3 phases: latent period, contraction phase & relaxation phase
-single twitch won’t produce normal movement, requires cumulative twitches
-repeat stimulation will result in higher tension due Ca2+ not being fully absorbed -> more cross bridges
latent period (frequencey stimuluation: twitch)
post stimulation but no tension: action potential moves across sarcolemma, Ca2+ released
contraction phase (frequencey stimuluation: twitch)
peak tension production: active cross bridge formation
relaxation phase (frequencey stimuluation: twitch)
decline in tension: Ca2+ reabsorbed, cross bridge decline
treppe
stepping up of tension production to max level with repeat stimuluation of same fiber following relaxation phase
wave summation
repeat stimulation before relaxation phase ends results in more tension production that max treppe (typical muscle contraction)
incomplete tetanus (way to summate)
rapid cycles of contraction & relaxation produce max tension
complete tetanus (way to summate)
relaxation eliminated, fiber in prolonged state of contraction, produces 4x more tension than maximum treppe, but quick to fatigue
most skeletal ->
cardiac muscle ->
complete tetanus when contracting
incomplete tetanus only to prevent seizure of heart
what does tension produced in the whole muscle depend on?
internal vs. external tension & number of muscle fiber stimulated
internal tension
produced by sarcomeres, not all transferred to load, some lost due to elasticity of muscle tissues
external tension
tension applied to load
number of muscle fibers stimulated
-each skeletal muscle has thousands of fibers organized into motor units
-fibers from different motor units intermingled in muscle so activation of one unit will produce equal tension across whole muscle
motor unit
-all fibers controlled by single motor neuron (axon branches to contact each fiber)
-number of fibers in motor unit depends on function:
*fine control: 4/unit ex: eye muscles
*gross control: 2000/unit ex: legs
recruitment
order of activation of motor units: slower weaker first, stronger units added to produce steady increasee in tension
-some units rest while others contract to avoid fatigue
-for maximum tension all units in complete tetanus but leads to rappid fatigue
muscle tone
maintaining shape/definition of muscle: some units always contracting: excerise = increase units contracting -> increase metabolic rate -> speed of recruitment (better tone)
isotonic contractions
muscle length changes resulting in movement
isometric contraction
tension is produced with no movement
how does a muscle return to resting length, expansion via what?
- elastic recoil after contraction
- opposing muscle contractions
- gravity
muscle metabolism
-1 fiber ~15 billion thick filaments
-1 thick filament ~2500 ATP/sec
-1 glucose (aerobic respiration) =36 ATP
-each fiber needs 1 x 10^12 glucose/sec to contract
-muscle store respiration energy on creatine as creatine phosphate (CP)
-creatine phosphokinase transfers P from CP to ADP when ATP needed to reset myosin for next contraction
-each cell has only ~20 sec energy reserve
at rest (muscle metabolism)
use glucose and fatty acids with O2 (from blood) -> aerobic respiration, resulting ATP used to build CP reserves, excess glucose stored as glycogen
moderate activity (muscle metabolism)
CP used up, glusoce & fatty acids with O2 (from blood) used to generate ATP (aerobic respiration)
high activity (muscle metabolism)
O2 not delivered adequately, glucose from glycogen reserves used for ATP via fermentation (glycolysis only), pyruvic acid converted to latic acid
muscle fatigue
-state where muscle can no longer contract due to:
1. depletion of reserves (glycogen, ATP, CP)
2. decreased pH due to lactic acid
to restore function muscle fatigue, cell needs:
- intracellular energy reserves (glycogen, CP)
- good circulation (nutrients in, wastes out)
- normal O2 levels
- normal pH
lactic acid disposal
-lactic acid diffuses into blood
-filtred out by liver
-converted back to glucose
-returned to blood for use by cells
-when O2 returns, remaining lactic acid in muscle is converted to glucose and used in aerobic cellular respiration
what does muscle performance depend on?
- types of fibers
- physical conditioning
fiber types (muscle performance)
types of fibers in a muscle are genetically determined and mixed
fast glycolytic fibers (fast twitch)
-myosin ATPase work quickly
-anerobic ATP production (glycolysis only)
-large diameter fibers
-more myofilamnets & glycogen
-few mitochondria
-fast to act, powerful, but quick to fatigue
-catabolize glucose only
slow oxidative fiber (slow twitch)
-myosin ATPase woeks slowly
-specialized for aerobic respiration: many mitochondria, extensive blood supply, myoglobin
-smaller fibers for better diffusion
-slow to contract, weaker tension, but resist fatigue
-catabolize glucose, lipids & amino acids
intermediate/fast oxidative fibers
-qualities of both fast glycolytic & slow oxidative fibers
-fast acting but perform aerobic respiration so resist fatigue
-physical conditioning cn convert some fast fibers into intermediate fibers for stamina
aerobic excerise (physical conditioning)
increase in capillary density -> increase in mitochondria & myoglobin
both then:
increase efficiency of muscle metabolism -> strength & stamina -> decrease in fatigue
resistance excerise (physical conditioning)
-results in hypertrophy: fibers increase in diameter but not number
-increase in glycogen, myofibrils & myofilaments results in increase tension production
muscle enlargement
growth hormone & testosterone stimulates syntheisis of contractile proteins
what does epinephrine stimulate?
increase in muscle metabolism = increase force of contraction
without stimulation muscles will atrophy:
fibers shrink due to loss of myofilament proteins, loss up to ~5%/day
cardiac muscle tissue
-forms the majority of heart tissue
-one or two nuclei
-no cell division
-long branched cells
-myofibrils organized into sarcomeres (striated)
-no triads
-T tubules encircle Z-lines
-aerobic respiration only
-mitochondria & myoglobin rich
-glycogen & lipid energy reserves
-intercalated discs at cell junctions
intercalated discs
located at cell junctions (gap junctions & desmosomes) allow transmission of action potentials & link myofibrils from one cell to next
features of cardiac muscle
- contact without neural stimuluation, automaicity due to pacemaler cells that generate action potetials spontaneously
- pace & amount of tension can be adjusted by nervous system
3.contraction 10x longer than skeletal muscle - only twitches, no coplete tetanus
smooth muscle tissue
-lines hollow organs
-forms arrector pili muscles
-usually organized into two layers: circular & longitundinal
-spindle shaped cells
-central nucleus
-cells capable of division
-no myofibrils, sarcomeres, or T tubules
-thick filaments scattered
-thin filaments attached to dense bodies on desmin cytoskeleton (web)
-adjacent cells attach at dense bodies with gap junctions (linkage & communication)
-no tendons
-contraction compresses whole cell
smooth muscle excitation-contraction
different than striated muscle: no troponin so active sites on actin always exposed
smooth muscle excitation-contraction events 1-5:
- stimuluation causes Ca+ release from SR into cytiplasm
- Ca2+ binds calmodulin
- calmodulin activates myosin light chain kinase
- MLC kinase converts ATP -> ADP to cock myosin head
- cross bridges form -> contraction, cells pull toward center
how is smooth muscle cells stimulated?
-involuntary control from:
1. automatic nervous system (ANS)
2. hormones
3. other chemical factors
what control skeletal muscle and cardiac muscle?
motor neurons & automaticity
effects of aging
-skeletal muscle fibers become thinner: decrease in myofibrils & energy reserves = decrease in strength, endurance but increase in fatigue
decrease in cardiac and smooth muscle function equals what?
cardiovascular performance
what happens when there is an increase in fibrosis (CT)?
skeletal muscle less elastic
decrease in ability to repair equals what?
decrease in satellite cells & increase scar formation
