Physio Nerve Muscle 2006

8/13/2019 Physio Nerve Muscle 2006

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M1 Nerve/Musc le

Phys io logy Exam

Review

9/1/04

Stacy Trent and Joe Walsh


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Test Details:

1) Approx. 3 questions per lecture

2) 1.2 minutes per question

3) Department practice exam on

Blackboard

4) TLEs on M1 website (go to: Class

Materials then Physiology)


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Membranes

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Fluid Mosaic Model

Phospholipid bilayerwith proteins and cholesterol embeddedwithin bilayer.

Cholesterol makes bilayerstiffer or more viscous!!

Membrane composition depends on function (ie. More lipid in

Schwann cells and more protein in mitochondria).

Intrinsic/Integral vs. Extrinisic/Peripheral Proteins

Intrinsicproteins span the entire membrane and contain

hydrophillic ends and a hydrophobic core, often serving as

transporters. Extrinsicproteins are present on one side of the bilayer or the

other and are anchored by electrostatic interactions.

Glycolipidscan be conjugated with either an intrinsic or extrinsic

protein and serve as a surface marker for the cell.




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Transport

1) Simple Diffusion

- small, nonpolar > large, polar

2) Osmosis

- water follows solute

3) Facilitated Diffusion

- notenergy dependent transport of solute down itsconcentration gradient

4)Active Transport

- energy dependent transport of solute against itsconcentration gradient

Note: All transport mechanisms exhibit saturation kinetics,chemical specificity and competitive inhibition. Whenthe [substrate] increases, the transportation rateincreases until transport mechanism becomessaturated.




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Diffusion

Diffusionis driven by concentrationgradients.

Ficks 1st Law of Diffusion: Use to calculate Rate of Diffusion Note: C = C1-C2where C1= target compartment

Stokes-Einstein Equation: Use to calculate Diffusion Coefficient

Partition Coefficient() Expresses relative Lipid Solubility

0 (lipid insoluble) 1 (completely lipid soluble)



J DAC

X

D kT

6r




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Which factors allow fast

diffusion?1. Lipid solubility ()- the morelipid soluble, the

faster the diffusion.

2. C- the greaterthe change in concentration,

the faster the diffusion.3. Membrane thickness- the thinnerthe

membrane, the faster the diffusion.

4. Viscosity of membrane- the lessviscous the

membrane, the faster the diffusion.5. Radius of molecule- the smallerthe radius of

the molecule, the faster the diffusion.




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Osmosis

Vant Hoffs Law: =RT(iC)o Use to calculate osmotic pressure

o = pressurerequired to oppose the movement ofwater from an area of high [H2O] (low osmolarity)to an area of low [H2O] (high osmolarity).

Osmotic Flow Rateo Vw=Lo Use to calculate the osmotic flow rate of water

when the membrane is permeable to both water

and solute.o = reflection coefficient(0-1) - a high reflection

coefficient reflects a solute that does NOTpermeate the membrane well.




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Hypertonic vs. Hypotonic

Solutions Hypotonicsolutions have a lowerosmolarity

than cellular osmolarity (0.3 osm) and thus the

cell will swell when placed in a hypotonic

solution. Cell will swell in hypOtonic solution

Hypertonicsolutions have a higherosmolarity

than cellular osmolarity and thus the cell will

shrink when placed in a hypertonic solution.




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Facilitated Diffusion

Helps larger, less soluble molecules cross

the membrane

Dependent on concentration gradient

No Energy Needed!






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Active Transport

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Active Transport

Againstconcentration gradient Requires Energy (ATP)

Primary Active Transport Transporter directlybreaks down an energy

molecules (mostlyATPNa+/K+pump)

Secondary Active Transport Transporter is indirectlydependent on energy

expenditure from another transporter

ex. Na/glucose co-transporter fueled by Na+/K+pump

NOTE: Na+/K+pump = PumpKin(Pump K+in)




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Gated Channels

Utilize gradient: high to low[ ]

Ligand Gated Channels- passivediffusionthrough a

channel opened through ligand binding(hormone or

neurotransmitters)

Voltage Gated Channels- passivediffusionthrough a

channel opened by changes in the membrane potential

Vesicle Mediated Transport

Requires Energy!!

Endocytosis- into cell

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Membrane Potentials

Results because of an unequaldistribution of charge across a

membrane

Two equations you need to know:1) Nernst Equation

2) Goldmans Equation

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Nernst Equation:

(Dont forget about zvalence of ion)

- Use to calculate the membrane potentialof an

ion atequilibrium

- Represents the electrical potentialnecessary tomaintain a certain concentration gradient of a

permeable solute.

E 60mV

z

log

X AX

B




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Goldmans Equation

Used to calculate overall membrane potential whenmultiple ionsare involved.

Incorporates permeabilityof each ion.

Permeability of K+> Na+> Cl- thus..

K+drives Resting

Membrane Potential

Em (60mv)log

Pk K o PNa Na o PCl Cl i

Pk K

i P

Na Na

i P

Cl Cl

o




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Neurotransmitters

Acetylcholine(ACh) SomaticNS

At neuromuscular junction

AutonomicNS

Preganglionic PNS and SNS neurons Postganglionic PNS

Norepinephrine ANS- postganglionic SNS neurons

GABA Inhibitoryneurotransmitter of brain

Glutamate Excitatoryneurotransmitter of brain


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Receptors

Ionotropic- binding of

NT opens ion channel nACh receptors- Na+

and K+ channels

At neuromuscularjunction and autonomic

ganglion GABA receptors- ligand

gated Cl- channels

Glutamate receptors

Non-NMDA - ligandgated Na+ and K+

channels NMDA

Must bind glycine tobe active

Ligand gated Na, Kand Ca channels

blocked by Mg at rest

Metabotropic- binding

of NT generates a 2ndmessenger which

opens an ion channel

Binding activates G-

proteinwhich activatesand enzyme serving as a

2nd messenger

mAChreceptors

At PNS effector

organs

1, 2, 1, 2, and 3 At SNS effector

organs


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SNS Receptors

1- contraction (sphincters) 2- decreases sections (salivary glands) 1- heart (excitatory) and kidney 2- lungs, pupil (relaxation)Mnemonic: 1, 2 lungs


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Agonists and Antagonists

Pro-PNSEffects Neostigmine- Inhibits Acetylcholinesterase prolonging ACh

activity

Propanolol- antagonist

Pro-SNSEffects Isoprotenerol- agonist Belladonna and Atropine- mACh antagonist

Anti-ANS(both PNS and SNS) Hexamethonium- nACh antagonist (ganglia)

Anti-Skeletal MuscleContraction Curare- nACh antagonist (NMJ)


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Action Potentials (APs)

APsare the result of timeand voltagedependent changes in ionic permeabilityofexcitable cells (i.e. neurons).

Na+

and K+

channelsthat generateAPsare onlyfound at the axon hillock. Any otherdepolarization in a neuron is called a receptorpotential.

APsare ALL-OR-NOTHINGevents. A strongerstimulus only increases the frequencyof firing.

Ph f A ti


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Phases of Action

Potentials1. Slow depolarizationto

threshold

2. Rapid depolarizationdueto opening of voltagedependent Na+channelsleading to Na+influx(Hodgkin Cycle!)

3. Repolarizationdue toincreased K+

conductance leading toK+efflux

4. Hyperpolarization(refractory period)

5. Resting membranepotential


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Refractory Periods

AbsoluteRefractory Period- due to time

dependence of Na+channel

Noamount of inward current will generate another AP

Due to the Na+inactivationgate which is slow to closewhen triggered at threshold

RelativeRefractory Period

Need an excess of currentto generate an APbecause the Na+ channels are still inactivated until

the end of repolarization phase


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Velocity of Conduction

of AP Velocity increaseswith

increaseddiameter of

axon.

Velocity increaseswhenmembrane resistance

increases(myelination!)




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Synaptic Transmission

Presynaptic Membrane:

APCa+2channelsopening Ca+2 influx synaptic vesicle fusion release of NTs

Post-synaptic membrane:

Neurotransmitter binds to

postsynaptic neuron or

muscle leading to

increased conductance

of Na+ and K+ causing agenerator or action

potential.

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Response of Post-Synaptic Cell

Responsemay be inhibitory or excitatory depending on thenature of postsynaptic cell (NOTNeurotransmitter!!)

Temporal or Spatial Summation

Temporal- multiple signals from 1 axon firing in rapid

succession such that successive inputs add to the still-

existent present inputs. Spatial- multiple signals from different axons occurring

simultaneously.

Repetitive Stimulations

Facilitation- successive APs cause postsynaptic membrane

potential to grow more and more intense in amplification

Post-tetanic Potentiation- after repetitive firing, Ca+2

channels are synchronized resulting in a more amplified

EPSP following tetanus

Synaptic Fatigue- delay in response after synapse following

prolonged tetanus (NTs have to be re-packaged)


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Generator vs. Action Potentials

Generator Potentials

Subthreshold

Graded

Intensity of signal =larger response

Decremental

conductance

Longer length constant =less decrement

Larger nerves = longer

length constant

Action Potentials

Over threshold

All or Nothing!!!

Intensity of signal =more frequent Aps

No decrement in

signal

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Autonomic vs. Somatic NS

Somatic NS Acts on skeletal

muscles

1 neuron

ACh nACh (motorend plate)

Controlled by

voluntarythought

(motor cortex)

Autonomic NS Acts on smooth muscle,

glands, cardiac muscle

2 neurons: post andpreganglionic

PreG: ACh nACh

Post G: PNS: ACh mACh SNS: NE or

Controlled by hypothalamus(involuntary)

Associated w/ limbic systemleads to emotionally linkedresponse

Ablation (cant respond tochanges)



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Autonomic NS

Sympathetic Cell bodies of

postganglionicnerves are inganglia near spinal

cord Diffuse control (1:10

ratio of pre to postGfibers)

Shortpreganglionicnerves (ACh nACh receptors)

Longpost ganglionicnerves (NE1,2,

1 and 2)

Parasympathetic Cell bodies of

postganglionicnerves are inganglia near organ

Precise control (1:3ratio of pre to postGfibers)

Longpreganglionicnerves (ACh nACh receptors)

Short postganglionicnerves (ACh mACh receptors)

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SNS vs. PNS

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SNS vs. PNS

SNS = fight or flight

Dilates pupils

Opens airways

Increases heart rate and

BP

Increases blood flow toheart, brain and skeletal

muscle

Inhibits digestion

Piloerection

Gluconeogenesis andglycogenolysis (makes

glucose available)

PNS = rest and digest

Constricts pupils

Restricts airways

Decreases heart rate and

BP

Promotes digestion Increases blood flow to

gut

Increase saliva

Glyconeogenesis (stores

glucose as glycogen)






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SNS vs. PNS

Salivary Secretions: SNS: salivary amylase production PNS: watery saliva

Defecation SNS: motility of colon until appropriate time PNS: motility of colon leads to expulsion of stool

Urination SNS: Relaxation of bladder to allow for fill-up

PNS: Contraction of bladder Erection

SNS: Ejaculation and psychogenic erections

PNS: Erection (ACh NO release

vasodilation)


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Muscle


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Skeletal Muscle

Controlled by Somatic NS

Skeletal muscle specific terms:

Neuromuscular junction

Motor endplateskeletal muscle on thereceiving end of nm junction

End Plate Potential (EPP)generatorpotential of skeletal muscle

ACh release is quantal (miniature endplate potential = 0.4 mV)


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Organization and

Structure of Muscle


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Classification of Muscle

Striated

Muscle

Smooth

Muscle

Multi-Unit

Single-UnitCardiac

Skeletal

FunctionalSyncytium

Automaticity

Motor Unit

Composition

Motor Nerve

Required


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Connective Tissue (Know

this!) Epimysium

surrounds entire muscle

Perimysium separates muscle into bundles of muscle fibers (fascicles)

contains blood vessels Endomysium

separates muscle fascicles into individual muscle cells(myofibers)

contains capillaries

Epimys ium, perimys ium , and endomysium all com e together at

the ends of m uscles to form TENDONS


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Anatomy of a Muscle

c

Nerves and blood vessels are embedded in connective tissue. The major

connective tissue components are collagen and elastin. Muscles are attached

to bones by tendons at their origin and insertion.


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Muscle Growth During Development

Activated

by injury

or trauma

Cell Div is ion

(Hyperplasia)Cell Fusion

Cell Growth

(Hypertrophy)

Satellite Cell

(quiescent)

Re-Enter

the

Cell Cycle

Myoblasts Myotubes

Myofibers


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The SarcomereBasic Contractile Unit in Muscle

M line


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Myofilament Arrangements

I IA

When muscle contracts, the

sarcomere shortens. The I band

and H Zone also shorten. But

the length of the A band remains

the same.

A cross-section through

the A Band/I Band overlap

shows the hexagonal arrayof thick and thin myofilaments

The Thick Myofilament


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The Thick Myofilament

The thick myofilaments are composed of myosin molecules arranged in an

end to end fashion at the M-line. Each myosin is composed of two myosin

heavy chain subunits and two pair of myosin light chains.

Myosin Light Chains

MHC220,000 Daltons

MLC1520,000 Daltons


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Thin myofilaments Actin core

Tropomyosin

Filamentous proteinblocks myosin bindingsite on actin

Troponin Tattaches troponin

complex totropomyosin

Ialong withtropomyosin inhibitsmyosin binding site onactin

Cbinds freeintracellular calcium to

produce aconformationalchange in tropomyosin


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Other Structural Proteins Titin

keeps thick myofilaments centered in sarcomere

extends from M line to Z line, largest MW protein known

Nebulin determines length of thin myofilaments, molecular ruler

Alpha Actininanchors thin myofilaments to the Z-line

Beta Actinindetermines length of thin filaments

Myomesinbinds titin, aligns thick filaments into hexagonal array

Desmincytoskeletal protein, connects adjacent sarcomeres

C-, H-, and X- proteinsform rings around thick filaments, maintains thickfilament structure during contraction

Cap-Z and tropomodulinassociated with opposite ends of growing thinfilaments, regulates length Dystrophinanchors actin filaments to sarcolemma, defective in MD

Myotilininteracts with alpha actinin and Z-lines, sarcomeric organization


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NerveMuscle

Relation


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Some definitions

Motor Unit

Composed of an alpha motorneuron and allthe myofibers innervated by that neuron

Motor Endplate The region of the myofiber directly under the

terminal axon branches

Neuromuscular junction

Where the axon terminal and the motorendplate meet

Size Principle of Motor Unit


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Size Principle of Motor Unit

Recruitment

Input from CNSCorticospinal Tract

Small Cell Body

few myofibers

easily recruited

Large Cell Body

Type IType II

Recruited First

Finesse Contractions

Recruited Last

Forceful ContractionsSpinal chord

Two different motor units within the same myofiber

Acetylcholine receptor


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Acetylcholine receptor


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T-tubules are aligned w/ ends of A band(near myosin heads).


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Excitation-Contraction CouplingResting Muscle

DHP

Receptor

RyR

Receptor

Ca++

Ca++Calsequestrin

Ca++

Ca++

Ca++

Ca++

Ca++

Ca++

Ca+++ +

_ _Ca++

ATP

No

at resting membrane potential

SR-Ca++ATPase


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Excitation-Contraction CouplingContracting Muscle

DHP

Receptor

RyR

Receptor

Ca++

Ca++

Calsequestrin

Ca++

Ca++

Ca++

Ca++

Ca++

Ca++

Ca+++ +

+ +Ca++

ATP

Depolarized

Crossbridge

Formation

Sarcomeric Shortening

Ca++

Ca++SR-Ca++ATPase


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Excitation-Contraction CouplingRelaxing Muscle

DHP

Receptor

RyR

Receptor

Ca++

Ca++Calsequestrin

Ca++

Ca++

Ca++

Ca++

Ca++

Ca++

Ca+++ +

_ _Ca++

ADP + Pi

No

at resting membrane potential

Ca++ SR-Ca++ATPase

Tension is longer than electrical or biochemical events


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Steps in excitation-contraction coupling:

1) Action Potential

2) Depolarization of the T-Tubules - Causes conformationalchange in the DHPR - opens Ca2+channels(Ryr) on

sacroplasmic reticulum

3) Ca2+released from SR into ICF

4) Ca2+ binds to Troponin C cooperatively - causes

conformational change

5) Tropomyosin is out of way

6) Cross-bridge cycling

7) Relaxation via Ca2+ATPase

The Crossbridge Cycle


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Crossbridge

detachmentATP

ADP + Pi

AM

AMATP AMADPPi

A + MADPPi(Charged Intermediate)

Relaxed state

Rigor mortis if no ATP

Crossbridge

energized

Crossbridge

attachment

Crossbrige

Motion

Ca2Actin-Myosin

Binding Sites

3

The Crossbridge Cycle

Features of the


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Crossbridge Motion

Changes in the conformation of the hinge

region of the myosin molecule allow for

swivel motion of the crossbridges that

produces sarcomeric shortening.

Features of the

Crossbridge Cycle

1) CB cycle is repetitive2) CB cycle is asynchronous

3) Tension is proportional to CB number

4) Velocity is proportional to cycle rate

5) Velocity is inversely proportional to load


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Sliding Filament Theory

Describes the mechanism of muscle contraction

Free energy from cleavage of Mg*ATP induces abend in myosin head from a 90 to 45 degreeangle

Actin filaments slide toward the H zone, pullingthe Z lines inward

Sarcomere shortens and muscle contracts

This happens in a wave - not synchronous foreach sarcomere


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Sample Question #1

Lengths at rest:

A band = 1.5 mI band = 1.0 m

H zone = 0.7 m

What is the length of the

a) sarcomere?

b) thin filament?

c) overlap?


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Sample Question #1

Lengths at rest:

A band = 1.5 mI band = 1.0 m

H zone = 0.7 m

What is the length of the

a) sarcomere? 1.5 + 1.0 = 2.5 mb) thin filament? (2.50.7) / 2 = 0.9 mc) overlap? 1.50.7 = 0.8 m


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Sample Question #2

Lengths at rest:A band = 1.5 mI band = 1.0 mH zone = 0.7 mSarcomere = 2.5 m

During contraction, the muscle shortens by 20%. What is the length of the

a) sarcomere?

b) thick filament?

c) I band?

d) H zone?

e) overlap?


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Sample Question #2

Lengths at rest:A band = 1.5 mI band = 1.0 mH zone = 0.7 mSarcomere = 2.5 m

During contraction, the muscle shortens by 20%. What is the length of the

a) sarcomere? 2.50.5 = 2.0 mb) thick filament? 1.5 m (no change!)c) I band? 2.01.5 = 0.5 md) H zone? 2.0[(2) x (0.9)] = 0.2 me) overlap? 1.50.2 = 1.3 m

Length Tension


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LengthTension

Relationship Generation of tension in a muscle depends on its initial

length

Maximal tensioncan be developed at a sarcomeresoptimal length, usually its resting length

At the optimal length, a maximum number of cross-

bridge sites are accessible to the actin molecules forbinding and bending

When a muscle is passively stretched, the thin filamentsare pulled out and there are less actin sites available forcross-bridge binding, decreasing tension

When a muscle is shorter than its optimal length, tensiondecreases because the thin filaments overlap and thethick filaments become forced against the Z-lines

Length vs. Tension


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Length vs. Tension

AT OPTIMAL LENGTH

- maximum # of crossbridges

> OPTIMAL LENGTH

- thin filaments pulled away and less

room on actin for binding = less tension

< OPTIMAL LENGTH

- thin filaments overlap, thick filaments

run into Z lines = less tension

Active State


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Active State

Describes criteria which must be met for

contraction to occur:

a) binding of calcium to troponin C

b) cross-bridge formation

c) ATP splitting

d) cross-bridge motion

Twitch force

Ca-troponin

complex

Myoplasmic [Ca]

Action potential

El ti d C t til C t


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Elastic and Contractile Components

Contractile

Component

Parallel Elastic

Component

Series Elastic

Component

1) Contractile Component: Responsiblefor Active Tension(proportional to # of

crossbridges that cycle)

2) Parallel Elastic Component:

Responsible for Passive Tension

3) Series Elastic Component: Must be

stretched in order to develop active

tension


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Modulation of Muscle

Contraction


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Summation

Muscle force can be modulated by the frequencyof stimulation

Depends on active state and refractory period

Skeletal muscle exhibits a long active state anda short refractory period

Allows a second action potential long before theinitial twitch response is complete

Subsequent twitches build upon the one before,ultimately achieving a tetanus state


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Summation of Twitches

The force of muscle contraction can be increased by increasing the frequency

of nerve stimulation. The key is the difference in the time course for the

action potential, calcium transient, and mechanical response.


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Tetanus and Fatigue

1/sec 5/sec 10/sec 50/sec

Stimulation at low frequencies produces summation of twitches andtetanus. However, when stimulation frequency reaches a rate rapid

enough to produce a complete tetanus, fatigue will develop.

Fatigue in tetany is due to fast twitch muscles

Onset of

Fatigue


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Muscle Architecture

Force production and velocity of shortening of the whole muscle depends

on the architecture. It is important to remember that force is proportional

to myofiber number, while velocity is proportional to myofiber length.

Therefore, strap-like muscles provide the greatest velocity of shortening,

while pennate muscles can generate more force.


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Leverage

Because muscles operate across joints, theforce applied to move an object depends on theleverage factor

LF = Leverage arm / Distance from joint

The farther away from the joint a muscle isinserted, the smaller the leverage factor and theeasier it is to move an object (example: doorhinge)

The closer a muscle is inserted to the joint, thelarger the leverage factor (mechanicaldisadvantage), but the more maneuverable theobject is

Preload Afterload and the Latent Period


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Preload, Afterload and the Latent Period(influence on twitch force)

Preloaded with 10 kg Afterloaded with 10 kg

8 msec latent period 12 msec latent period

Preloaded with 20 kg

8 msec latent period

Afterloaded with 20 kg

20 msec latent period

Action

Potential

Action

PotentialAction

Potential

Action

Potential

Muscle

Twitch

Muscle

Twitch

Muscle

Twitch

Muscle

Twitch

The latent period isprolonged in an after-

loaded muscle because

it takes time to stretch

the series elastic

component.

The length of the latent

period is dependent on

load for afterloaded

muscle, but independent

of load for preloaded

muscle.

Increasing load

decreases twitch

shortening independent

of effects on latent

period.

ExtentofShortening

ExtentofShortening

ExtentofShortening

ExtentofShortening


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Load-Velocity Relationship

As load increases the velocity of shortening decreases.


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Sample Question #3

A muscle which weighs 12 g and is 100 cm long isstimulated for a total of one hour at a frequency

of 4/min. Upon each stimulation the muscle lifts

204 g and shortens 0.5 meters. What is the

work and power output of that muscle?


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Sample Question #3

A muscle which weighs 12 g and is 100 cm long isstimulated for a total of one hour at a frequencyof 4/min. Upon each stimulation the muscle lifts204 g and shortens 0.5 meters. What is thework and power output per hour of that muscle?

Force produced per stimulation = 0.204 kg x 9.81 m/s2= 2.00124 N

Work done during 1 contraction = 2 N x 0.5 m = 1.0 Joules

Work done per hour = 1.0 J x 4/min x 60 min = 240 JPower output over 1 hour = 240 J / 3600 sec = 0.067 Watts

Total work per gram of muscle = 240 J / 12 g = 20.0 J/g


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Rate of Onset of Energy Pathways

Aerobic

Mechanisms

Anaerobic

Glycolysis

Creatine

PhosphatePercentCapacity

ofEnergy

GeneratingSystem

Exercise Duration

10 sec. 30 sec. 2 min. 5 min.

100


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Biochemical Profile Performance Profile

Fiber Type Glycolytic Oxidative MHC-ATPase Fatigue Activity ProfileActivity Activity Twitch Speed Resistance

Fast Twitch White V. High Low High Low Short term phasic

IIB

Fast Twitch Red Moderate V. High High High Sustained phasic

IIA

Slow Twitch Low Moderate Low V. High Sustained Tonic

I

Characteristics of Muscle Fiber Types

The activity profile of the major muscle fiber types matches the biochemical

and contractile profiles for these fiber types.

Anaerobic Threshold


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Anaerobic Threshold

OxygenConsu

mption

(ml/kg/min)

Exercise Work LoadREST

30

45

60

100

20

40

60

80

Blood

Lactate(mg/dL

)

Anaerobic

Threshold

Untrained Trained

Oxygen Debt


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Oxygen Debtoxygen debt and oxygen repayment are equal

Rate

ofEnergyExpen

diture

Time (minutes)

Oxygen Debt

Oxygen Repayment

O

xygenConsump

tion

0 2 8


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Parameters of Endurance Training

Time (months)

AdaptiveR

atio

(Control/Tra

ined)

TCA Cycle

Enzymes

Oxidative Potential

of Fast Fibers

Capillary Density

Slow twitch fiber diameter

VO2Max

1 12 24 6

Training De-training

Effi i C l l ti


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Efficiency Calculations

A 70-kg individual does 20 pullups, lifting his body weight 1 meter eachtime. In doing so, he consumes 4 liters of O2. Baseline is 400 ml ofO2/min. Total exercise time is 5 mins. What is his gross and netmechanical efficiency.

1 L O2 = 4.8 kcal

1 cal = 4.186 J

Effi i C l l ti


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1 L O2 = 4.8 kcal

1 cal = 4.186 J

W = mgh = (70 x 9.8 x 1) x 20 reps = 13.7 kJ

= 13.7 kJ/4.186 kJ/kcal = 3.3 kcal

Effi i C l l ti


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1 L O2 = 4.8 kcal

1 cal = 4.186 J

W = mgh = (70 x 9.8 x 1) x 20 reps = 13.7 kJ

= 13.7 kJ/4.186 kJ/kcal = 3.3 kcal

Total E = 4 L x 4.8 kcal = 19.2 kcalNet E = (4 L0.4 L x 5 min) x 4.8 kcal = 9.6 kcal

Effi i C l l ti


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1 L O2 = 4.8 kcal

1 cal = 4.186 J

W = mgh = (70 x 9.8 x 1) x 20 reps = 13.7 kJ

= 13.7 kJ/4.186 kJ/kcal = 3.3 kcal

Total E = 4 L x 4.8 kcal = 19.2 kcalNet E = (4 L0.4 L x 5 min) x 4.8 kcal = 9.6 kcal

Gros s Efficienc y = W/E = 3.3 kcal/19.2 kcal = 17%

Net Eff ic iency = 3.3/9.6 = 34%

Fib T


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Fiber Types

Metabolism ATPase

activity

Fatigue

Resistance

Contraction Adaptation Example

White

Fast

Glycolysis + - Short term

phasic

hypertrophy Power lift

Slow Red Oxidative - ++ Sustained

tonic

Incr mt

myoglobin

Postural mm

Fast Red Oxid/Glyc + + Sustained

phasic

both rowing

S th M l U it


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Smooth Muscle: Unitary

Present in GI tract, bladder, uterus, and ureter

Contracts in coordinated fashion b/c of gap jxns

Modulated by NTs and hormones

Has pacemaker activity, slow waves

S th M l M lti it


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Smooth Muscle: Multiunit

Found in iris, ciliary muscels of lens, and the vas deferens

Cells dont communicate w/ each other electrically

Densely innervated by autonomics

E it ti C t ti i S th M l


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Excitation-Contraction in Smooth Muscle

1) Action potential opens Ca2+ channels in sacrolemmal membrane

2) Rise in intracellular Ca2+concentration causes Ca2+bind to calmodulin -the Ca2+ - Calmodulin complex binds to and activates myosin light chainkinase(MLCK)

3) Activated MLCK phosphorylates myosin, which can now form an breakcross-bridges

*amount of cross-bridges=tension=intracellular Ca2+

4) Intracellular Ca2+decreases(b/c of SRs Ca2+ATPase) and myosin isdephosphorylated by myosin light chain phosphatase(MLCP)

Ratio of MLCK:MLCP is main determinant of tension in smooth muscle


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Practice Questions for

Nerve/Muscle Physio

Test

9/1/2004


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Choose the correct sequence of events

during excitation/contraction coupling:

a) Action potential, calcium release, depolarization ofthe t-tubules, contraction, calcium re-uptake

b) Action potential, depolarization of the t-tubules,calcium release, contraction, calcium re-uptake

c) Action potential, depolarization of the t-tubules,calcium re-uptake, contraction, calcium release

d) Action potential, calcium release, contraction,depolarization of the t-tubules, calcium re-uptake

C f


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Choose the correct sequence of events

during excitation/contraction coupling:

a) Action potential, calcium release, depolarization ofthe t-tubules, contraction, calcium re-uptake

b) Action potential, depolarization of the t-tubules,calcium release, contraction, calcium re-uptake

c) Action potential, depolarization of the t-tubules,calcium re-uptake, contraction, calcium release

d) Action potential, calcium release, contraction,depolarization of the t-tubules, calcium re-uptake

At equilibrium the concentration of Na + is 5

M i id th ll d 500 M t id th


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mM inside the cell and 500 mM outside the

cell. What is the Na + equilibrium potential

for this cell?

a) +90 mV

b) -90 mVc) +120 mV

d) -120 mV

e) +60 mV

At equilibrium the concentration of Na + is 5

M i id th ll d 500 M t id th


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mM inside the cell and 500 mM outside the

cell. What is the Na + equilibrium potential

for this cell?

a) +90 mV

b) -90 mVc) +120 mV

d) -120 mV

e) +60 mV

A di t th " i i i l " hi h f


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According to the "size principle" which of

the following statements would be true?

a) large motor units are recruited first but generate less force

b) large motor units are recruited first and generate more force

c) small motor units are recruited first and generate more force

d) small motor units are recruited first but generate less force

e) motor unit size and force production are not related so noneof the above are true.

A di t th " i i i l " hi h f


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According to the "size principle" which of

the following statements would be true?

a) large motor units are recruited first but generate less force

b) large motor units are recruited first and generate more force

c) small motor units are recruited first and generate more force

d) small motor units are recruited first but generate less force

e) motor unit size and force production are not related so noneof the above are true.

According to the sliding filament theory,


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which of the following occurs during a

muscle contraction:

a) The thin filaments pull the H zone to the center of thesarcomere.

b) The Z lines pull the thick filaments in the overlapping region.

c) The area of overlap between the thick and thin filamentsincreases, however the actual lengths of the thick and thethin filaments remain unchanged.

d) The width of both the I band and the A band decreases whilethe H zone increases.



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g g y,

which of the following occurs during a

muscle contraction:

a) The thin filaments pull the H zone to the center of thesarcomere.

b) The Z lines pull the thick filaments in the overlapping region.

c) The area of overlap between the thick and thin filamentsincreases, however the actual lengths of the thick and thethin filaments remain unchanged.

d) The width of both the I band and the A band decreases whilethe H zone increases.

W i th bl d l t th


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Warming the blood supply to the

hypothalamus causes

a) shivering.

b) increased pulmonary circulation.

c) piloerection.

d) increased cutaneous circulation.

e) increased mesenteric circulation.

Warming the blood s ppl to the


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Warming the blood supply to the

hypothalamus causes

a) shivering.

b) increased pulmonary circulation.

c) piloerection.

d) increased cutaneous circulation.

e) increased mesenteric circulation.

Which of the following features are the same


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g

in the sympathetic and parasympathetic

nervous system?

a) Average length of preganglionic fibers.

b) Average length of postganglionic fibers.

c) Neurotransmitter in preganglionic fibers.

d) Neurotransmitter in postganglionic fibers.

Which of the following features are the same


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g

in the sympathetic and parasympathetic

nervous system?

a) Average length of preganglionic fibers.

b) Average length of postganglionic fibers.

c) Neurotransmitter in preganglionic fibers.

d) Neurotransmitter in postganglionic fibers.

The following data are given for a skeletal muscle fiber:

Length of thin filament: 0 8um


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a) 1.20 um

b) 1.60 um

c) 1.76 um

d) 2.08 um

e) Cannot be determined from above data.

Length of thin filament: 0.8um

Length of H-zone: 0.4um

The muscle is stimulated under isotonic conditions and

it shortens 20%. What is the approximate length of the

sarcomere in the contracted muscle according to the

sliding filament theory?


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QuickTime and a


H-zone = 0.4 um

Thin Filaments = 0.8 um


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0.8 + 0.8 + 0.4 = 2.0 um

2.0 x 80% = 1.6 um

QuickTime and a


The following data are given for a skeletal muscle fiber:

Length of thin filament: 0 8um


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a) 1.20 um

b) 1.60 um

c) 1.76 um

d) 2.08 um

e) Cannot be determined from above data.

Length of thin filament: 0.8um

Length of H-zone: 0.4um

The muscle is stimulated under isotonic conditions and

it shortens 20%. What is the approximate length of the

sarcomere in the contracted muscle according to the

sliding filament theory?

GOOD LUCK!!


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GOOD LUCK!! http://www2.uic.edu/stud_orgs/prof/M1/courses/physiology/

[email protected]

[email protected]

[email protected]

BIOCHEM REVIEW NEXT WEEK, SAME TIME,

ROOM TBA

Obi Ekwenna and Jason Emer

QuickTime and a

http://www2.uic.edu/stud_orgs/prof/M1/courses/physiology/mailto:[email protected]:[email protected]:[email protected]:[email protected]:[email protected]:[email protected]://www2.uic.edu/stud_orgs/prof/M1/courses/physiology/

Physio Nerve Muscle 2006

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