Dr. Lo'ay al-hammad

1. Contraction of
Skeletal Muscle
Dr. loa’y Hammad
Oral & maxillofacial resident in RMS

2. Chapter 6 Outline
Skeletal Muscles structure
Mechanisms of Contraction
Characteristics of Muscle contraction
Muscle length & tension relation
Muscle load & velocity of contraction relation
Motor unit summation & Tetanization
Energetic of contraction & muscle fatigue
Adaptation of skeletal muscle to demands
Skeletal muscle pathology
12-2

3. Skeletal Muscles
12-3

4. Skeletal Muscles
 These muscles are called skeletal because they are attached to
the bones of the skeletal system
 Are attached to bone on each end by tendons
Insertion is the more movable attachment; is pulled toward
origin-the less moveable attachment
Contracting muscles cause tension on tendons which move
bones at a joint
Flexors decrease angle of joint
Extensors increase angle of joint
 Prime mover of any skeletal movement is agonist muscle
 Antagonistic muscles are muscles (flexors and extensors) that
act on the same joint to produce opposite actions
12-4

5. Skeletal Muscle Structure
 Fibrous connective
tissue from tendons
forms sheaths
(epimysium) that
extend around and
into skeletal muscle
 Inside the muscle
this connective
tissue divides
muscle into
columns called
fascicles
 Connective tissue
around fascicles is
called perimysium
12-5

6. *What is Epimysium?
-It is:
1.A fibrous connective tissue.
2. The most outer layer that covers the muscle fibers.
3. It's continuous with tendons where it becomes thicker.
4. It divides the muscle into columns or bundles called
fascicles and these fascicles are surrounded by Perimysium.

7.  Muscle fibers are muscle cells
Ensheathed by thin connective tissue layer called
endomysium
 Plasma membrane is called sarcolemma
 Muscle fibers are similar to other cells except are multinucleate
and striated
Skeletal Muscle Structure continued
12-6

8. Most distinctive feature of skeletal muscle is its
striations
Skeletal Muscle Structure continued
12-7

9. *summary:
→ TheEpimysiumsurroundstheentiremuscleand act asa
fascia, whilethePerimysiumsurroundsbundlesof muscle
fibers(fascicles) and theEndomysiumsurroundsthefibers
insidethebundle.

10. Structure of Muscle Fiber
 Each fiber is packed with myofibrils
Myofibrils are 1µ in diameter and extend length of fiber
Packed with myofilaments
 Myofilaments are composed of thick and thin filaments
that give rise to bands which underlie striations
12-16

11. *Thearrangement from outsidethemuscleto theinside:
ThewholeMuscle→ → musclebundles(fascicles) → → musclefibers
→ → myofibrils→ → Myofilaments

12. *Sarcolemma: it is thecell membraneof themusclefiber.
-Thesarcolemmaconsistsof atruecell membrane, called theplasma
membrane
-At each end of themusclefiber, thissurfacelayer of thesarcolemma
fuseswith atendon fiber, and thetendon fibersin turn collect into
bundlesto form themuscletendonsthat then insert into thebones

13. *Sarcoplasm.
-Themany myofibrilsof each musclefiber aresuspended sideby sidein the
musclefiber.
-Thespacesbetween themyofibrilsarefilled with intracellular fluid called
sarcoplasm
-Sarcoplasm iscontaining largequantitiesof potassium, magnesium, and
phosphate, plusmultipleprotein enzymes.
-Also present aretremendousnumbersof mito cho ndria that lie parallelto the
myofibrils. Thesesupply thecontracting myofibrilswith largeamountsof energy
in theform of adenosinetriphosphate(ATP) formed by themitochondria
*Sarcoplasmic Reticulum….. Located in thesarcoplasm surrounding the
myofibrilsof each musclefiber
-This reticulum has a specialo rganizatio n that isextremely important in
controlling musclecontraction

14.  A band is dark, contains
thick filaments (mostly
myosin)
Light area at center of
A band is H band
= area where actin
and myosin don’t
overlap
 I band is light, contains
thin filaments (only actin)
At center of I band
is Z line/disc where
actins attach
Structure of Myofibril
12-17

15. 12-18

16.  Are contractile units of skeletal muscle consisting of
components between 2 Z discs
 M lines are structural proteins that anchor myosin during
contraction
 Titin is elastic protein attaching myosin to Z disc that contributes
to elastic recoil of muscle
Sarcomeres
12-19

17. *Notes:
1-Myofilamentsarethefilamentsof Myofibril that constructed from thick (myosin)
and thin (actin) proteins, theseproteinsarethesourceof striation of theskeletal
muscles.
2-Myofibril arecomposed of repeating sectionsof sarcomeres

18. 3-Titin isoneof thelargest protein found in thehuman body; it isan elastic
protein that attachesmyosin to Z disk which contributeto elastic recoil of the
muscle.
4-when wetalk about myofilaments, weshould recall that wehave2 actin
filamentsand 1 myosin filament.
5-Each myofibril iscomposed
of about 1500 adjacent myosin
filamentsand 3000 actin
filaments, which arelarge
polymerized protein molecules
that areresponsiblefor the
actual musclecontraction

19. 6-When themusclefiber iscontracted, as
shown at thebottom of Figure6–4, thelength
of thesarcomereisabout 2 micrometers. At
thislength, theactin filamentscompletely
overlap themyosin filaments, and thetipsof the
actin filamentsarejust beginning to overlap one
another. Wewill seelater that, at thislength,
themuscleiscapableof
Generating itsgreatest forceof contraction.

20. Neuromuscular Junction
12-8

21. Neuromuscular Junction (NMJ)
 Includes the single synaptic ending of the motor neuron
innervating each muscle fiber and underlying specializations of
sarcolemma
12-9

22. Place on
sarcolemma
where NMJ
occurs is the
motor end
plate
Neuromuscular Junction (NMJ) continued
12-10

24. Motor Unit
12-11

25.  Each motor neuron
branches to innervate
a variable # of muscle
fibers
 A motor unit includes
each motor neuron
(coming from the
anterior horn of the
spinal cord) and all
fibers it innervates
Motor Unit
12-12

26. -MotorUnit…. Each motoneuron that leavesthespinal cord
innervatesmultiplemusclefibers, thenumber depending on thetype
of muscle.
*In general, small musclesthat react rapidly and whosecontrol must beexact
havemore nervefibersfor fewer musclefibers(for instance, asfew astwo or
threemusclefibersper motor unit in someof the laryngeal muscles).
*Conversely, largemusclesthat do not requirefinecontrol, such asthe soleus
muscle, may haveseveral hundred musclefibersin amotor unit
-Themusclefibersin each motor unit arenot all bunched together in themusclebut
overlap other motor unitsin microbundlesof 3 to 15 fibers.
-Thisinterdigitation allowstheseparatemotor unitsto contract in support of one
another rather than entirely asindividual segments.

27.  When a motor neuron is activated, all muscle fibers in its motor
unit contract
 Number of muscle fibers in motor unit varies according to
degree of fine control capability of the muscle…?!!
*Explanation: the muscles that act on the largest body masses (i.e. thigh muscle)
have motor units that contain more muscle fibers, whereas smaller muscles (i.e.
Extraocular Muscles) contain fewer muscle fibers in each motor unit.
Innervation ratio is # motor neurons : muscle fibers
Vary from 1:100 to 1:2000
Fine control occurs when motor units are small, i.e. 1 motor
neuron innervates small # of fibers
Motor Unit continued
12-13

28. Since individual motor units fire "all-or-none," how do
skeletal muscles perform smooth movements?
Recruitment is used:
Brain estimates number of motor units required
and stimulates them to contract
It keeps recruiting more units until desired
movement is accomplished in smooth fashion
More and larger motor units are activated to
produce greater strength
Motor Unit continued
12-14

29. Mechanisms of Contraction
12-15
How Fiber Contracts

30. Sliding Filament Theory of Contraction
Muscle contracts because myofibrils get shorter
Occurs because thin filaments slide over and
between thick filaments towards center
Shortening distance from Z disc to Z disc
12-21

31. Sliding Filament Theory of Contraction continued
 During contraction:
 A bands (containing actin)
move closer together, do
not shorten
 I bands shorten because
they define distance
between A bands of
successive sarcomeres
 H bands (containing
myosin) shorten
12-22

32. 12-23

33. *MolecularCharacteristics of the Contractile Filaments
1-Myosin Filament.
-Themyosin filament iscomposed
of multiplemyosin molecules,
Figure6–5Asho ws an individual
molecule; Figure6–5Bsho ws the
o rganizatio n of many moleculesto
form amyosin filament, aswell as
interaction of thisfilament on one
sidewith theendsof two actin
filaments
-Themyo sin mo lecule (see Figure 6– 5A)
is co mpo sed of six polypeptidechains—
two heavy chains and four light chains

34. -Thetwo heavy chainswrap spirally around
each other to form adoublehelix, which is
called thetail o f the myosin molecule.
-Oneend of each of thesechainsisfolded
bilaterally into aglobular polypeptide
structurecalled amyosin head. Thus,
there are two free heads at oneend of the
double-helix myosin molecule.
-Thefour light chainsarealso part of the
myosin head, two to each head. Theselight
chainshelp control thefunction of thehead
during musclecontraction
-Thetailsof themyosin moleculesbundled
together to form thebody of thefilament
shown in Figure(6–5B) while many heads o f
the moleculeshang outward to thesidesof the
body.

35. -part of thebody of each myosin
moleculehangsto thesidealong with the
head, thusproviding an armthat extends
thehead outward from thebody,
-Theprotruding armsand heads
together arecalled cross-bridges.
* Each cross-bridgeisflexibleat two
pointscalled hinges….onewherethe
arm leavesthebody of themyosin
filament, and theother wherethehead
attachesto thearm.

36. Cross Bridges
 Are formed by heads of myosin molecules that extend toward
and interact with actin
 Sliding of filaments is produced by actions of cross bridges
Each myosin head contains an ATP-binding site which
functions as an ATPase -enzyme
12-24

37. *ATPase Activity of the Myosin Head :
-This property allows the head of myosin to cleave ATP and to
use the energy derived from the ATP’s high-energy phosphate
bond to energize the contraction process

38. Cross Bridges continued
 Myosin can’t bind to actin unless it is “cocked” by ATP
After binding, myosin undergoes conformational change
(power stroke) which exerts force on actin
After power stroke myosin detaches
12-25

39. 12-26

40. 2-Actin Filament….The actin filament is also complex.
-It iscomposed of threeprotein components: actin, tropomyosin, and
troponin.
*MolecularCharacteristics of the Contractile
Filaments
*Tropomyosin Molecules:
-Thesemoleculesarewrapped
spirally around thesidesof theF-actin
helix.
- In theresting state, thetropomyosin
moleculeslieon top of theactivesites
of theactin strands, so that attraction
cannot occur between theactin and
myosin filamentsto causecontraction

41. *Troponin molecules:
-thesemoleculesareAttached intermittently along thesidesof the
tropomyosin molecules.
-Theseareactually complexesof threeloosely bound protein subunits, each
of which playsaspecific rolein controlling musclecontraction.
-Oneof thesubunits(troponin I) hasastrong affinity for actin
- another (troponin T) for tropomyosin
- and athird (troponin C) for calcium ions.
*Thiscomplex (troponin) isbelieved to attach thetropomyosin to theactin.
* Thestrong affinity of thetroponin for calcium ionsisbelieved to initiate
thecontraction process

42. Control of Contraction
 Control of cross bridge attachment to actin is via troponin-
tropomyosin system
Serves as a switch for muscle contraction and relaxation
The filament tropomyosin lies in grove between double row
of G-actins (that make up actin thin filament)
Troponin complex is attached to tropomyosin at intervals of
every 7 actins
12-27

43. Control of Contraction continued
 In relaxed muscle,
tropomyosin blocks
binding sites on actin so
crossbridges can’t occur
This occurs when Ca++
levels are low
 Contraction can occur
only when binding sites
are exposed
12-28

44. Role of Ca++
in Muscle Contraction
When Ca++
levels rise, Ca++
binds to troponin causing
conformational change which moves tropomyosin and
exposes binding sites
Allowing crossbridges and contraction to occur
Crossbridge cycles stop when Ca++
levels decrease
12-29

46. -When amusclecontracts, work isperformed and energy isrequired. Large
amountsof ATParecleaved to form ADPduring thecontraction process; the
greater theamount of work performed by themuscle, thegreater theamount of
ATPthat iscleaved, which iscalled theFenn effect.
*Thefollowing sequenceof eventsisbelieved to bethemeansby which this
occurs:
1. Beforecontraction begins, theheadsof thecrossbridgesbind with ATP. The
ATPaseactivity of themyosin head immediately cleavestheATPbut
leavesthecleavageproducts, ADPplusphosphate ion, bound to thehead. In this
state, theconformation of thehead issuch that it extendsperpendicularly toward
theactin filament but isnot yet attached to theactin.
2. When thetroponin-tropomyosin complex bindswith calcium ions, activesites
on theactin filament areuncovered, and themyosin headsthen bind
with these.

47. 3. The bond between the head of the cross-bridge and the active site of the
actin filament causes a conformational change in the head, prompting the
head to tilt toward the arm of the cross-bridge.
-This provides the power stroke for pulling the actin filament. The energy
that activates the power stroke is the energy already stored, like a
“cocked” spring, by the conformational change that occurred in the head when
the ATP molecule was cleaved earlier.
4. Once the head of the cross-bridge tilts, this allows release of the ADP and
phosphate ion that were previously attached to the head. At the site of
release of the ADP, a new molecule of ATP binds….. This binding of new ATP
causes detachment of the head of myosin from the actin.
5. After thehead hasdetached from theactin, thenew moleculeof ATP
iscleaved to begin thenext cycle, leading to anew power stroke.
-That istheenergy again “cocks” thehead back to itsperpendicular
condition, ready to begin thenew power strokecycle.

48. 6. When thecocked head (with itsstored energy derived from thecleaved ATP)
bindswith anew activesiteon theactin filament, it becomesun-cocked and
onceagain providesanew power stroke.
-Thus, theprocessproceedsagain and again until theactin filamentspull theZ
membraneup against theendsof themyosin filamentsor until theload on
themusclebecomestoo great for further pulling to occur

49. Interaction Between the“Activated” Actin Filament and the
Myosin Cross-Bridges—The“Walk-Along” Theory of
Contraction.
*onehypothesisfor which considerableevidenceexistsisthe “walk-along”
theory or “ratchet” theory of contraction.

50. Role of Ca++
in Muscle Contraction
 Ca++
levels decrease
because it is
continually pumped
back into the
sarcoplasmic
reticulum (SR - a
calcium reservoir in
muscle)
 Most Ca++
in SR is in
terminal cisternae
 Running along
terminal cisternae are
T tubules
12-30

51. Excitation-Contraction Coupling
 Skeletal muscle
sarcolemma is
excitable
Conducts Action
Potentials
 Release of ACh at
NMJ causes large
depolarizing end-plate
potentials and APs in
muscle
 APs race over
sarcolemma and
down into muscle via
T tubules
12-31

52. Excitation-Contraction Coupling continued
 T tubules are extensions
of sarcolemma
 Ca++
channels in SR are
mechanically linked to
channels in T tubules
 APs in T tubules cause
release of Ca++
from
cisternae via V-gated
and Ca++
release
channels
Called
electromechanical
release
channels are 10X
larger than V-gated
channels 12-32

54. 12-20
Neuromuscular Junction

55. *General Mechanism of Muscle Contraction (the whole
story)
-Theinitiation and execution of musclecontraction occur in thefollowing
sequential steps:
1. An action potential travelsalong amotor nerveto itsendingson muscle
fibers.
2. At each ending, thenervesecretesasmall amount of theneurotransmitter
substanceacetylcho line.
3. Theacetylcholineactson alocal areaof themusclefiber membraneto open
multiple“acetylcholine-gated” channels through protein moleculesfloating in
themembrane4. Opening of theacetylcholine-gated channelsallowslargequantitiesof sodium
ionsto diffuseto theinterior of themusclefiber membrane. Thisinitiatesan
action potential at themembrane.

56. 5. Theaction potential travelsalong themusclefiber membranein the
sameway that action potentialstravel along nervefiber membranes.
6. Theaction potential depolarizesthemusclemembrane, and much of the
action potential electricity flowsthrough thecenter of themusclefiber.
- Hereit causesthesarcoplasmic reticulum to releaselargequantitiesof
calcium ionsthat havebeen stored within thisreticulum.
7. Thecalcium ionsinitiate attractiveforcesbetween theactin and myosin
filaments, causing them to slidealongsideeach other, which isthecontractile
process.
8. After afraction of asecond, thecalcium ionsarepumped back into the
sarcoplasmic reticulum by aCa++ membranepump, and they remain stored
in thereticulum until anew muscleaction potential comesalong; this
removal of calcium ionsfrom themyofibrilscausesthemusclecontraction to
cease.

57. Excitation-Contraction Coupling continued
12-33

59. Muscle Relaxation
Ca++
from SR diffuses to troponin to initiate crossbridge
cycling and contraction
When APs cease, muscle relaxes
Because Ca++
channels close and Ca++
is pumped
back into Sarcolplamic Reticulum by Ca++-ATPase
pumps.
Therefore, ATP is needed for relaxation as well as
contraction!!!.
12-34

60. *Muscle length &tension relation:
(Effect of Amount of Actin and Myosin Filament Overlap on Tension)
Developed by the Contracting Muscle
-At point D on thediagram, theactin
filament haspulled all theway out to
theend of themyosin filament, with
no actin-myosin overlap. At this
point, thetension developed by the
activated muscleiszero.

61. -asthesarcomereshortensand the
actin filament beginsto overlap the
myosin filament, thetension
increasesprogressively until the
sarcomerelength decreasesto about
2.2 micrometers….. At thispoint,
theactin filament hasalready
overlapped all thecross-bridgesof
themyosin filament but hasnot
yet reached thecenter of themyosin
filament.
-With further shortening, thesarcomeremaintainsfull tension until point B is
reached, at asarcomerelength of about 2 micrometers. At thispoint, theendsof
thetwo actin filamentsbegin to overlap each other in addition to overlapping the
myosin filaments.

62. -Asthesarcomerelength fallsfrom 2 micrometersdown to about 1.65
micrometers, at point A, thestrength of contraction decreasesrapidly. At
thispoint, thetwo Z discsof thesarcomereabut theendsof themyosin
filaments
-ascontraction proceedsto still shorter
sarcomerelengths, theendsof the
myosin filamentsarecrumpled and, as
shown in thefigure, thestrength
of contraction approacheszero, but the
entiremusclehasnow contracted to its
shortest length

63. Effect of Muscle Length on Force of
Contraction in the Whole Intact Muscle.
*Thetop curveof Figure6–9 issimilar to
that in Figure6–8, but thecurvein Figure6–9
depictstension of theintact, wholemusclerather
than of asinglemusclefiber.
- Thewholemuscle hasalargeamount of
connectivetissuein it; also, thesarcomeres
in different partsof themuscledo not always
contract thesameamount. Therefore, thecurve
hassomewhat different dimensionsfrom those
shown for theindividual musclefiber, but it
exhibitsthesamegeneral form for theslopein
thenormal rangeo f co ntractio n,
asnoted in Figure6–9.

64. *Notein Figure6–9 that when themuscle
isat itsnormal resting length, which isat
asarcomerelength
of about 2 micrometers, it contractsupon
activation with theapproximate
maximum forceof contraction.
-However, theincreasein tension that
occursduring contraction, called active
tension, decreasesasthemuscleis
stretched beyond itsnormal length—that
is, to asarcomere length greater than
about 2.2 micrometers.
-Thisisdemonstrated by thedecreased
length of thearrow in thefigureat greater
than normal musclelength.

65. Relation of Velocity of Contraction to Load
*A skeletal musclecontractsextremely rapidly when it
contractsagainst no load—to astateof full contraction
in about 0.1 second for theaveragemuscle.
*When loadsare applied, thevelocity of contraction
becomesprogressively lessastheload increases, as
shown in Figure6–10. That is, when theload hasbeen
increased to equal themaximum forcethat themusclecan
exert, thevelocity of contraction becomeszero and no
contraction results, despiteactivation of themusclefiber.
*Thisdecreasing velocity of contraction with load is
caused by thefact that a load on acontracting muscle
isareverseforcethat opposesthecontractileforce
caused by musclecontraction. Therefore, thenet force
that isavailableto causevelocity of shortening is
correspondingly reduced.

66. *Energetics of Muscle Contraction
Work Output During Muscle Contraction
-When amusclecontractsagainst aload, it performs work.
-Thismeansthat energy istransferred from themuscleto theexternal load to
lift an object to agreater height or to overcomeresistanceto movement.
-In mathematical terms, work isdefined by thefollowing equation:
W = L * D
W: thework output
L :theload
D: thedistanceof movement against theload.
*NOTE: Theenergy required to perform thework isderived from the
chemical reactionsin themusclecellsduring contraction.

67. Sources of Energy forMuscle
Contraction
-musclecontraction dependson energy supplied by ATP.
*Most of thisenergy isrequired to actuatethewalk-along mechanism by
which thecross-bridgespull theactin filaments, but small amountsarerequired for:
(1) pumping calcium ionsfrom thesarcoplasm into thesarcoplasmic reticulum after the
contraction isover.
(2) Pumping sodium and potassium ionsthrough themusclefiber membraneto maintain
appropriateionic environment for propagation of musclefiber action potentials.
*Theconcentration of ATPin themusclefiber issufficient to maintain full contraction
for only 1 to 2 secondsat most.
-TheATPissplit to form ADP, which transfersenergy from theATPmolecule
to thecontracting machinery of themusclefiber. Then, theADPisre-phosphorylated
to form new ATPwithin another fraction of asecond, which allowsthemuscleto continue
itscontraction…… Thereareseveral sourcesof theenergy for thisre-phosphorylation.

68. 1) thesubstancephosphocreatine.
-It carriesahigh-energy phosphatebond similar to thebondsof ATP…. Thehigh-energy
phosphatebond of phosphocreatinehasaslightly higher amount of freeenergy than that of
each ATPbond Therefore, phosphocreatineisinstantly cleaved, and itsreleased energy
causesbonding of anew phosphateion to ADPto reconstitutetheATP.
- However, thetotal amount of phosphocreatinein themusclefiber isalso very little—
only about fivetimesasgreat astheATP. Therefore, thecombined energy of both the
stored ATPand thephosphocreatinein themuscleiscapableof causing maximal muscle
contraction for only 5 to 8 seconds!!!
2) Thesecond important sourceof energy, which isused to reconstituteboth ATPand
phosphocreatine, is“glycolysis” of glycogen previously stored in themusclecells.
- Rapid enzymatic breakdown of theglycogen to pyruvic acid and lactic acid liberatesenergy
that isused to convert ADPto ATP; theATPcan then beused directly to energizeadditional
musclecontraction and also to re-form thestoresof phosphocreatine.

69. AdvantagesVs. Disadvantagesof glycolysis
-Theimportanceof thisglycolysismechanism istwofold:
* First, theglycolytic reactionscan occur even in theabsenceof
oxygen, so that musclecontraction can besustained for many seconds
and sometimesup to morethan aminute, even when oxygen delivery
from theblood isnot available.
*Second, therateof formation of ATPby theglycolytic processis
about 2.5 timesasrapid asATPformation in responseto cellular
foodstuffsreacting with oxygen.
-However, so many end productsof glycolysisaccumulatein the
musclecellsthat glycolysisalso losesitscapability to sustain
maximum musclecontraction after about 1 minute.

70. 3) Oxidativemetabolism.
-Thismeanscombining oxygen with theend productsof glycolysisand with
variousother cellular foodstuffsto liberateATP.
-Morethan 95% of all energy used by themusclesfor sustained, long-term
contraction isderived from thissource.
-Thefoodstuffsthat areconsumed arecarbohydrates, fats, and protein. For
extremely long-term maximal muscleactivity—over aperiod of many hours—
by far thegreatest proportion of energy comesfrom fats, but for
periodsof 2 to 4 hours, asmuch asonehalf of theenergy can comefrom
stored carbohydrates.

71. Efficiency of Muscle Contraction.
- Theefficiency of an engineor amotor iscalculated asthepercentageof
energy input that isconverted into work instead of heat.
-Thepercentageof theinput energy to muscle(thechemical energy in nutrients)
that can beconverted into work, even under thebest conditions, islessthan 25% ,
with theremainder becoming heat.
-Thereason for thislow efficiency isthat about onehalf of theenergy
in foodstuffsislost during theformation of ATP, and even then, only 40 to 45 %
of theenergy in theATPitself can later beconverted into work.
-Maximum efficiency can be realized only when themusclecontractsat a moderate
velocity.
-If themusclecontractsslowly or without any movement, small amountsof maintenance
heat arereleased during contraction, even though littleor no work isperformed, thereby
decreasing theconversion efficiency to aslittleaszero.

72. -Conversely, if contraction istoo rapid, largeproportionsof theenergy are
used to overcomeviscousfriction within themuscleitself, and this, too,
reducestheefficiency of contraction.
*Ordinarily, maximum efficiency isdeveloped when thevelocity of
contraction isabout 30 % of maximum.

73. *Characteristics of Whole Muscle Contraction
-Many featuresof musclecontraction can bedemonstrated
by eliciting single muscle twitches. This can be accomplished by instantaneous
electrical excitation of thenerveto amuscleor by passing ashort electrical
stimulusthrough themuscleitself, giving riseto asingle, sudden contraction
lasting for afraction of asecond.
*Isometric Versus Isotonic Contraction.
-Musclecontraction issaid to be isometric when the muscle do es no t sho rten
during contraction and isotonic when it doesshorten but thetension on the
muscleremainsconstant throughout thecontraction.
-- Systemsfor recording thetwo typesof musclecontraction areshown in
Figure6–11.

74. *In theisometric system, themusclecontracts
against aforcetransducer without decreasing the
musclelength, asshown on theright in Figure6–11.
*In theisotonic system, themuscleshortensagainst
afixed load; thisisillustrated on theleft in the
figure, showing amusclelifting apan of weights.
-Thecharacteristicsof isotonic contraction depend
on theload against which the musclecontracts, as
well astheinertiaof theload.
-However, theisometric system recordsstrictly
changesin force of musclecontraction itself.
-Therefore, the isometric system is most often
used when comparing thefunctional characteristics
of different muscletypes.

75. *Characteristics of Isometric Twitches Recorded from
Different Muscles.
-Thehuman body hasmany sizesof skeletal muscles—from thevery small
stapediusmusclein themiddleear, measuring only afew millimeterslong and
amillimeter or so in diameter, up to thevery largequadricepsmuscle, ahalf
million timesaslargeasthestapedius.
Finally, theenergeticsof musclecontraction vary considerably from onemuscleto
another. Therefore, it isno wonder that themechanical characteristicsof muscle
contraction differ among muscles.
*Figure6–12 showsrecordsof isometric contractionsof threetypesof skeletal muscle:
1)an ocular muscle, which hasaduration of iso metric co ntractio n o f less than 1/40
second.
2) thegastrocnemiusmuscle, which hasaduration of contraction of about 1/15 second.
3) Thesoleusmuscle, which hasaduration of contraction of about 1/3 second.

76. -It isinteresting that thesedurationsof
contraction areadapted to thefunctions
of therespectivemuscles…
* Ocular movementsmust be
extremely rapid to maintain fixation of
theeyeson specific objectsto provide
accuracy of vision.
*Thegastrocnemiusmusclemust
contract moderately rapidly to provide
sufficient velocity of limb movement
for running and jumping.
* thesoleusmuscleisconcerned
principally with slow contraction for
continual, long-term support of the
body against gravity

77. Isotonic, Isometric, Eccentric, and
Concentric Contractions
During isotonic contraction, force remains constant
throughout shortening process, length changes
During isometric contraction, exerted force does not
cause load to move and length of fibers remains
constant
During eccentric contraction, load is greater than
exerted force and fibers lengthen despite its
contraction
During concentric contraction, muscle tension is
greater than the load and muscle shortens
12-40

78. - every muscleof thebody is
composed of amixtureof so-called
fast and slow muscle fibers, with still
other fibersgradated between these
two extremes.
-Themusclesthat react rapidly are
composed mainly of “fast” fibers
with only small
numbersof theslow variety.
- Conversely, themusclesthat
respond slowly but with prolonged
contraction are
composed mainly of “slow” fibers.
Fast Versus Slow Muscle Fibers.

79. *Characteristics of Fast muscle Fibers.
(1) Largefibersfor great strength of contraction.
(2) Extensivesarcoplasmic reticulum for rapid releaseof calcium ionsto
initiatecontraction.
(3) Largeamountsof glycolytic enzymesfor rapid releaseof energy by
theglycolytic process.
(4) Lessextensiveblood supply becauseoxidativemetabolism isof
secondary importance.
(5) Fewer mitochondria, also becauseoxidativemetabolism issecondary.

80. *characteristics of Slow muscle Fibers.
1 ) Smaller fibers.
(2) Also innervated by smaller nervefibers.
(3) Moreextensiveblood vessel system and capillariesto supply extraamountsof
oxygen.
(4) Greatly increased numbersof mitochondria, also to support high levelsof oxidative
metabolism.
(5) Fiberscontain largeamountsof myoglobin, an iron-containing
protein similar to hemoglobin in red blood cells.
-Myoglobin combineswith oxygen and storesit until needed; thisalso greatly speeds
oxygen transport to themitochondria.
-Themyoglobin givesthe slow muscleareddish appearanceand thename red muscle,
whereasadeficit of red myoglobin in fast musclegivesit thename white muscle.

81. Twitch, Summation, and Tetanus
 A single rapid contraction and relaxation of muscle fibers is a
twitch
 If 2nd stimulus occurs before muscle relaxes from 1st, the 2nd
twitch will be greater (summation)
 Contractions of varying strength (graded contractions) are
obtained by stimulation of varying numbers of fibers
12-36

82. *Muscle Contractions of Different Forces—Force Summation.
-Summation meanstheadding together of individual twitch contractionsto increasethe
intensity of overall musclecontraction.
-Summation occursin two ways:
(1) by increasing the number of motor unitscontracting simultaneously, which iscalled
multiplefiber summation.
(2) by increasing thefrequency of contraction, which iscalled frequency summation and
can lead to tetanization.
*Multiple Fibers Summation.
-When thecentral nervoussystem sendsaweak signal to contract amuscle, the
smaller motor unitsof themusclemay bestimulated in preferenceto thelarger motor
units. ….Then, asthestrength of thesignal increases, larger and larger motor
unitsbegin to beexcited aswell, with thelargest motor unitsoften having asmuch as50
timesthecontractileforceof thesmallest units. Thisiscalled the size principle.

83. *Frequency Summation and Tetanization.
Figure6–13 showstheprinciplesof frequency
summation and tetanization. To theleft aredisplayed
individual twitch contractionsoccurring oneafter
another at low frequency
of stimulation.
-Then, asthefrequency increases, therecomesa
point whereeach new contraction occurs
beforethepreceding oneisover. Asaresult, the
second contraction isadded partially to thefirst, so
that thetotal strength of contraction rises
progressively with increasing frequency.
-When thefrequency reachesacritical level, the
successivecontractionseventually
becomeso rapid that they fusetogether, and the
wholemusclecontraction appearsto becompletely
smooth and continuous, asshown in thefigure. This
iscalled tetanization.

84. Twitch, Summation, and Tetanus continued
 If muscle is stimulated by an increasing frequency of electrical
shocks, its tension will increase to a maximum (incomplete
tetanus)
 If frequency is so fast that no relaxation occurs, a smooth
sustained contraction results called complete tetanus or tetany
12-37

85. Twitch, Summation, and Tetanus continued
If muscle is repeatedly stimulated with maximum
voltage to produce individual twitches, successive
twitches get larger
This is Treppe or staircase effect
Caused by accumulation of intracellular Ca++
 increasing calcium ionsin thecytosol becauseof thereleaseof moreand
moreionsfrom thesarcoplasmic reticulum with each successivemuscle
action potential and failureof thesarcoplasm to recapturetheions
immediately.
12-38

86. Velocity of Contraction
For muscle to shorten it must generate force greater
than the load
The lighter the load the faster the contraction and vice
versa
12-39

87. *Muscle Fatigue.
-Prolonged and strong contraction of amuscleleadsto thewell-known stateof muscle
fatigue.
-Studiesin athleteshaveshown that musclefatigueincreasesin almost direct proportion to
therateof depletion of muscleglycogen.
- fatigueresultsmainly from inability of thecontractileand metabolic processesof the
musclefibersto continuesupplying thesamework output.
*However, experimentshave also shown other 2 causesof musclefatigue:
1-thetransmission of thenervesignal through theneuromuscular junction can diminish at
least asmall amount after intenseprolonged muscleactivity, thusfurther diminishing
musclecontraction.
2- Interruption of blood flow through acontracting muscleleadsto almost completemuscle
fatiguewithin 1 or 2 minutesbecauseof thelossof nutrient supply, especially lossof
oxygen.

88. *Remodeling of Muscle to Match Function
(adaptation of skeletal muscle to demands)
-All themusclesof thebody arecontinually being remodeled to match thefunctionsthat
arerequired of them.
-Their diameters arealtered, their lengths arealtered, their strengths arealtered, their
vascularsupplies arealtered, and even the types of muscle fibers arealtered at least
slightly
*Note: Thisremodeling processisoften quiterapid, within afew weeks!!!
1) Muscle Hypertrophy and Muscle Atrophy.
- musclehypertrophy :when the total massof amuscleincreases.
-muscleatrophy: When thetotal massof amuscledecreases.

89. -Virtually all musclehypertrophy resultsfrom an increasein thenumber of
actin and myosin filamentsin each musclefiber thisiscalled simply fiber
hypertrophy.
-Hypertrophy occursto amuch greater extent when themuscleisloaded during
thecontractileprocess.
-Only afew strong contractionseach day arerequired to causesignificant
hypertrophy within 6 to 10 weeks.
-In turn, someof themyofibrilsthemselveshavebeen observed to split within
hypertrophying muscleto form new myofibrils

90. -Along with theincreasing sizeof myofibrils, the enzymesystemsthat provide
energy also increase. Thisisespecially trueof the enzymes forglycolysis, allowing
rapid supply of energy during short-term forceful musclecontraction.
-When amuscleremainsunused for many weeks, therateof decay of thecontractile
proteinsismorerapid than therateof replacement. Therefore, muscle atrophy
occurs.
2)Adjustmentof MuscleLength.
-Another typeof hypertrophy occurswhen musclesarestretched to greater
than normal length.
-Thiscausesnew sarcomeresto beadded at theendsof themusclefibers,
wherethey attach to thetendons.
-Conversely, when amuscle continually remainsshortened to lessthan itsnormal
length, sarcomeresat theendsof themusclefiberscan actually disappear.
- It isby theseprocessesthat musclesarecontinually remodeled to havethe
appropriatelength for proper musclecontraction.

91. 3)Hyperplasia of Muscle Fibers.
-Under rareconditionsof extrememuscleforcegeneration, theactual
number of musclefibershasbeen observed to increase(but only by afew
percentagepoints).
- Thisincreasein fiber number iscalled fiberhyperplasia.
The lecture almost done be
patient plz !!!

92. *skeletal muscle pathology.
*muscles denervation:
-occursWhen amusclelosesitsnervesupply, it no longer receivesthe
contractilesignalsthat arerequired to maintain normal musclesize. Therefore,
atrophy beginsalmost immediately.
- After about 2 months, degenerativechangesalso begin to appear in the
musclefibersthemselves.

93. -If thenervesupply to themusclegrowsback rapidly, full return of function can
occur in aslittle as3 months, but from that timeonward, thecapability of functional
return
becomeslessand less, with no further return of function after 1 to 2 years.
-In thefinal stageof denervation atrophy, most of themusclefibersaredestroyed and
replaced by fibrousand fatty tissue.
-Thefibroustissuethat replacesthemusclefibersduring denervation atrophy also
hasatendency to continueshortening of musclefor many months, which iscalled
contracture.
-Therefore, oneof themost important problemsin thepracticeof physical therapy isto
keep atrophying musclesfrom developing debilitating and disfiguring
contractures.
-Thisisachieved by daily stretching of themusclesor useof appliancesthat keep the
musclesstretched during theatrophying process.

94. *poliomyelitis:
-Poliomyelitis often called polio or infantile paralysis, is
an infectiousdisease caused by the poliovirus.
-Approximately 90% to 95% of infectionscauseno
symptoms. Another 5 to 10% of peoplehaveminor symptoms
such as: fever, headache, vomiting, diarrhea, neck stiffnessand
painsin thearmsand legs….Thesepeopleareusually back to
normal within oneor two weeks.
-In about 0.5% of casesthereis muscleweakness resulting in
an inability to move….. Thiscan occur over afew hoursto few
days.
-
Theweaknessmost often involvesthelegsbut may less
commonly involvethemusclesof thehead, neck and diaphragm.
--Many but not all peoplefully recover. In thosewith muscle
weaknessabout 2% to 5% of children and 15% to 30% of adults
die.

95. *Recovery of Muscle Contraction in Poliomyelitis :
Development of MacromotorUnits.
-When somebut not all nervefibersto amusclearedestroyed, ascommonly
occursin poliomyelitis, theremaining nervefibersbranch off to form new axons
that then innervatemany of theparalyzed musclefibers.
-Thiscauseslargemotor unitscalled macromotorunits, which can contain as
many asfivetimesthenormal number of musclefibersfor each motoneuron
coming from thespinal cord.
-Thisdecreasesthefinenessof control onehasover themusclesbut doesallow the
musclesto regain varying degreesof strength.

96. *RigorMortis
-Several hoursafter death, all themusclesof thebody go into astateof
contracturecalled “ rigo r mo rtis” ; that is, themusclescontract and become
rigid, even without action potentials.
-Thisrigidity resultsfrom lossof all theATP, which isrequired to cause
separation of thecrossbridgesfrom theactin filamentsduring the
relaxation process.
-Themusclesremain in rigor until themuscleproteinsdeteriorateabout 15
to 25 hourslater, which presumably resultsfrom autolysiscaused by
enzymesreleased from lysosomes….. All theseeventsoccur morerapidly
at higher temperatures.