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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
Depend on glycolysis for energy
Relatively low number of mito
White appearance

Slow twitch fibers

Contain a myosin ATPase that slowly hydrolyzes ATP
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

-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


covers the active sites to prevent myosin binding when it's not time for that


associated w/ actin
I: intimately binds actin
T: ties together tropomyosin
C: binds Ca2+

The A band is

purely myosin
-These segments move w/ contraction

H zone:

between adjacent actin filaments

I band:

between adjacent myosin filaments

Z disks

anchor actin filaments


Anchors all myofibrils to the sarcolemma
Binds the actin filaments
Defective or absent in muscular dystrophy pts


Anchors myosin to the Z disk
Also centers the thick filaments


Assoc w/ actin
Serves as a "molecular ruler," controlling the length of the actin filaments


Anchors actin to the Z disk

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...


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 muscle contraction

Botulinum toxin

Decreases the release of ACh
-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


-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


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


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


Discrete bundles that only contract in response to innervation
Ex: vas deferens, iris, piloerectors
Very efficient


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


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


-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


-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


fused state of contraction caused by high AP freq. no individual contractions and instead a


actin & myosin increase


new fibers; due to endurance training?

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