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55 terms

Muscle Contraction

STUDY
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What are the steps in muscle contraction
1. Efferent motor cortex axons synapse on the spinal cord and generate an action potential in the α-motor neuron.
2. The action potential travels to the axon terminal, releasing acetylcholine into the synaptic cleft.
3. Acetylcholine binds a receptor on the skeletal muscle cell and generates an action potential, increasing Ca++ release from the sarcoplasmic reticulum.
4. Ca++ initiates contraction, resulting in shortening of the muscle cell and, consequently, movement.
Fast twitch fibers
Contain a myosin ATPase that rapidly hydrolyzes ATP
Thus, develop tension quickly; short bursts of activity
Large
Depend on glycolysis for energy
Relatively low number of mito
White appearance
Slow twitch fibers
Contain a myosin ATPase that slowly hydrolyzes ATP
Small
Depend on oxidative phosphorylation for energy
Develop tension more slowly
More resistant to fatigue
High number of mito
Red appearance
What are the qualities of a muscle fiber
-Multinucleated
-Surrounded by a memb called a sarcolemma
-Contains myofibrils
Contractile elements
Immersed in a matrix called sarcoplasm
Each myofibril is composed of
actin & myosin filaments
What are the qualities of myosin Myosin
The thicker filament
Contains a "head" region that is the site of ATPase activity
What are the qualities of Actin?
The thinner filament
Tethered at one end to the Z disk
Contain active sites where myosin heads will bind
Tropomyosin covers the active sites to prevent myosin binding when it's not time for that
Tropomyosin
covers the active sites to prevent myosin binding when it's not time for that
Troponin
associated w/ actin
I: intimately binds actin
T: ties together tropomyosin
C: binds Ca2+
The A band is
purely myosin
IT DOES NOT SHORTEN
-These segments move w/ contraction
H zone:
between adjacent actin filaments
I band:
between adjacent myosin filaments
Z disks
anchor actin filaments
Dystrophin
Anchors all myofibrils to the sarcolemma
Binds the actin filaments
Defective or absent in muscular dystrophy pts
Titin
Anchors myosin to the Z disk
Also centers the thick filaments
Nebulin
Assoc w/ actin
Serves as a "molecular ruler," controlling the length of the actin filaments
Alpha-actinin
Anchors actin to the Z disk
MECHANISM OF MUSCLE CONTRACTION
Walk Along Theory
Ca2+ binds to C-troponin
-This triggers a conformational change in tropomyosin
-Active sites on actin are uncovered
-Myosin heads bind to actin spontaneously
-With ATP, myosin head releases while the ATP binds
-Hydrolyze the ATP
-Myosin head is "cocked" and attaches to next active site
-This is the POWER STROKE
-ADP is released...
NMJ
Specialized synapse between a motor neuron and a muscle fiber
Occurs at a structure on the muscle fiber called the MOTOR END PLATE
-Contains an invagination called the synaptic trough
Space is called the synaptic cleft
-Contains large quanities of acetylcholinesterase (AChE)
-Smaller subneural clefts project into the post synaptic memb
-These increase the surface area
-ACh gated channels at the tops
-Voltage-gated Na+ channels in the valleys
ACh release
-Impulse begins in the ventral horn of the SC
-Local depol opens voltage-gated Ca2+ channels
ACh release
Impulse begins in the ventral horn of the SC
-Local depol opens voltage-gated Ca2+ channels
These are located on linear structures on the axon terminal called dense bars
-Influx of Ca2+ triggers fusion of 125 synaptic vesicles w/ the presynaptic memb
-ACh is released and binds to nicotinic ACh receptors on the muscle fiber memb
-Opening of the nicAChRs produces an END PLATE POTENTIAL
-(AChE terminates the effects of ACh in the synapse)
Curariform drugs
Block nicAChRs
-No EPP
-No muscle contraction
Botulinum toxin
Decreases the release of ACh
-No EPP
-No muscle contraction
ACh-like drugs
-Bind and activate nicAChRs
-Not destroyed by AChE, so prolonged effect!
-Ex: methacholine, carbachol, nicotine
Anti-AChE drugs
Block the degradation of ACh
-Prolong its effects
-Ex: neostigmine, "nerve gas"
Myasthenia gravis
Sx: paralysis
-An autoimmune dz characterized by presence of antibodies against nicAChRs
-Subsequently, these nicAChRs are destroyed
-Results in weak EPPs
-Tx: neostigmine increases the amount of ACh in the NM
Lambert-Eaton syndrome
Sx: muscle weakness, paralysis
-An autoimmune dz that attacks voltage-gated Ca2+ channels on the presynaptic memb
-Thus, little ACh can be released
-Results in weak EPPs
-Tx: neostigmine increases the amount of ACh in the NMJ
T-tubules
-Invaginations of the sarcolemma
-Filled w/ extracellular fluid
-Penetrate the muscle fiber, branch and form networks
-Transmit APs deep into the muscle fiber
-Skeletal muscle has two per sarcomere; cardiac muscle has one per sarcomere
Sarcoplasmic reticulum
Specialized smooth ER
-Form terminal cisternae adjacent to the T-tubules
-Intracellular storage compartment for Ca2+
A protein called calsequestrin cuddles w/ calcium when not in use
Triad
The junction between two terminal cisternae & one T-tubule
-Dihydropyridine receptor (DHPR)
Voltage sensitive
Embedded in the T-tubule
-Ryanodine Ca2+ release channel
Embedded in the terminal cisternae
Sequence of Events
-EPP moves along the T-tubule
-The DHP receptor senses the voltage change
-Triggers the opening of the RyCR channel
-Calcium is released
-Contraction occurs
-SERCA pumps calcium back into the SR
-Calcium binds to calsequestrin to facilitate storage
-Contraction is terminated
The contractile force of skeletal muscle increases in a calcium-dependent manner
Cardiac muscle
-Similar to skeletal muscle w/ a few exceptions
One is that the trigger for calcium release is calcium, not voltage
Malignant Hyperthermia
Autosomal dominant dz that disturbs calcium homeostasis in muscles
-Can be life-threatening
-Sx: muscle rigidity, high temperature, lactic acidosis, tachycardia, rhabdomyolysis
-Triggered by anestetics like halothane or ether
-Due to a constant leak of SR calcium thru the ryanodine channels
This makes SERCA work so, so hard to maintain the calcium gradient
This generates lots of heat
-Tx: IV dantrolene
This is a muscle relaxant that "plugs" the ryanodine receptor
Central Core Dz
-Rare autosomal dominant trait
-Sx: muscle weakness
-Again, a mutated ryanodine channel may allow too much calcium into the sarcoplasm
Mito absorb this extra calcium and die
This leads to a lack of mito in the central core of muscle fibers
Brody's Dz
-Sx: PAINLESS muscle cramping and impaired muscle relaxing during exercise
Exacerbated by cold weather
-Results from the decreased activity of SERCA found in fast-twitch skeletal muscle
SMOOTH MUSCLE
Mononucleate cells w/ no striations
Unitary Organization of smooth muscle
Sheets of electrically coupled cells which act in unison
Often spontaneously active
Ex: gut, blood vessels
Multiunitary
Discrete bundles that only contract in response to innervation
Ex: vas deferens, iris, piloerectors
Very efficient
LATCH STATE
maintainence of force for long periods of time
Difference between smooth and striated muscle contraction
Contraction occurs by the same actin-myosin interaction as in striated muscle
-However, the troponin complex is absent
-Myosin does not hydrolyze ATP unless it is first phosphorylated
An enz called Myosin Light Chain Kinase (MLCK) does this
MLCK is active only in the presence of a small, calcium-binding protein called calmodulin
Myosin Light Chain Kinase (MLCK
enzyme active only in the presence of a small, calcium-binding protein called calmodulin. phosphorylates myosin
Sequence of events in smooth muscle contraction
-Calcium initiates contraction
-It binds to calmodulin
Instead of troponin as in skeletal muscle!
-The calcium-calmodulin-MLCK complex leads to phosphorylation of the myosin light chain
-The phosphorylated myosin head binds to actin and power stroke occurs automatically
-A 2nd ATP is required to release the myosin head from actin
-Subsequent relaxation requires a MLCPhosphatase to remove the phosphate from myosin
Tension is a measure of
cross-bridging
Maximum tension developed by
the sarcomere is at the middle of the length-tension curve
This is when every myosin head is across from an actin molecule
At lengths longer than optimal
some myosin heads are not across from an actin
The optimal length of a sarcomere is
2.2 microns
PRELOAD
-For cardiac muscle, the amount of stretch before a contraction
How do you measure active tension
Active tension cannot be directly measured
You can measure the total tension and subtract the passive tension to get it tho
Stages of Muscle Contraction
1. Muscle at rest
2. After stimulation, there is an increase in tension and force develops
This is the isometric phase
Tension is still insufficient to lift a weight
3. At some point, the tension equals the weight.
Further sarcomere contraction will result only in shortening of the muscle
This now becomes the isotonic phase
4. WIthout a weight, tension (tone) momentarily stays the same as contraction stops and the muscle lengthens.
5. Finally, the muscle resumes its original length and resting tone.
The speed of muscle contraction is determined by how quick the myosin ATPase is.
-NB: This enz breaks down ATP so the next power stroke can occur
In any muscle, there is a mixture of slow and fast fibers
-All fibers in a certain motor unit will be of the same type
Small motor units (10 fibers per neuron) are for
precise control & rapid rxns
Ex: larynx, extraocular
Large motor units (1000 fibers per neuron) are for
coarse control & slow rxns
Ex: quadriceps
...
Different people have different proportions of these types
Evidence says that training does not alter these proportions
Summation
-An increase in the contraction intensity as a result of the additive effect of individual twitch contractions
-Can be due to multiple fiber recruitment or freq stimulation of the same fiber
Staircase Effect
Aka treppe effect
-Strength of a muscle contraction is increased by previous activity
-Due to enhanced intracellular calcium levels
-If a muscle is stimulated before a complete relaxation, the new twitch will sum w/ the previous one
TETANUS
fused state of contraction caused by high AP freq. no individual contractions and instead a
Hypertrophy
actin & myosin increase
Hyperplasia
new fibers; due to endurance training?