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Motor unit
nerve body
axon
muscle fiber innervated
Nerve conduction
action potential passed down nerve segments
signal remains same voltage throughout nerve
Frequency modulation
increased frequency of action potentials → increased intensity of muscle contraction
Electrical potential
ability of electrons to do work/generate energy
dependent on gradient of electrons (comparison of two sides)
Membrane potential
potential for electrons to flow across cell membrane and do work
excitable cells = higher potential
Nernst/Goldman equations
concentration of ions on both sides & permeability of membrane determines membrane potential
Resting membrane potential
K+ is main contributor, ATP-dependent Na+/K+ pump maintains
K+ is very permeable when membrane is in resting/inactive state
-90mV charge compared to outside of cell
high K+ concentration in the cell, high Na+ & Cl- concentration outside of the cell
Excitable cells
higher resting membrane potential
ability to rapidly depolarize (change potential)
ex: muscle & nerve cells
Action potential
stimulus causes membrane to completely depolarize
occurs when stimulus reaches threshold (~ -60mV)
cell becomes hyperpolarized before returning to resting potential
unidirectional down the axon
Excitability
difference between resting potential & threshold
lower threshold/higher resting potential = more excitable
low extracellular K+/high extracellular Ca++ = decreased excitability
high extracellular K+/low extracellular Ca++ = increased excitability
K+ influences resting potential, Ca++ influences threshold
Depolarization
rapid entry of Na+ via voltage-gated Na+ channels when membrane potential hits threshold value
positive feedback loop (Na+ channels opening causes more channels to open)
Repolarization
K+ channels always open to allow K+ to leak out of the cell
slower process
Refractory period
period of time after an action potential in which the cell membrane is unable to mount another action potential
voltage-gated Na+ channels can’t open again for a period of time
Absolute refractory period
no impulse can cause action potential
during action potential
Relative refractory period
maximal/suprathreshold impulse can cause action potential but normal threshold stimulus will not cause action potential
Total refractory period
absolute + relative refractory periods
Neuromuscular junction
junction between the terminal nerve fiber & the muscle fiber
voltage-gated Ca++ channels open at end of nerve & Ca++ enters cell
vesicles from cell release acetylcholine into cleft to bind with cholinergic nicotinic receptors on motor end plate of muscle
can re-bind or get degraded
Na+ channels on motor end plate open & cause end plate potential
A band
dark/myosin w/overlapping actin/thick filaments
remains same length
finger-like projections w/resting potential energy
I band
light/actin/thin filaments
varies in length depending on contraction
binding sites w/high affinity for myosin, covered by tropomyosin w/troponin in resting state
Sarcomere
between Z lines (where actin filaments of two sarcomeres join), center M line (myosin)
Contraction
Ca++ contained in sarcoplasmic reticulum released to actin molecule, binds to troponin & displaces tropomyosin
myosin heads bind to actin
ATP releases myosin head from actin
ATP breakdown to ADP resets myosin head to potential energy
Relaxation
Ca++ pumped back into sarcoplasmic reticulum + released from troponin
actin binding sites re-covered, cross-bridges detached
Passive tension
tension generated by inherent elasticity of muscle
increases as length increases
Active tension
created by myosin-actin cross-bridges
tension wanes at very high length - maximum tension when all myosin heads engaged
total tenson follows curve
Summation
multiple firings in short period of time that increases force of contraction