day 11 - muscle anatomy + phys. Flashcards
heart “wants to” beat at BLANKbpm
100bpm
is skelital muscle striated or non-striated
striated
skelital muscles are under voluntary/involuntary control
voluntary (exept respiratory muscles are weird)
name the three types of muscle tissue
skelital muscle, cardiac muscle, smooth muscle
cardiac muscles are striated/smooth
striated
cardiac muscles are under voluntary/involuntary control
involuntary
smooth muscle is striated/non-striated
non-striated (smooth)
smooth muscle is voluntary/involuntary
involuntary
what type(s) of muscle cells are multinucleated
skelital muscles
what type(s) of muscle cells are not ultinucleated
cardiac + smooth muscle
action potential(s) can/cannot go through connective tissue
canNOT
in what type of muscle cell does an action potential travel as a wave accross the whole muscle (as opposed to action potentials effecting only one motor unit)
cardiac muscle
in skelital muscle, muscle fibers are structurally BLANK from neighboring fiber(s)
structurally INDEPENDANT
fibers contract without the fiber next to it contracting
neuromuscular junction (def)
synapse between a neuron and muscle fiber
what neurotransmitter is released at neuromuscular junction
ACh
what happens when ACh is released into a neuromuscular junction
ACh stimulates muscle fiber(s) by causing action potential
action potential starts cascade of events that causes contraction through that entire muscle CELL
muscle cell contracts, producing maximal force, until action potential is stopped (muscle cells are all or none force production)
force production of a full muscle contracting is due to BLANK
the amount of muscle fibers recruited NOT how hard the fibers are pulling – muscle fibers are all or none force production
muscle twitch (def)
contraction as the result of one action potential from a single stimulus
tetanus (def)
high frequency stimulation that leads to a sustained contraction
electromyography (def)
recording of electrical signals being sent to the muscle (NOT measuring what the muscle is actually doing)
myocyte (def)
muscle cell
sarcolemma (def)
muscle cell membrane
sarcoplasm (def)
muscle cell cytoplasm
connective tissue (def)
very strong supporting tissue(s)
what connective tissue connects bone to bone
ligaments
what connective tissue connects muscle to bone
tendons
tendon (def)
connect muscle to bone and transfer force production from muscle to bone
how is connective tissue organized in a muscle
connective tissue wraps around each indivdual muscle fiber in many layers then wraps around groups of muscle fibers and eventually wraps around whole muscle
connective tissue wraps extend past the end of the muscle fibers/last muscle fiber to connect to bone
true/false: tendons are stuck onto the ends of muscles and attach muscle to bone
FALSE THEY ARNT JUST STUCK ON THE END THEY ARE WRAPPED
tendons are vascular/avascular
avascular – take much longer than muscle to heal
myofiliment (def)
structural proteins in muscle fibers that cause shortening
myofiliment types
actin and myosin
actin (def)
thin filament, double helix shape
has CA2+ binding site, when CA2+ binds it causes conformational change
myosin (def)
thick filament, arm like cross bridges that firm strong bonds with actin when CA2+ is bound (conformational change makes it possible for myosin to get a good grip/strong bond w/actin)
how many actin per each myosin
6 actin per one myosin
sarcomere (def)
section of muscle, structural + functional unit of muscle cell
how do you define a sarcomere
from one z-line to the next z-line
explain the basic mechanism of muscle contraction
action potential occurs (due neural stimulation)
ACh released into the neuromuscular junction which causes the release of Ca2+ in the muscle cell from the sarcoplasmic reticulum
Ca2+ binds to binding site on acting, causing conformational change
myosin binds to actin after conformational change (can now get a good grip)
myosin pulls on actin toward the midline, z-lines become closer to eachother = sarcomeres shorten
who developed the sliding filament theory
huxely
sarcoplasmic reticulum (def)
organell that acts as a storage site for Ca2+ in muscle cells + sucks Ca2+ back in once neural stimulation ends
step one in sliding filament theory (diagram)
energized, but weak bond (myosin in wrong position to pull)
step two in sliding filament theory (diagram)
energized, Ca2+ binds to binding sites on actin = strong bond (myosin in position to pull)
steps three + four in sliding filament theory (diagram)
myosin uses strong bond formed with actin and pulls
now un energized, and uncocked
what happens to muscle contraction if there is no atp
always contracted (rigor mortis)
best/most accepted theory of fatigue in muscles at a cellular level
H+ ions associated with lactate production may interfere with muscle contraction
how do H+ ions possibly cause peripheral fatigue
H+ interferes with Ca2+ binding sites on actin and blocks Ca2+ from binding
H+ blocking Ca2+ = less force production = cant do another rep etc.
central fatigue (def)
“i just dont want to do this anymore” even if one physically could
periferal fatigue (def)
accumulation fatigue (accumulation of H+ due to lactate production)
muscle fatigue
what type of muscle fibers have the most mitochondria
slow oxidative
what type of muscle fiber is best at adaptation
FOG
henneman size principle (def)
increased frequency/magnitude of stimulation will sum to reach threshold of more and faster fibers
true/false: body will let you recruit all FG fibers but only after all SO and FOG fibers are also recruited
FALSE
your body will NEVER let you recruit all you FG fibers because then you would tear the muscle from the tendon
fiber type and performance: elite power atheletes
ex. sprinters, jumpers, throwers, volleyball, american football, etc.
high percentage of FG fibers, up to 70%
fiber type and performance: elite endurance atheletes
ex. distance running, nordic skiing, cyclists, triathletes, etc.
high percentage of SO fibers, up to 85%
why do elite endurance atheletes have up to 85% SO fibers but elite power atheletes only have up to 70% FG fibers
because all postural muscles are SO and everyone has postural muscles so those get lumped in with the SO fibers in endurance atheletes althogh they dont actually have to do with thier sport and eveyrone has them
fiber types and performance: regular people/the rest of us
have more ballanced mix of slow + fast fibers determined by genetics
can adapt, but there is genetic ceiling (not going to be elite)
muscle fibers can change characteristics (FOG look + act more like FG), but cannot actually change type
adaptation of muscle fiber types to training: endurance (aerobic/oxidative) training
- greatest adaptation in SO fibers (increased mitochondria)
- can result in a shift in characteristics of FOG + FG fibers toward more oxidative capacity
- possible increase in muscle size due to additional acting + myosin
adaptation of muscle fiber types to training: resistance/high intensity (anaerobic/glycolydic) training
- greatest adaptation in FG + FOG fibers (more phosphocreatine stores, greater increase in muscle size from additional actin + myosin)
- can result in a shift in characteristics of SO + FOG fibers (more glycolidic capacity + increased muscle size)
muscle fiber adaptation through overload (greater than normal physical stress)
causes microtears in fibers and trigger immune response including inflamation and formation of new proteins (DOMS)
delayed onset muscle soreness (DOMS) steps
1) structural damage to muscle cells (microtears)
2) membrane damage
3) calcium leaks from sarcoplasmic reticulum
4) protease activated which results in breakdown of cellular proteins
5) inflammatory response
6) edema (swelling) and pain (particularly when moving bc swelling hits free nerve endings)
overtraining (def)
accumulation of training stress that is detramental to ones health and performanceo
overtraining symptoms
- elevated HR at rest + at fixed work rate
- physchological staleness
- increased rate of illness
- loss of appetite + decrease in bodyweight
- decrease(s) in performance
progression causes BLANK
hypertrophy (increase in cell size due to additional actin + myosin)
