1.

02
19, June, 2015

Dr. KATHERINE MUNARRIZ | Muscle Physiology

SKELETAL MUSCLE
The skeletal muscle is multinucleated, striated and moves
voluntarily
Each muscle covered by an EPIMYSIUM
Each muscle is composed of FASCICLES which are
covered by the PERIMYSIUM
Each fascicle is composed of several MUSCLE FIBERS
(cells) which are covered by an ENDOMYSIUM
A muscle fiber is composed of several MYOFIBRILS
which are covered by the SARCOPLASMIC
RETICULUM (SR) and invaginated by T-TUBULES
(transverse tubules)
SARCOLEMMA is a thin membrane enclosing a
skeletal muscle fiber. Through this, the action
potential passes towards the T tubules.
The T tubules are extensions or invaginations of the
sarcolemma that brings the action potential rapidly
to the innermost part of the muscle.
Myofibrils consist of SARCOMERES that contain the
Actin (Thin Filament) and Myosin (Thick Filament)
SARCOPLASM is the intracellular fluid between
myofibrils that contains large quantities of K, Mg and
PO4, plus multiple protein enzymes. Also present are
tremendous numbers of mitochondria that lie
parallel to the myofibrils. These supply the
contracting myofibrils with ATP. Mitochondria also
store Ca++ that adds to intracytosolic Ca++ during
depolarization.

composition:
a. large protein that consists of six different polypeptides
b. one pair of large heavy chains
c. two pairs of light chain
Thin Filament (Actin)
formed by the aggregation of actin molecules (Gactin) into a two-stranded helical filament (F-actin)
Tropomyosin inhibits binding of myosin to actin by covering
the binding site
Troponin complex
a. Troponin T -Has strong affinity to tropomyosin
-Attaches the troponin complex to
tropomyosin
-No. 1 inhibitor of Cross-bridge formation
b. Troponin I- Has strong affinity to actin
-Inhibits interaction of actin and myosin
c. Troponin C -Ca++ protein that once bound permits
myosin and actin interaction by the
movement of tropomyosin, thereby
exposing the myosin binding sites.
*A thin/actin filament is made-up of the following proteins:
actin globules, tropomyosin and troponin (T, I, and C).

Parts of a myofibril
Sarcomere - segment of myofibril between two Z
lines/disc
Z line bisects the I-band; attachment of the actin
filament
I band (Isotropic) contains only actin (thin)
filaments
H Zone light are between the A-band contains only
myosin (thick) filaments
A band (Anisotropic) dark striation of the myofibril
that contains both actin and myosin
M line bisects the H zone
*In a normal contraction/ regular contraction, it is the H zone
and I band which shorten.
*The I band, A band and Z disc/ line give the skeletal muscles
its striated appearance.
Muscle filaments
Thick Filament (Myosin)
tethered to the Z-lines by a cytoskeletal
protein called titin
Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

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1.02 PHYSIOLOGY
Muscle Physiology
Dr. MUNARRIZ |

SKELETAL MUSCLE CONTRACTION

Neuromuscular Junction Transmission

4.
5.

6.

7.

Ca++ entry triggers the release of Ach from the axon

terminals
Ach diffuses from axon terminals to the synaptic
cleft and attaches to the receptor sites at the motor
end plate/sarcolemma of the muscle
The binding of the Ach to the receptors opens Ca++
channels at the end plate and causes and influx of
Ca++ and an efflux of K+, depolarizing the membrane
(sarcolemma), producing the EPP.
EPP depolarizes the adjacent muscle cell plasma
membrane to its threshold potential, generating an
AP that propagates the muscle fiber surface

Nerve Cell Resting Membrane Potential (RMP): -70mV

Nerve Cell Threshold Potential: -55mV
Skeletal Muscle Cell RMP: -90mV
Skeletal Muscle Cell Threshold Potential: -75mV
8.

1.
2.

3.

SYNAPSE is the area between a nerve and a muscle

cell
LOWER MOTOR NEURON (LMN) supplies the muscle
cell and synapses with the SkM fiber
SOMATIC NEURON supplies the Skeletal
muscle
AUTONOMIC NEURON supplies the
Smooth muscles
END PLATE the part of the muscle where Ach
attaches to the receptor sites
ACETYLCHOLINE the only neurotransmitter found
in the NMJ
NEUROMUSCULAR JUNCTION (NMJ) -End Plate +
Post Synaptic Axon Terminal
END PLATE POTENTIAL (EPP) a localized nonpropagated potential that could produce an AP in
the muscle when threshold is reached
An Action Potential (AP) is received by a neuron and
travels down the axon to the axon terminal
The AP causes an influx of Na+ which causes a
depolarization while an efflux of K+ will cause a
repolarization. The repolarization causes the
regeneration of the AP and the next depolarizing
event occurs at the Node of Ranvier and continues
to the next until it reaches the axon terminal.
Some Notes:
-Upper motor neuron- located in brain cortex
-mostly excitatory (Na+ influx)
-Interneuron- mostly inhibitory (K+ efflux; Cl- influx)
-Lower Motor Neuron-found in spinal cord
-Axon Hillock- where action potential is generated.
The AP at the axon terminal allows the opening of
the voltage-gated Ca++ channels which causes an
influx of Ca++

9.

The AP travels from the sarcolemma towards the Ttubules

From the T-tubules, the AP reaches the Ca++ channel
DHPR ( Dihydropyridine Receptor) and activates the
RYR (Ryanodine Receptor) which releases Ca++ from
the terminal cisternae of the Sarcoplasmic Reticulum
(SR) into the myoplasm

T-tubules are extensions/invaginations of the

Sarcolemma that extends into the muscle fiber,
forming a close association with the two terminal
cisternae of the SR
This association of the T-tubule with the terminal
cisternae is called a triad
The T-tubule and the terminal cisternae are
connected by bridging proteins called feet
These feet are the RYR through which the Ca++ is
released in response to an AP
At the T-tubule membrane, the RYR interacts with
the DHPR which is an L-type voltage gated Ca++
channel with five subunits

Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

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1.02 PHYSIOLOGY
Muscle Physiology
Dr. MUNARRIZ |

10.

11.
12.
13.

14.

15.

One of the subunits of the DHPR appears to

be critical for the ability of the AP in the T-tubule to
induce release of the Ca++ from the SR
However, influx of Ca++ into the cell through the
DHPR is not needed for the initiation of Ca++ release
from the SR
Instead, release of the Ca++ from the terminal
cisternae of the SR is thought to result from a
conformational change in the DHPR as the AP passes
down the T-tubule
This conformational change, by means of a proteinprotein interaction, opens the RYR (like a mechanical
opening of a door) and releases the Ca++ into the
myoplasm
When the Ca++ is released, it binds to Troponin C
which promotes the lateral movement of the
Troponin-Tropomyosin complex, exposing the
myosin-binding site on the actin filament
Immediately, myosin heads bind to the sites on the
actin filament and contraction happens
The Ca++ that was previously bound to Troponin C is
reabsorbed by the tubules of the SR
The reabsorption of the Ca++ causes the
Tropomyosin to cover again the binding sites,
releasing the interaction of the myosin head and the
actin filament
Ca++ uptake in to the SR (Ca++ ATPase) is due to the
action of SERCA (Sarcoplasmic Endoplasmic
Reticulum Calcium ATPase)
From the tubules of the SR, the Ca++ is brought back
to the terminal cisternae where it is stored
Calsequestrin is a low affinity Ca++ binding
protein that helps accumulate Ca++ in the
terminal cisternae

ECF Ca++: 10-3 mol/L

ICF Ca++: 10-8 mol/L resting; 10-5 mol/L contracted
Ca++ is more concentrated in the ECF
Cross-Bridge Cycle

a.
b.
c.

d.

In the relaxed state, ATP is partially hydroyzed by

Myosin
In the presence of elevated myoplasmic Ca++,
myosin binds to actin
Myosin releases ADP and phosphate ion. Hydrolysis
of ATP is completed and causes a conformational
change in the myosin molecule that pulls the actin
filament toward the center of the sarcomere
(powerstroke) and contraction occurs.
A new ATP binds to myosin and causes release of
cross-bridge. Partial hydrolysis of the newly bound
ATP recocks the myosin head, returning to the
resting state. Myosin head is now ready to bind
again and again.

The cycle continues until the SERCA pumps back Ca++ into
the SR. As Ca++ concentration falls, Ca++ dissociates from
Troponin C, and the troponin-tropomyosin complex moves
and blocks the myosin binding site on the actin filament. If
myoplasmic Ca++ is still elevated, the cycle repeats, if
myoplasmic Ca++ is low, relaxation occurs.
Roles of ATP
Cross Bridge Cycling: 1 Cross bridge = 1 ATP
ATP causes both contraction (indirectly) and
relaxation (directly)
Decreased production of ATP ->Rigor Mortis at
death; In living persons, delayed contraction and
relaxation
Mechanisms that Prolong Contraction
Factors that prolong cytosolic Ca++
a. Increased frequency of AP
b. Defective Na+ inactivation: continued Na+ influx
->muscle membrane will be depolarized
->conformational change in DHPR leading to RYR
activation ->hyperkalemic periodic paralysis
c. Defective Ca++ RYR: continued Ca++ release
->Malignant Hyperthermia
Mechanisms for Relaxation:
Relaxation occurs by decreasing the
cytosolic/intracellular Ca++ or by detaching the myosin head
to actin.
1. Via SERCA (sarcoplasmic endoplasmic reticulum
calcium ATPase):
Ca++ resequestered to SR due to Ca++ ATPase, an
active pump
SERCA is the most abundant protein in the SR of
skeletal muscles
Transports 2 Ca++ for each hydrolyzed ATP
2. Decreasing the action potentials
Decreases DHPR and RYR Decreased cytosolic
Ca++
3. Myosin ATPase

Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

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1.02 PHYSIOLOGY
Muscle Physiology
Dr. MUNARRIZ |

Attachment of ATP to the myosin head

detachment of myosin head to actin eventually
relaxes muscles
Phases of the Muscle Twitch
1. Latent phase
As action potential reaches sarcolemma and down
the T-tubules and starts the excitation-contraction
coupling
2 ms
2. Contraction phase
Cross-bridge formation (Actin-myosin interaction)
Includes isometric and isotonic phases of
contraction
Maximum tension (TM) depends on the number of
muscle fibers that are recruited during the
contraction
15 ms
3. Relaxation phase
Ca++ reuptake decreased tension in the
sarcomere
25 ms
Phases of Contraction
1. Isometric Phase
No isotonic phase of contraction
No change in muscle length.
Tension
TM is reached at end of the isometric phase of
contraction, and is maintained thereafter;
Load (TL) TM, the muscle does not shorten and
the load is not moved; there is simultaneous
contractions (co-contraction) of agonist and
antagonist muscles
TL <TM (-) shortening but (+) movement of load
TL =TM (-) shortening and movement of load
2. Isotonic Phase
Isometric phase + isotonic phase
(+) change in muscle length (most of the time,
shortens)
Concentric contraction: shortening of the muscle
during contraction
Eccentric contraction: lengthening of the muscle
during contraction
Tension
TM is reached at end of the isometric phase of
contraction, or during the isotonic phase
When TL TM, the muscle shortens and the load is
moved
TL > TM (+) LENGTHENING and movement of
load
TL =TM (-) shortening and movement of load
Muscle Tension

Tension refers to the interaction of actin and myosin.

1. Active tension
Generated when the opposing actin filament is
almost equal to myosin filament exerted during
the cross-bridge formation.
How to increase the active tension?
Spatial summation: increase number of crossbridges (length of actin-myosin overlap)
Temporal summation: increase number of
action potentials by increasing UMN LMN
sarcolemma stimulation (frequency of stimulus)
2. Passive tension
Tension between connective tissues or cell elements
Lo (optimal length), which is between 2.0 2.2 m in
both skeletal and cardiac muscle, and 90 110% of the
original muscle length.
Lo = start of passive tension (refer to the picture
below)
Change in passive tension is directly proportional to
muscle length
Usually the tension measured before muscle
contraction.
Refer to the picture below:

Clinical importance of providing passive tension after an

extensive exercise (i.e. cool-down/stretching) Allows
muscle to go back to its LO Increasing efficiency of muscle
length and avoids muscle pain induced after the exercise
(delayed-onset muscle soreness/DOMS)
Relationships between
MUSCLE TENSION AND MUSCLE LENGTH
LO = 2.0 - 2.2 m for skeletal and cardiac muscles
Active tension: As stress increases, muscle length also
increases up to LO. Beyond this point, contractile force
(stress) decreases.

Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

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1.02 PHYSIOLOGY
Muscle Physiology
Dr. MUNARRIZ |

Passive tension: When muscle is at rest,

stretching of the muscle length initially increases stress
slowly, and then more rapidly as the extent of stretch
increases.

Length-Tension Relationship

Optimal length of sarcomere prior to

contraction = 2.0 2.2 m

The Third Law of Newton: When a mass exerts a

force on another mass, the second mass
simultaneously exerts a force equal in magnitude but
opposite in direction to that of the first mass.
PASSIVE Tension
When all the muscle fibers in the muscle bundle have

been recruited
to carry the load the tension
PHYSIOEX experiments.
At 2.2
there is the beginnings
of passive
generated
by that muscle bundle is maximal (see point
tension (0.2 g).
B of the power-stress curve)
Yellow-box region: isotonic concentric contraction
If you dont stretch your muscles
Green-box
region:
isotonic eccentric contraction
prior to exercising
them, and you
do
prolonged exercises,
willC:
you
cause
Point
isometric
contraction (no change in muscle
[
contractures, or length)
[
power?

initial length
# cross-bridges tension in fibers
MUSCLE TENSION AND FREQUENCY OF STIMULATION
Dependent on motor unit activity.
Summation of muscle contractions
Spatial summation
o cross-bridges of muscle fibers or increasing the
tension twice as its original load
Temporal summation (Tetanus)
o number of action potentials or frequency of
stimulation
o Results to prolonged cytosolic Ca++ increased
number of cross-bridges increased active
tension

MUSCLE TENSION AND VELOCITY OF SHORTENING or

LENGTHENING

Poin
t

Load

Tension

Velocity of
shortening
/lengtheni
ng

No load

Submaxim
al

Maximal

Submaxim
al

Submaxim
al

Submaxima
l

Maximal

Maximal

Zero

Max. to
decreasin
g

**Increasin
g from
point
C/isometric
phase
(doesnt

Supramax.

Increasing the load will increase the cross-bridges:

Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

Other
notes:
No power
since no
distance
was
covered
Max
power
No power
since work
velocity is
zero;
Maximum
tension
Velocity of
lengtheni
ng

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1.02 PHYSIOLOGY
Muscle Physiology
Dr. MUNARRIZ |

mean that
eccentric
contractio
n is faster
than
concentric)

Recruited later as more and more force is needed

since these fibers are large and more difficult to
excite.
For high-intensity activity that entails great power.

Muscle Fiber Types

Recruitment of muscle fibers (accdg. to Size Principle of
Recruitment):
Simultaneous activation of muscle fibers done to
increase force of contraction
Muscle fibers with lower thresholds are stimulated
first
Weak stimulus: activates neurons with low
threshold (small motor units at the level of UMN)
Strong stimulus: activates neurons with high
threshold

Summary of basic classification of skeletal muscle fiber types

Types of fibers:
1. Type I (Slow-oxidative fibers)
Slow twitch
Uses aerobic respiration (consumes oxygen,
glucose, fatty acids, and lastly the 30-32 ATPs)
Less fatigable; hence, good for prolonged activities
Recruited first than fast-twitch fibers since these
fibers are small and are easily excited.
For mild-moderate intensity activities that
requires control and endurance
2. Type II (Fast twitch)
May be Type IIa (Fast-oxidative) or Type IIb (Fastglycolytic focus)
Type IIa (intermediate): uses aerobic respiration
(consumes oxygen, glucose, fatty acids, and lastly
the 30-32 ATPs)
Type IIb: uses anaerobic respiration (ADP and
creatine phosphate/CrP)
More fatigable

Muscle Tone
Muscle tone refers to the tautness of a muscle, even
at rest.
Mechanisms for Muscle Tone:
At rest, type II afferents (sensory nerves at the
muscle spindle) tonically send afferent
proprioceptive impulses towards the spinal cord
where they synapse with the lower motor
neurons (LMN).
1. The alpha MN synapses with the extrafusal
muscle fibers, while the gamma MN synapses
with the intrafusal muscle fibers, or the
muscle spindles.

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1.02 PHYSIOLOGY
Muscle Physiology
Dr. MUNARRIZ |

2. The afferents synapse monosynaptically with

the alpha MN, and polysynaptically with the
gamma MN.
*More on this concept, in the Study Guide on the
Autonomic Nervous System, where the myotatic
/ stretch reflexes will be discussed.
Muscles are arranged in antagonist pairs and
groups. As one muscle exerts a little contraction
in response to the impulses passing thru the
reflex arc, it stretches its antagonists, causing
them to send proprioceptive sensory information
back to the spinal cord. Thus, a normal state of
involuntarily controlled contractions of various
skeletal muscle fibers in different muscle groups
occurs, which keeps all individual muscles in a
state of partial contraction, and ready to
contraction more forcefully if voluntary
commands are received from the cortical motor
areas.
Muscle Fatigue
Prolonged and strong contraction of a muscle
inability of the contractile and metabolic processes
of the muscle fibers to continue supplying the same
work output FATIGUE!
Mechanisms of (peripheral) muscle fatigue:
Failure of nerve impulses to release enough ACh
Depletion of ATP, glycogen, creatine PO4
Build-up of ADP inhibits CB cycling
Depletion of ICF K+ or accumulation of ECF K+
Release of Ca++ ions from SR
protons ( pH) changes protein conformation

CARDIAC MUSCLES

Cardiac muscle is STRIATED and INVOLUNTARY.

Some cardiac fibers are connected by intercalated
disks.
Cardiac muscle is capable of self-excitation.
FASCIA ADHERENS and DESMOSOMES provide
mechanical connection.
GAP JUNCTIONS in between cells provide electrical
connection.

1. Excitation of cardiac muscle results from:

a. Primarily by:
i. Pacemaker potentials
ii. Electrical coupling, or depolarization via gap junctions
-these will result in depolarization of the cardiac
muscle, and activate the DHPR. In contrast to the skeletal
muscle wherein DHPR mechanically changes the RYR to
release Ca++ from the SR, activation of the DHPR in cardiac
muscle fibers result in a small flux of Ca++ into the
sarcoplasm -> small increase in cytosolic Ca++ will open the

RYR channels (Ca++-induced Ca++ release from SR) -> large

increase in cytosolic Ca++ -> cardiac muscle contraction.
b. Modulation by:
-neuromuscular transmission, via autonomic nerves release
of neurotransmitters.
2.Action Potential
a. Fast Response (happens in the atrial and ventricular
cardiac cells and in the Purkinje fibers)
Phase 0: Rapid Na+ influx caused reversal of polarity from (-)
to (+) depolarization.
Phase 1: K+ efflux causes an EARLY REPOLARIZATION.
Phase 2: Ca++ influx maintains impulse (plateau)
Phase 3: continuous K+ efflux makes the cells polarity
become more (-) than the previous (+) it was (repolarization).
Phase 4: Resting state achieved.
b.Slow Response (happens in the sinoatrial node and
atrioventricular node via cardiac conduction system)
Why does the duration of the action potential make tetanic
contractions impossible in cardiac muscle fibers?
Cardiac muscle and skeletal muscle differ, however, in the
level of intracellular [Ca++] attained after an action potential
and hence in the number of actin-myosin interactions are high
after an action potential. In cardiac muscle, the rise in
intracellular Ca++ can be regulated, which affords the heart an
important means of modulating the force of contraction
without recruitment of more muscle cells or undergoing
tetany. Recall that in the heart all the muscle cells are activated
during a contraction, so recruiting more muscle cells is not an
option. Moreover, tetany of cardiac muscle cells would
prevent any pumping action and thus be fatal. Consequently,
the heart relies on different means of increasing the force of
contraction, including varying the amplitude of the
intracellular Ca++ transient.
3.Contraction Events
What are the mechanisms for the increase in cytosolic Ca++ in
cardiac muscle?
-influx through voltage-gated L-type Ca++ channel
-Ca++-induced Ca++ release (CICR) from the SR (DHPR -> Ca++
bind with RYR
-through -adrenergic agonists (activation of -receptors ->
activates adenylyl cyclase -> ^ cAMP -> phosphorylation -> ^
Ca++ in SR
4.Relaxation Events
ICF Ca++ through
-Ca-ATPase/ SERCA
-Ca-ATPase/ sarcolemma
-Ca++-Na+ antiporter (secondary active transport: 3Na in, 1Ca
out)

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1.02 PHYSIOLOGY
Muscle Physiology
Dr. MUNARRIZ |

5.Muscle Tension
^muscle tension, contraction force
^cytosolic Ca++ - by -agonists
^sensitivity of myofilaments to cytosolic Ca++ - ^ stretch by
^preload (Frank-Starling Mechanism)

ii & iii. Anything that ^afterload ->shortening of myocardial

fibers during systole -> systolic volume

*Phospholamban- protein which activates SERCA when there

is no epinephrine or -agonist present upon phosphorylation.
SERCA- involve in muscle relaxation.

10. Muscle Fiber Type of Cardiac Muscle: Slow-twitch muscle

fiber type

-1 agonists -> ^rate of contraction -> ^peak tension -> rate

of relaxation

There is only ONE PHYSIOLOGICAL MECHANISM for SkM,

SmM, CM hypertrophy: ^ AFTERLOAD.

11. Energy Sources of cardiac muscles:

Approximately 70-90% of energy is normally derived form
oxidative metabolism of fatty acids with abou 10-30% coming
from other nutrients, especially lactate and glucose.

6.Summation of muscle contractions:

Spatial & temporal summation: seen on individual CICR
events
SMOOTH MUSCLES
7. Isometric and isotonic phases of cardiac muscle
contractions
a. Isometric phase= isovolumic contractions; (-) muscle
shortening; T ~ ventricular pressure
b. Isotonic phase= occurs during ejection; muscle shortening
occurs here

Accdg. kay Doc, ang importanteng malaman ditto ay ang

contraction-relaxation mechanisms at yung iba ay hindi
masyado dahil sa discussion ng ANS pa ang mga yun.
Excitation of smooth muscle results from:
Pacemaker potentials
Electrical coupling, or depolarization via gap
junctions
Neuromuscular transmission, via autonomic nerves
release of neurotransmitters (further discussed in
the Study Guide and Lecture on the Autonomic
Nervous System)
Hormone activation of receptors
*Signal Transduction mechanisms will be further discussed in
the Study Guide for the Autonomic Nervous System.

9. Preload vs. Afterload of Cardiac Muscle

a. Preload= load on non-contracting ventricular or atrial
muscle
-filling of blood in ventricles during diastole
-PASSIVE TENSION
b. Afterload= load on contracting ventricular or atrial muscle.
-ACTIVE TENSION
i. What constitutes the afterload on atrial muscle? On
ventricular muscle?
Arterial pressure (will be increased by ^cross bridges ->
hypertrophy) , aortic impedance to blood flow, ventricular
volume
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1.02 PHYSIOLOGY
Muscle Physiology
Dr. MUNARRIZ |

Relaxation Events:
1. Dephosphorylation of light chains by myosin lightchain phosphatase (MLCP) to decrease intracellular
Ca++
2. Stress-relaxation phenomenon
Ability to return to nearly its original force of
contraction seconds/minutes after it has been
elongated or stretched.
3. Reverse stress-relaxation phenomenon
Ability to return to nearly its original force of
contraction seconds/minutes after it has been
shortened.
Relaxation Events:

Contraction Events
Calcium ions bind to calmodulin, instead of troponin
C.
MLCK phosphorylates the myosin light chains, and
energizes the myosin head to bind with the actin
filament (crossbridge).

1.

2.

Ligand action
NE, AII, and ET-1 alpha-receptor
stimulation of Gq PL-C PIP2 + IP3
increase Ca++
DHPR CICR
Not as prominent as in cardiac muscle

Must-know concepts (Summary):

I talked to Dra. Munarriz at sabi niya ay halos lahat ng nasa
table raw na ito ang lalabas sa exam. (Yanna)

Nuclei

DHPR and RYR

Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

SKELETAL

CARDIAC

SMOOTH

Multinucleated
;
Subsarcolemm
al (peripheral)

1-2 nuclei;
cytoplasmic
(central)

Single nucleus;
cytoplasmic
(central)

DHPR opens
channels of
RYR to release
Ca++ from SR

The DHPR (Ltype) contains

the Ca++
channel to
release Ca++

(-) DHPR and

RYR
Ca++ ions are
released
through the

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1.02 PHYSIOLOGY
Muscle Physiology
Dr. MUNARRIZ |

activation of IP3
receptor, the
RYR of striated
muscles
Regulatory
proteins for
muscle
contraction (for
Ca++ binding)
Ca++ Source (SR
or ECF, or
both?)

Troponin C

SR

Troponin C

Both
Action
potential
opens voltagegated Ca++

Events of
Contraction

Action
potential Ttubules
Ca++ from SR
inc. Ca++

Hormones and
transmitters
open IP3-gated
Ca++ in SR

Calmodulin

Both
(sometimes
with
mitochondria)
Influx of Ca++
during plateau
of action
potential ->
calmodulin
Activation of
MLCK
phosphorylates
regulatory MLC
Inc Ca++

Events of
Relaxation

Main Sources
of Energy
(glucose or
fatty acids, or
both?)
Motor neuron
(somatic or
autonomic, or
both?)
Neurotransmit
ters (for
cardiac,
smooth)

Signal
transduction
mechanisms
(for cardiac,
smooth)

Via SERCA,
decreasing
action
potentials, or
myosin ATPase

Reaccumulatio
n of Ca++ by SR
via Ca++
ATPase

Both

Fatty acids

Somatic

Autonomic

ACh

Epinephrine

cAMP for
adenyl cyclase
inhibitition (via
beta-2 and
alpha-2
receptors)

Mechanisms
that increase
ICF Ca++

Cross-bridging
StressRelaxation
mechanism,
Dephosphoryla
tion of light
chains by
myosin lightchain
phosphatase
(MLCP)

Mechanisms
that decrease
ICF Ca++

Mechanisms
or
Contraction
Force

Depolarization
of T-tubules to
activate DHPR
and RYR

Increase heart
rate;
Sympathetic
stimulation; (+)
of cardiac
glycosides

Reuptake of
Ca++ by the SR
Ca++
released from
troponin C
low crossbridge cycling

Parasympatheti
c stimutation
(Ach) via
muscarinic
receptors

Summation,
recruitment,
and preload
are varied to
varying force

Contractility
and preload
are varied to
varying force;
Changing
contractility
affects speed
of contraction

Ligand action;
and DHPR
activating CICR

Recruitment,
summation,
preload, and
contractility are
varied to
varying force.
Formation of
latch-bridges
reduces speed
of contractility.

Reminders:
For the First Long Quiz, 40 questions regarding muscle
physiology
15 questions about each specific concept (with
asterisk) in the table below
15 questions about the concepts outlined or
discussed above
10 questions for the specific differences between
skeletal, cardiac and smooth muscle

Legend: ^- increase
If you dont go after what you want, youll never have it. If
you dont ask, the answer is always no. If you dont step
forward, youre always in the same place. (Nora Robert

Autonomic
Several
neurotransmitt
ers depending
on the location
of muscle
*See picture of
smooth muscle
sig. trans.
cGMP for
smooth muscle
relaxation;
cAMP for
glycogen
synthesis

Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

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