muscular system Flashcards
myofibrils
contain sarcomere for contraction, actin/myosin
actin = thick
myo = thin
satellite cells
undifferentiated cells, gives nuclei to muscle fibres
imp role in musc growth and repair…activated by training
initiates divide to inc nuclei…inc nuceli makes PROTEIn
motor unit
1 motor neuron and all assoc fibres it innervations
AP travels down t tubules into cell
NMJ
neuromuscular junction, where motor neuron and muscle cell meet
AP comes from nervous sys/somatic motor neuron
synaptic cleft separates neuron and cell
- AP stims NT release i.e. ACh in synaptic vessels
- travels across cleft to open Na channels
- generates end plate potential that continues AP
- AP travels along musc fibre membrane down t tubules, impacting all myofibrils
sliding filament theory
calcium released by of ATP, shortening of sarcomere
myosin binding site on actin opens for myosin head
- ca binds, shifting troponin-tropomyosin to allow myo head binding
2 ATP/crossbridge cycle…ATP needed to detach and reattach
excitation-contraction coupling
events causing depolarization of muscle that lead to muscle shortening
- AP from motor neuron releases ACh in NMJ
- ACh binds to receptors, causes end-plate potential
- depolarization of muscle leads to ca release from SR
- ca binds to troponin, which MOVES tropomyosin from myo binding site
- myosin head binds to actin = crossbridge
- power stroke, actin is PULLED and muscle shortens
when impulse ends, ca reputake into SR so muscle relaxes
ATPase breaks down ATP attached to crossbridge so myosin can bind to another actin
concentric contraction
musc length shortens, force > load
series elastic component
cross-bridge BRAKING EFFECT, process hindered if myosin-actin are bound too long
eccentric contraction
muscle elongates even tho trying to shorten
braking effect HELPS contraction, trying to resist lengthening
improves strength of contraction
what determines force of contraction
- type and number of MUs recruited
- more MU and fast twitch = inc force - initial muscle length: if optimal
- nature of neural stimulation of MUS: freq of stimulation
- summation
- tetanus - contractile history: fatigued or primed
muscle twitch
one full contraction response
latent period, contraction, relaxation
orderly recruitment
small MUs have small threshold, are recruited first
large MUs are last to be recruited and first to be de-recruited
length-tension relationship
optimal length produces most force, falls off at greater length
optimal myosin-actin overlap to contract
tetanus vs summation
summation: fast firing so muscle doesn’t fully relax, force compounds
tetanus: maximum force production when optimal activation frequency
trained ppl recruit fewer MUs for easy motions
why don’t we recruit 100% muscle fibres
would tear muscle from tendon
post activation potentiation
when previous activity was non-fatiguing, will increase force production of contraction
because of more efficient cross bridges, ca sensitivity
not applicable to real life
force-velocity relationship
as velocity inc, force dec
muscle fibre types
type 1/slow twich: slow oxidative
- red bcs low myosin ATPase
- activities less than 25% vo2max
type 2a: fast oxidative glycolytic
type 2x: fast glycolytic
- white bcs rich w myosin ATPase
fibre type distribution
depends on muscle and needed function
- most ppl have 45-55% slow twitch
- genetics
- hormone concentrations
- exercise habits
biochemical properties of musc fibres
- oxidative capacity: number of capillaries, myoglobin, mitochondria
- type of myosin ATPase isoform: speed of ATP degradation, fast twitch degrades fastest
- amount of contractile proteins in fibres: amount of act/myo determines number of crossbridges
contractile properties of musc fibres
- max force production: force/unit of cross sectional area
- large fibres = inc force - speed of contraction: Vmax
- myosin ATPase activity
- rate of cb cycling - max power output: power = force x velocity
- muscle fibre efficiency
types of muscle biopsy
muscle biopsy: remove muscle piece, may NOT represent whole body
stain for ATPase isoform
- immunohistochemical staining: antibody binds to myosin protein, fibre determined by colour
- gel electrophoresis: ID myosin isofroms specific to fibre type
why are muscle fibres different colours
myoglobin carries iron, which carries o2
- this is red in colours
oxidative fibres are red bcs are oxygenated, non-oxi are white
fatigue
decline in muscle power output
- decrease in force generation and decrease in shortening velocity
in exercise:
- inability to maintain exercise intensity or power output
- sensations of tiredness and assoc w dec musc fatigue
reversible w recovery
causes of fatigue in high intensity exercise vs long duration
high intensity: 60s
- accumulation of lactate, H, ADP, Pi, free radiacals
- diminishes cross bridges bound to actin
long duration exercise: 2-4hr
- musc factors i.e. accumulation free radicals, glyogen depletion, electrolyte imbalance
system causes of muscular fatigue
CV system: delivery o2 blood, removal metabolites
energy supply system: inadequate ATP, issues w susbtrate depletion
neuromuscular system: dec neural drives, dec respond to MAPs
psychology: inc RPE
central governer model: must maintain homeostasis, prevent catastrophic failure
- body won’t let continue
thermoregulatory: critical core temp
central vs peripheral fatigue
central fatigue: occurs w/in CNS…motor cortex –> SC
- pain, dec motivation
- reduced firing frequency of MUs
peripheral fatigue: w/in PNS…NMJ, sarcolemma, actin-myosin interaction
- impaired neuromuscular transmission leads to dec AP conductance to sarcolemma
- dec ca impairs cross-bridge cycling
why is it hard to discover origin of fatigue
in muscle, compartmentalization w/in cell inc difficulty to determination
i.e. ATP may be depelted by myosin head, but is adequate in other cell areas
diffusion is often origin of fatigue
- i.e. dehydration, factors contrib to homeostasis distribution
- easier to ID correlations than causes of fatigue
depletion hypothesis
peripheral fatigue
depletion of energy susbtrates i.e. ATP, PCr, glycogen
- must match restoration from other metabolic pathways or cause fatigue
initial rate of decline and extent of decline related to exercise intensity
glycogen: moderate intensity
- uniform depletion from fibre tupes
- carb loading can inc performance
- caffeine offsets fatigue
blood glucose:
- inc during short intense bursts
- falls w prologned exercise
TCA intermediates: decline causes dec capacity of krebs
accumulation hypothesis
peripheral fatigue
buildup of lactate, pi, ca, ammonia
muscle acidosis: inhibits important processes
- ATP production releases H ions, cause pain
Po = max isometric force
ca accumulation is linked to mitochondrial coupling efficiency
- alteration in membrane potential
- can be caused by lactate
- dec ca leads to dec SR uptake…impaired EC coupling
- dec responsiveness to ca: H interference on troponin
- dec sensitivity to ca leads to dec force for given amount of ca -> musc can’t contract
other metabolites involved in peripheral fatigue
potassium: released from contracting muscle
- dec cytosolic and inc plasma k content: release high enough to block nerve transmission in t tubules
sodium: increased na disrupts normal cell excitability
high na/k pump will inc performance
oxygen and fatigue
o2 depletion in muscle can cause fatigue i.e. altitude, circulation issues
low o2 indicated by lactate accumulation and pcr depletion
can double oxidative capacity w training
- inc ffa use, spare glycogen
neuromuscular fatigue
in CNS
exercise-induced decline in ability of musc to gen force/power that recovers w rest
- is MEASURABLE, not subjective like physical fatigue
neuromuscular fatigue model
how interactions in brain impact muscle
fatigue can be bcs of nerve or muscle failure
original vs new central fatigue hypotheses
origianl: to pass blood brain barrier and enter brain, transport protein binds to branched amino acid
- as prolong exercise, FFA primary source
- FFAs displace tryptophan from carriers and enter bloodstream
- compete w branched a.as to enter CNS
- in brain, tryptophan converted to serotonin
- serotonin causes lethargy
dopamine dec w activity = fatigue
- inc dopaminergic activity to prolong activity
superimposed twitch technique
central fatigue
if superimposed twitch occurs, bcs CNS failed toa ctivate all MUs and is experiencing fatigue
apply shock when “contract as hard as you can”
- if 100% musc recruited, no twitch would occur
supraspinal fatigue
produced by failure to generate output from motor cortex
brain or cortical fatigue
