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stimulation and contraction of single skeletal muscle cells
excitability
contractility
extensibility
elasticity
excitability
aka responsiveness or irritability
ability to receive and respond to a stimulus
electrical signal gets sent to muscle immediately
contractility
ability to shorten (contract) when an adequate stimulus is received
second signal
extensibility
ability of muscle cells to be stretched
elasticity
ability to recoil and resume resting length after stretching, reset
depolarization
electrical contractility
ex.) heartbeat, moving a muscle
the nerve stimulus and action potential
skeletal muscles must be stimulated by a motor neuron (nerve cell) to contract
motor unit
neuromuscular junction
synaptic cleft
action potential (electrical impulses) reaches the axon terminal of the motor neuron (efferent)
calcium channels open and calcium ions enter the axon terminal
efferent
nerve and muscles: DO NOT TOUCH
motor unit
one motor neuron and all the skeletal muscles stimulated by that neuron
neuromuscular junction
association site of axon terminal of the motor neuron and muscle
entire area involved in transmission of nerve impulse to muscle
axon terminal
end of nerves
gold bulb
synaptic cleft
gap between nerve and muscle
nerve and muscle do not make contact
area between nerve and muscle is filled with interstitial fluid
efferent
fibers that go from spinal cord into muscles (going away from nervous system)
nerves that come out of spinal cord that go to muscles come out of anterior/ventral side
transmission of nerve impulse to muscle
1.) action potential (electrical impulse) travels down the axon terminal of motor neuron, jumpstarting mitochondria
2.) calcium channels open up and Ca2+ (as released by sarcoplasmic reticulum) enters the axon terminal
3.) Ca2+ entry causes some synaptic vesicles to release their contents (pops) (acetylcholine, a neurotransmitter) by exocytosis
4.) acetylcholine goes across synaptic cleft and binds to receptors (purple channels) in the sarcolemma (gray membrane)
5.) ACh binds sarcolemma making cellular membrane permeable, so Na+ can go in and K+ rushes out
the sliding filament theory of muscle contraction
activation by nerve causes myosin heads (cross bridges) to attach to binding sites on the thin filament
cross bridges allows to hook on actin
myosin heads then bind to the next site of the thin filament and pull them toward the center of the sarcomere
when calcium comes in, the actin spins, revealing their binding sites and cross bridges form, and ADP gets converted to ATP
this continued action causes a sliding of the myosin along the actin
the result is that the muscle is shortened (contracted)
graded responses
different degrees of skeletal muscle shortening
graded responses can be produced by changing
the frequency of muscle stimulation
the number of muscle cells being stimulated at one time
types of graded responses
twitch
summing of contractions
unfused (incomplete) tetanus
fused (complete) tetanus
twitch
single, brief contraction
not a normal muscle function
summing of contractions (summation)
one contraction is immediately followed by another
the muscle does not completely return to a resting state due to more frequent stimulations
the effects are added
treppe: starts to relax, then gets more tense
unfused (incomplete) tetanus
looks like big stairstep, building upon one another
some relaxation occurs between contractions but nerve stimuli arrive at an even faster rate than summing on contractions
unless the muscle contraction is smooth and sustained, it is said to be unfused tetanus
fused (complete) tetanus
no evidence of relaxation before the following contractions
frequency of stimulations does not allow for relaxation between contractions
the result is a smooth and sustained muscle contraction
spasm that is maintained (does not relax)
muscle response to strong stimuli
muscle force depends on the number of fibers stimulated
more fibers contracting results in greater muscle tension
muscles can continue to contract unless they run out of energy
energy for muscle contraction
initially, muscles used stored ATP for energy
ATP bonds are broken to release energy
only 4-6 seconds worth of ATP is stored by muscles
after this initial time other pathways must be utilized to produced ATP
direct phosphorylation of ADP by creatine phosphate (CP)
aerobic respiration
anaerobic glycolysis and lactic acid formation
direct phosphorylation of ADP by creatine phosphate (CP)
muscle cells store CP
CP is a high-energy molecule
after ATP is depleted, ADP is left
when ADP and creatine phosphate join together, they make ATP
creatine separates by itself, phosphate joins ATP
CP + ADP = creatine + ATP
makes quick energy
CP supplies are exhausted in less than 15 seconds
about 1 ATP is created per CP molecule (1:1 ratio)
aerobic respiration
most efficient way to create ATP
uses oxygen
glucose is broken down to carbon dioxide and water, releasing energy (about 32 ATP)
a series of metabolic pathways occur in the mitochondria
this is a slower reaction that required continuous oxygen
glucose turns into pyruvic acid, and since oxygen is present, allows the use of fatty acids and amino acids (proteins)
anaerobic glycolysis and lactic acid formation
reaction that breaks down glucose without oxygen
glucose is broken down to pyruvic acid to produce about 2 ATP
pyruvic acid is converted to lactic acid via glycolysis
this reaction is not as efficient, but is fast
huge amounts of glucose are needed
lactic acid produces muscle fatigue
muscle fatigue and oxygen deficit
when a muscle is fatigued, it is unable to contract even with a stimulus
common cause for muscle fatigue is oxygen debt
oxygen must be “repaid” to tissue to remove oxygen deficit
oxygen is required to get rid of (wash out) accumulated lactic acid
increasing acidity (from lactic acid) and a lack of ATP causes the muscle to contract less