Muscle Physiology Flashcards
structure of skeletal muscle
structure of skeletal muscle
structure of skeletal muscle
skeletal muscle cells
skeletal muscle cells are long and cylindrical - length = 1-12 cm
they are striated (banding pattern under light microscopy)
striations caused by the arragement of the thin and thick myofilaments
they are multinucleated and contain a lot of mitocondria
number of cells depends on size of muscle
structure of skeletal muscle fiber
myofibrils and myofilaments
a muscle cell/fiber is composed of a bundle of myofibrils
myofibril = organelle composed of bundles of myofilaments
striated appearance - darker and lighter bands
composed of repeating units of contractile proteins = sarcomeres = contractile unit of myofibril
~100,000 sarcomeres in bicep branchii from one end to the other
thin myofilaments
actin (G-actin) - globular protein linked to form helical strands
- each has one myosin binding site
- associated with two regulatory proteins
tropomyosin - rod-shaped protein composed of two alpha helical chains wrapped in a supercoil
- found in grooves made by actin
- partically covers the myosin binding site
troponin - three-protein complex attatched to both actin and tropomyosin
- holds tropomyosin over myosin binding site on actin
Troponin A - binds to actin
Troponin C - binds calcium
Troponin T - binds tropomyosin
thick myofilaments
myosin - protein made of two polypeptide strands, each forming part of the tail, hinge, arm and head
- thick myofilaments are made of many individual myosin molecules
- head has an actin binding site and an ATP binding site (location of ATPase)
- undergoes conformational change to generate contraction
myosin molecule
each myosin molecule is made of 2 long polypeptide chains each forming part of the tail and one head of the myosin molecule
each myosin head contains:
- a binding site for actin and ATP (ATPase)
thin and thick myofilament in sarcomere
sliding filament theory
myosin binds to actinm forming a cross-bridge
myosin heads undergo power-strokes
thin filament slides over thick filament
sarcomere shortens - muscle contracts
thin and thick myofilament length do not change
sarcomere length does change
neuromuscular junction
neuromuscular junction
- action potential travels down motor neuron, to presynaptic terminal
- activation and opening of the voltage-gated Ca2+ channels
- ACh-containing vesicles fuse with the post-synaptic membrane and release ACh
- binding of neurotransmitter to ligand-gated ion channels on muscle
- change in membrane permeability
- opening of ion channels - ACh broken down by acetylcholinesterase
excitation-contraction coupling
where an action potential on the sarcolemma of the muscle cell leads to the release of Ca++ from the sarcoplasmic reticulum (SR), leading to crossbridge activity and muscle contraction
the neuromuscular junction
step 1 - the neuromuscular junction (NMJ)
- action potential travels down motor neuron, to presynaptic terminal
- activation and opening of the voltage-gated Ca2+ channels
- Ach-containing vesicles fuse with the post-synaptic membrane and release ACh
- binding of neurotrasmitter to ligand-gated ion channels on muscle
- change in membrane permeability
- opening of ion channels - ACh broken down by acetylcholinesterase
excitation contraction coupling (step 1,2)
- AP generated at end plate of the muscle cell (End Plate Potential)
- AP propagates over sarcolemma and down T-tubules
excitation contraction coupling (step 3,4,5)
- voltage sensors on T-tubule detects AP and changes shape
- Voltage sensor opens Ca2+ release channels on lateral sac of SR, Ca2+ is released from SR
- Ca2+ binds to troponin pulling tropomyosin off the myosin binding sites found on actin
excitation contraction coupling (step 6,7)
- myosin attaches to actin (crossbridge formation) and power stroke occurs
- thin filaments slides over thick filament and muscle contracts (sliding filaments - sarcomeres shorten)
How the muscle contraction stops
- Ca2+ is actively pumped back into SR by Ca2+ ATPase
- when Ca2+ is “removed”, tropomyosin covers myosin binding sites
- muscle relaxes
from NMJ signaling to muscle contraction
- AP travels down the motor neuron, causing ACh release
- AP travels down the T-tubule, to voltage sensor
- Voltage sensor changes conformation (shape)
- voltage sensor opens Ca2+ channel on SR and Ca2+ is released
- Ca2+ binds to troponin C, exposing the myosin binding site on actin
5a. myosin attaches to actin, forming a crossbridge and power stroke
5b. filaments slide past each other, shortening sarcomere - muscle contraction - Ca2+ is recycled back into the SR through the Ca2+ ATPase
actin-myosin-ATP cycle
- ATP has just attached to myosin, myosin is not attached to actin
- ATP is hydrolyzed to ADP and Pi; energy is transferred to myosin head; myosin now has high affinity for actin; myosin head is repositioned
between 2-3. AP causes Ca2+ release from SR; Ca2+ binds to troponin -> pulls tropomyosin off myosin binding sites; myosin binding sites; myosin attaches to actin forming crossbridge; no powerstroke yet
- Pi is released; powerstroke is triggered; muscle contraction occurs
- ADP is released; crossbridges still formed
- new molecule of ATP attaches to myosin; cross-bridge breaks; cycle repeats
the cycle keeps going as long as there is ATP and Ca2+
rigor mortis
the stiffening of muscles after death
- begins 3-4 hrs after death; reaches a maximum at 12 hrs; slowly disappears over next 24-48 hrs
cause
- no oxygen -> no ATP; no ATP -> Ca2+ cant be pumped back into SR -> crossbridges form
- no ATP -> actin and myosin cant dissociate -> muscle permanently fused until muscle decomposition
the motor unit
motor unit - one motor neuron + muscle fibers it innervates
one AP in motor neuron results in one ATP in all the muscle fibers it innervates
muscle twitch
twitch - muscle contraction in response to one action potential on the motor neuron
latency - time between an AP and the initiation of contraction
Contraction time (CT) vs relaxation time (RT)
duration of twitch 10-100 ms - depends on fiber type
grading muscle contraction
grading muscle contration: increased force of contraction
motor unit recuitment: as more motor units are recuited, more muscle fibers contract - higher contractile force
summation of twitch contractions: increased stimulus frequency
motor unit recuitment
motor unit recuitment - as more motor units are recuited, more muscle fibers contract - higher contractile force
summation
as summation (AP) frequency is increased, each muscle twitch has less “time” to relax before the next one occurs
-> twitch start to “stack up” on one another causing a more forceful contraction
unfused tetanus
increasing AP frequency increases the force of contraction
medium - high frequency - still some time to relax before next twitch
-> unfused tetanus
complete tetanus
at very high frequencies
- no time to relax between twitches
- all twitches summate to produce smooth sustained contraction called complete tetanus
