Physio Nerve Muscle 2006

M1 Nerve/Muscle
Physiology Exam
Review
9/1/04

Stacy Trent and Joe Walsh

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)
Membranes
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TIFF (Uncompressed) decompressor
are needed to see this picture.
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Fluid Mosaic Model
Phospholipid bilayer with proteins and cholesterol embedded
within bilayer.
Cholesterol makes bilayer stiffer 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
Intrinsic proteins span the entire membrane and contain
hydrophillic ends and a hydrophobic core, often serving as
transporters.
Extrinsic proteins are present on one side of the bilayer or the
other and are anchored by electrostatic interactions.
Glycolipids can 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
- not energy dependent transport of solute down its
concentration gradient
4) Active Transport
- energy dependent transport of solute against its
concentration gradient

Note: All transport mechanisms exhibit saturation kinetics,
chemical specificity and competitive inhibition. When
the [substrate] increases, the transportation rate
increases until transport mechanism becomes
saturated.
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Transport
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Diffusion
Diffusion is driven by concentration gradients.

Ficks 1st Law of Diffusion:
Use to calculate Rate of Diffusion
Note: C = C
1
-C
2
where C
1
= target compartment

Stokes-Einstein Equation:
Use to calculate Diffusion Coefficient

Partition Coefficient (|)
Expresses relative Lipid Solubility
0 (lipid insoluble) 1 (completely lipid soluble)

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J = DA
AC
AX

D=
kT
6trq
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Which factors allow fast
diffusion?

1. Lipid solubility (|) - the more lipid soluble, the
faster the diffusion.
2. C - the greater the change in concentration,
the faster the diffusion.
3. Membrane thickness - the thinner the
membrane, the faster the diffusion.
4. Viscosity of membrane - the less viscous the
membrane, the faster the diffusion.
5. Radius of molecule - the smaller the 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 = pressure required to oppose the movement of
water from an area of high [H
2
O] (low osmolarity)
to an area of low [H
2
O] (high osmolarity).
Osmotic Flow Rate
o V
w
=Lo
o Use to calculate the osmotic flow rate of water
when the membrane is permeable to both water
and solute.
o o = reflection coefficient (0-1) - a high reflection
coefficient reflects a solute that does NOT
permeate the membrane well.
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Hypertonic vs. Hypotonic
Solutions
Hypotonic solutions have a lower osmolarity
than cellular osmolarity (0.3 osm) and thus the
cell will swell when placed in a hypotonic
solution.
Cell will swell in hypOtonic solution

Hypertonic solutions have a higher osmolarity
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
Against concentration gradient
Requires Energy (ATP)

Primary Active Transport
Transporter directly breaks down an energy
molecules (mostly ATPNa
+
/K
+
pump)

Secondary Active Transport
Transporter is indirectly dependent 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 - passive diffusion through a
channel opened through ligand binding (hormone or
neurotransmitters)
Voltage Gated Channels - passive diffusion through a
channel opened by changes in the membrane potential

Vesicle Mediated Transport
Requires Energy!!
Endocytosis - into cell
Exocytosis - out of cell
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Membrane Potentials
Results because of an unequal
distribution 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 potential of an
ion at equilibrium
- Represents the electrical potential necessary to
maintain a certain concentration gradient of a
permeable solute.

AE =
60mV
z
|
\

|
.
|
log
X
+
| |
A
X
+
| |
B
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Goldmans Equation

Used to calculate overall membrane potential when
multiple ions are involved.

Incorporates permeability of each ion.

Permeability of K
+
> Na
+
> Cl
-
thus..
K+ drives Resting
Membrane Potential

E
m
= (60mv)log
P
k
K
| |
o
+ P
Na
Na
| |
o
+ P
Cl
Cl
| |
i
( )
P
k
K
| |
i
+ P
Na
Na
| |
i
+ P
Cl
Cl
| |
o
( )
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Neurotransmitters
Acetylcholine (ACh)
Somatic NS
At neuromuscular junction
Autonomic NS
Preganglionic PNS and SNS neurons
Postganglionic PNS
Norepinephrine
ANS- postganglionic SNS neurons
GABA
Inhibitory neurotransmitter of brain
Glutamate
Excitatory neurotransmitter of brain

Receptors
Ionotropic - binding of
NT opens ion channel
nACh receptors - Na+
and K+ channels
At neuromuscular
junction and autonomic
ganglion
GABA receptors - ligand
gated Cl- channels
Glutamate receptors
Non-NMDA - ligand
gated Na+ and K+
channels
NMDA
Must bind glycine to
be active
Ligand gated Na, K
and Ca channels
blocked by Mg at rest
Metabotropic - binding
of NT generates a 2nd
messenger which
opens an ion channel
Binding activates G-
protein which activates
and enzyme serving as a
2nd messenger
mACh receptors
At PNS effector
organs
o1, o2, |1, |2, and |3
At SNS effector
organs
SNS Receptors
o1 - contraction (sphincters)
o2 - decreases sections (salivary glands)

|1 - heart (excitatory) and kidney
|2 - lungs, pupil (relaxation)

Mnemonic: 1, 2 lungs
Agonists and Antagonists
Pro-PNS Effects
Neostigmine - Inhibits Acetylcholinesterase prolonging ACh
activity
Propanolol - | antagonist

Pro-SNS Effects
Isoprotenerol - | agonist
Belladonna and Atropine - mACh antagonist

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

Anti-Skeletal Muscle Contraction
Curare - nACh antagonist (NMJ)

Action Potentials (APs)
APs are the result of time and voltage
dependent changes in ionic permeability of
excitable cells (i.e. neurons).
Na
+
and K
+
channels that generate APs are only
found at the axon hillock. Any other
depolarization in a neuron is called a receptor
potential.
APs are ALL-OR-NOTHING events. A stronger
stimulus only increases the frequency of firing.

Phases of Action
Potentials
1. Slow depolarization to
threshold
2. Rapid depolarization due
to opening of voltage
dependent Na
+
channels
leading to Na
+
influx
(Hodgkin Cycle!)
3. Repolarization due to
increased K
+

conductance leading to
K
+
efflux
4. Hyperpolarization
(refractory period)
5. Resting membrane
potential
Refractory Periods
Absolute Refractory Period - due to time
dependence of Na
+
channel
No amount of inward current will generate another AP
Due to the Na
+
inactivation gate which is slow to close
when triggered at threshold

Relative Refractory Period
Need an excess of current to generate an AP
because the Na+ channels are still inactivated until
the end of repolarization phase
Velocity of Conduction
of AP
Velocity increases with
increased diameter of
axon.

Velocity increases when
membrane resistance
increases (myelination!)
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Synaptic Transmission
Presynaptic Membrane:
AP Ca
+2
channels
opening 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 a
generator or action
potential.
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http://mcb.berkeley.edu/courses/mcb136/topic/Tissue_Cells_Membranes/SlideSet3/AP%20review_files/slide0012_image012.gif
Response of Post-Synaptic Cell
Response may be inhibitory or excitatory depending on the
nature of postsynaptic cell (NOT Neurotransmitter!!)
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)
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 (motor
end plate)
Controlled by
voluntary thought
(motor cortex)
Autonomic NS
Acts on smooth muscle,
glands, cardiac muscle

2 neurons: post and
preganglionic

PreG: ACh nACh
Post G:
PNS: ACh mACh
SNS: NE o or |
Controlled by hypothalamus
(involuntary)
Associated w/ limbic system
leads to emotionally linked
response
Ablation (cant respond to
changes)
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Autonomic NS
Sympathetic
Cell bodies of
postganglionic
nerves are in
ganglia near spinal
cord
Diffuse control (1:10
ratio of pre to postG
fibers)
Short preganglionic
nerves (ACh
nACh receptors)
Long post ganglionic
nerves (NE o1,o2,
|1 and |2)

Parasympathetic
Cell bodies of
postganglionic
nerves are in
ganglia near organ
Precise control (1:3
ratio of pre to postG
fibers)
Long preganglionic
nerves (ACh
nACh receptors)
Short postganglionic
nerves (ACh
mACh receptors)
Qui ckTi me and a
TIFF (Uncompres sed) decompres sor
are needed to see thi s pi cture.
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 to
heart, brain and skeletal
muscle
Inhibits digestion
Piloerection
Gluconeogenesis and
glycogenolysis (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)
Muscle
Skeletal Muscle
Controlled by Somatic NS
Skeletal muscle specific terms:
Neuromuscular junction
Motor endplate skeletal muscle on the
receiving end of nm junction
End Plate Potential (EPP) generator
potential of skeletal muscle
ACh release is quantal (miniature end
plate potential = 0.4 mV)
Organization and
Structure of Muscle
Classification of Muscle
Striated
Muscle
Smooth
Muscle
Multi-Unit
Single-Unit Cardiac
Skeletal
Functional
Syncytium
Automaticity
Motor Unit
Composition
Motor Nerve
Required
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

Epimysium, perimysium, and endomysium all come together at
the ends of muscles to form TENDONS
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.
Muscle Growth During Development
Activated
by injury
or trauma
Cell Division
(Hyperplasia)
Cell Fusion
Cell Growth
(Hypertrophy)
Satellite Cell
(quiescent)
Re-Enter
the
Cell Cycle
Myoblasts
Myotubes
Myofibers
The Sarcomere
Basic Contractile Unit in Muscle
M line
Myofilament Arrangements
I I
A
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 array
of thick and thin myofilaments
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
MHC 220,000 Daltons
MLC 15 20,000 Daltons
Thin myofilaments
Actin core
Tropomyosin
Filamentous protein
blocks myosin binding
site on actin
Troponin
T attaches troponin
complex to
tropomyosin
I along with
tropomyosin inhibits
myosin binding site on
actin
C binds free
intracellular calcium to
produce a
conformational
change in tropomyosin
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 Actinin anchors thin myofilaments to the Z-line
Beta Actinin determines length of thin filaments
Myomesin binds titin, aligns thick filaments into hexagonal array
Desmin cytoskeletal protein, connects adjacent sarcomeres
C-, H-, and X- proteins form rings around thick filaments, maintains thick
filament structure during contraction
Cap-Z and tropomodulin associated with opposite ends of growing thin
filaments, regulates length
Dystrophin anchors actin filaments to sarcolemma, defective in MD
Myotilin interacts with alpha actinin and Z-lines, sarcomeric organization
Nerve Muscle
Relation
Some definitions
Motor Unit
Composed of an alpha motorneuron and all
the 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 motor
endplate meet
Size Principle of Motor Unit
Recruitment
Input from CNS
Corticospinal Tract
Small Cell Body
few myofibers
easily recruited
Large Cell Body
Type I
Type II
Recruited First
Finesse Contractions
Recruited Last
Forceful Contractions
Spinal chord
Two different motor units within the same myofiber
Acetylcholine receptor
T-tubules are aligned w/ ends of A band(near myosin heads).
Excitation-Contraction Coupling
Resting 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
Contracting 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
Relaxing 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
Steps in excitation-contraction coupling:
1) Action Potential
2) Depolarization of the T-Tubules - Causes conformational
change in the DHPR - opens Ca
2+
channels(Ryr) on
sacroplasmic reticulum
3) Ca
2+
released from SR into ICF
4) Ca
2+
binds to Troponin C cooperatively - causes
conformational change
5) Tropomyosin is out of way
6) Cross-bridge cycling
7) Relaxation via Ca
2+
ATPase

Crossbridge
detachment
ATP
ADP + P
i

AM
AMATP
AMADPP
i
A + MADPP
i
(Charged Intermediate)
Relaxed state
Rigor mortis if no ATP
Crossbridge
energized
Crossbridge
attachment
Crossbrige
Motion
Ca
2

Actin-Myosin
Binding Sites
3
The Crossbridge Cycle
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 repetitive
2) 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
Sliding Filament Theory
Describes the mechanism of muscle contraction
Free energy from cleavage of Mg*ATP induces a
bend in myosin head from a 90 to 45 degree
angle
Actin filaments slide toward the H zone, pulling
the Z lines inward
Sarcomere shortens and muscle contracts
This happens in a wave - not synchronous for
each sarcomere

Sample Question #1
Lengths at rest:
A band = 1.5 m
I band = 1.0 m
H zone = 0.7 m

What is the length of the
a) sarcomere?
b) thin filament?
c) overlap?
Sample Question #1
Lengths at rest:
A band = 1.5 m
I band = 1.0 m
H zone = 0.7 m

What is the length of the
a) sarcomere? 1.5 + 1.0 = 2.5 m
b) thin filament? (2.5 0.7) / 2 = 0.9 m
c) overlap? 1.5 0.7 = 0.8 m
Sample Question #2
Lengths at rest:
A band = 1.5 m
I band = 1.0 m
H zone = 0.7 m
Sarcomere = 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?
Sample Question #2
Lengths at rest:
A band = 1.5 m
I band = 1.0 m
H zone = 0.7 m
Sarcomere = 2.5 m

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

a) sarcomere? 2.5 0.5 = 2.0 m
b) thick filament? 1.5 m (no change!)
c) I band? 2.0 1.5 = 0.5 m
d) H zone? 2.0 [(2) x (0.9)] = 0.2 m
e) overlap? 1.5 0.2 = 1.3 m
Length Tension
Relationship
Generation of tension in a muscle depends on its initial
length
Maximal tension can be developed at a sarcomeres
optimal length, usually its resting length
At the optimal length, a maximum number of cross-
bridge sites are accessible to the actin molecules for
binding and bending
When a muscle is passively stretched, the thin filaments
are pulled out and there are less actin sites available for
cross-bridge binding, decreasing tension
When a muscle is shorter than its optimal length, tension
decreases because the thin filaments overlap and the
thick filaments become forced against the Z-lines
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
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
Elastic and Contractile Components
Contractile
Component
Parallel Elastic
Component
Series Elastic
Component
1) Contractile Component: Responsible
for 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
Modulation of Muscle
Contraction
Summation
Muscle force can be modulated by the frequency
of stimulation
Depends on active state and refractory period
Skeletal muscle exhibits a long active state and
a short refractory period
Allows a second action potential long before the
initial twitch response is complete
Subsequent twitches build upon the one before,
ultimately achieving a tetanus state

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.
Tetanus and Fatigue
1/sec 5/sec 10/sec 50/sec
Stimulation at low frequencies produces summation of twitches and
tetanus. 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
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.
Leverage
Because muscles operate across joints, the
force applied to move an object depends on the
leverage factor
LF = Leverage arm / Distance from joint
The farther away from the joint a muscle is
inserted, the smaller the leverage factor and the
easier it is to move an object (example: door
hinge)
The closer a muscle is inserted to the joint, the
larger the leverage factor (mechanical
disadvantage), but the more maneuverable the
object is
Preload, Afterload and the Latent Period
(influence on twitch force)
Preloaded with 10 kg Afterloaded with 10 kg
8 msec latent period
Preloaded with 20 kg
Afterloaded with 20 kg
Action
Potential
Action
Potential
Action
Potential
Action
Potential
Muscle
Twitch
Muscle
Twitch
Muscle
Twitch
Muscle
Twitch
The latent period is
prolonged 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.

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Load-Velocity Relationship
As load increases the velocity of shortening decreases.
Sample Question #3
A muscle which weighs 12 g and is 100 cm long is
stimulated 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?

Sample Question #3
A muscle which weighs 12 g and is 100 cm long is
stimulated 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 per hour of that muscle?

Force produced per stimulation = 0.204 kg x 9.81 m/s
2
= 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 J
Power 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

Rate of Onset of Energy Pathways
Aerobic
Mechanisms
Anaerobic
Glycolysis
Creatine
Phosphate
P
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r
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n
t

C
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a
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y

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a
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Exercise Duration
10 sec.
30 sec. 2 min. 5 min.
100
Biochemical Profile Performance Profile

Fiber Type Glycolytic Oxidative MHC-ATPase Fatigue Activity Profile
Activity 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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p
t
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n

(
m
l
/
k
g
/
m
i
n
)

Exercise Work Load

REST
30
45
60
100
20
40
60
80
B
l
o
o
d

L
a
c
t
a
t
e

(
m
g
/
d
L
)

Anaerobic
Threshold
Untrained Trained
Oxygen Debt
oxygen debt and oxygen repayment are equal
R
a
t
e

o
f

E
n
e
r
g
y

E
x
p
e
n
d
i
t
u
r
e

Time (minutes)
Oxygen Debt
Oxygen Repayment
O
x
y
g
e
n

C
o
n
s
u
m
p
t
i
o
n

0 2 8
Parameters of Endurance Training
Time (months)
A
d
a
p
t
i
v
e

R
a
t
i
o

(
C
o
n
t
r
o
l
/
T
r
a
i
n
e
d
)

TCA Cycle
Enzymes
Oxidative Potential
of Fast Fibers
Capillary Density
Slow twitch fiber diameter
VO
2
Max
1 12 24 6
Training
De-training
Efficiency Calculations
A 70-kg individual does 20 pullups, lifting his body weight 1 meter each
time. In doing so, he consumes 4 liters of O
2
. Baseline is 400 ml of
O
2
/min. Total exercise time is 5 mins. What is his gross and net
mechanical efficiency.

1 L O
2
= 4.8 kcal
1 cal = 4.186 J

2
O
2

1 L O
2
= 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

2
O
2

1 L O
2
= 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 kcal
Net E = (4 L 0.4 L x 5 min) x 4.8 kcal = 9.6 kcal

2
O
2

1 L O
2
= 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 kcal
Net E = (4 L 0.4 L x 5 min) x 4.8 kcal = 9.6 kcal

Gross Efficiency = W/E = 3.3 kcal/19.2 kcal = 17%
Net Efficiency = 3.3/9.6 = 34%

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

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
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
Excitation-Contraction in Smooth Muscle
1) Action potential opens Ca
2+
channels in sacrolemmal membrane

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

3) Activated MLCK phosphorylates myosin, which can now form an break
cross-bridges
*amount of cross-bridges=tension=intracellular Ca
2+

4) Intracellular Ca
2+
decreases(b/c of SRs Ca
2+
ATPase) and myosin is
dephosphorylated by myosin light chain phosphatase(MLCP)

Ratio of MLCK:MLCP is main determinant of tension in smooth muscle
Practice Questions for
Nerve/Muscle Physio
Test
9/1/2004
Choose the correct sequence of events
during excitation/contraction coupling:
a) Action potential, calcium release, depolarization of
the 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
Choose the correct sequence of events
during excitation/contraction coupling:
a) Action potential, calcium release, depolarization of
the 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
mM inside the cell and 500 mM outside the
cell. What is the Na + equilibrium potential
for this cell?

a) +90 mV
b) -90 mV
c) +120 mV
d) -120 mV
e) +60 mV
At equilibrium the concentration of Na + is 5
mM inside the cell and 500 mM outside the
cell. What is the Na + equilibrium potential
for this cell?

a) +90 mV
b) -90 mV
c) +120 mV
d) -120 mV
e) +60 mV
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 none
of the above are true.
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 none
of the above are true.
According to the sliding filament theory,
which of the following occurs during a
muscle contraction:
a) The thin filaments pull the H zone to the center of the
sarcomere.

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

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

d) The width of both the I band and the A band decreases while
the H zone increases.
According to the sliding filament theory,
which of the following occurs during a
muscle contraction:
a) The thin filaments pull the H zone to the center of the
sarcomere.

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

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

d) The width of both the I band and the A band decreases while
the H zone increases.
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 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
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
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.
a) 1.20 um
b) 1.60 um
c) 1.76 um
d) 2.08 um
e) Cannot be determined from above data.
The following data are given for a skeletal muscle fiber:
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?
QuickTime and a
H-zone = 0.4 um
Thin Filaments = 0.8 um
0.8 + 0.8 + 0.4 = 2.0 um
2.0 x 80% = 1.6 um
QuickTime and a
a) 1.20 um
b) 1.60 um
c) 1.76 um
d) 2.08 um
e) Cannot be determined from above data.
The following data are given for a skeletal muscle fiber:
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!!
http://www2.uic.edu/stud_orgs/prof/M1/courses/physiology/

jwalsh3@uic.edu
strent1@uic.edu
dgolde1@uic.edu

BIOCHEM REVIEW NEXT WEEK, SAME TIME,
ROOM TBA
Obi Ekwenna and Jason Emer
QuickTime and a

Physio Nerve Muscle 2006

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