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Exercise Physiology

) 1 (
1
Gad El - Mawla A. Gad .
Professor of Physiology
COLLEGE OF APPLIED MEDICAL CIE!CE
"I!G A#D #!I$E%I&'
Introduction:
There are no normal stresses to which the body is exposed reaches the
stress of heavy exercise. If extremes of exercise are continued for slightly
prolonged time, they may be fatal. Sports physiology is a study of the
ultimate limits to which most of the body mechanisms can be stressed. To
give an example; in a person who has high fever, the body metabolism
increases to about 100 above normal. !y comparison, the metabolism of
the body during a marathon race increases "000 above normal. #e try to
understand the changes which occur in the muscles during and after exercise.
$lso we try to %now the effects of muscular exercise on different systems
and organs of the body. $nd lastly we study the role of muscular exercise on
health and welfare, as well as the role of muscular exercise in control and
treatment of diabetes, hypertension, and obesity.
Neuro-muscular junction
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The s%eletal muscle fibers are innervated by large myelinated nerve
fibers &$ alpha' that originate form the motor neurons located in either the
spinal cord or the brain stem. Since the number of fibers in the muscle
greatly exceeds the number of fibers in the motor nerve, each nerve fibers
branches many times and stimulates a variable number of muscle fibers.
Thus, a single motor neuron innervates many muscle fibers. $ motor neuron,
plus the muscle fibers supplied by it is called a motor unit. In the muscles
which perform fine and delicate movements &e.g. eye muscles' only a few
&less than 10' muscle fibers are supplied by one motor neuron, while in
muscles used for coarse movements &e.g. gastrocnemius muscle' many
muscle fibers &1000("000' are supplied by a single neuron.
Functional anatomy of the neuro-muscular junction:
)ear the surface of the muscle, the motor nerve fiber loses its myelin
sheath and divides into many branches, each branch forms a *unction with a
single muscle fiber. The terminal branches of the axon are covered only by the
cytoplasm and the cell membrane of the Schwann cells &the neurilemma' which
fuses with the muscle membrane &the sarcolemma'. The terminal part of the
axon lies in a shallow groove on the surface of the muscle fiber.
The axon terminal &persynaptic terminal' contains small vesicles that carry
acetylcholine which is the chemical transmitter at the neuromuscular
*unctions.The presynaptic terminals contain also a large number of
mitochondria. These provide the metabolic energy for the synthesis of
acetylcholine and also for the )a ( + pumping mechanism that are necessary for
the recovery process that follow the action potential.
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The terminal part of the axon is separated from the muscle plasma
membrane by a space %nown as the synaptic cleft.
The post(synaptic membrane is the plasma membrane of the muscle fiber
under the terminal part of the axon; it is called the motor end plate. The surface
area of this membrane is greatly increased by the presence of numerous folds of
this membrane called the *unctional folds. The post(synaptic membrane
contains the receptors for the chemical transmitter acetylcholine &cholinergic
receptors'. These receptors are complex protein molecules that have a double
functions. ,ach receptor has a binding site for acetylcholine and also acts as an
ion channel. )ormally, the receptor is not permeable to ions, but when
acetylcholine is attached to the binding sites, )a
-
and +
-
ions can pass through
the chemically activated channels according to their electrochemical gradients.
The membrane of the motor end plate contains also an en.yme called
cholinestrase. This en.yme is essential for brea%ing down the acetylcholine to
an inactive form once it has done its action.
Mechanism of neuro-muscular transmission:
#hen a nerve impulse in a motor neuron reaches the axon terminal, it
opens the voltage sensitive /a
--
channels, and thus allowing the /a
--
ions to
diffuse into the axon terminal. The increase in the intracellular /a
--
ion causes
the synaptic vesicles that contain acetylcholine to move towards the membrane,
fuse with it, and lastly to rupture and release their content into the synaptic cleft.
$cetylcholine diffuses across the cleft to the postsynaptic membrane &motor end
plate' where it combines with the specific binding sites on the receptor. #hen
the binding occurs, the membrane channels becomes permeable to both )a
-
and
+
-
ions at the same time. !ecause of the differences in electrochemical
gradients across the membrane, more )a
-
move in, than +
-
moves out,
producing a local depolari.ation of motor end plate %nown as the motor end
plate potential.
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Mechanism of neuro-muscular transmission
The end plate potential causes small local currents which depolari.e the
ad*acent muscle plasma membrane to the threshold level for generation of an
action potential. This action potential propagates on both sides of the motor end
plate to the whole length of the muscle fiber leading to its contraction. $fter
passage of the action potential, the muscle membrane repolari.es and returns to
its resting potential.
0nce, acetylcholine produces its action, it is rapidly hydroly.ed by the
cholinestrase en.yme into choline and acetic acid. /holine is actively ta%en up
by the presynaptic terminal, where it is utili.ed again in the formation of
acetylcholine which re(fills the vesicles. 1egradation of acetylcholine is
necessary to prevent it from causing multiple muscle contractions.
Pro(er)ies o* +e,ro--,sc,lar )ra+s-issio+.
1) One way (unidirectional) conduction:
)euromuscular transmission occurs only from the nerve to the muscle
and not in the opposite direction because the chemical transmitter
acetylcholine is present only in the terminal parts of the nerve fiber
& presynaptic terminals' and not in the muscle &postsynaptic membrane' and
there is a synaptic cleft in between them.
2) There is a delay in conduction:
,lectrical recording shows that, there is a delay of about 0.2 m.sec
between the nerve impulse reaching the neuromuscular *unction and the action
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potential generated in muscle. This delay is due to the time needed for the
release of acetylcholine from the presynaptic terminals, its diffusion across the
synaptic cleft and its combination with the receptors which open the channels
leading to diffusion of ions and depolari.ation of the motor end plate.
3)Neuro-muscular transmission readily shows fatigue:
3atigue is caused by rapid repeated stimulation of the motor nerve which
leads to depletion of the acetylcholine vesicles. 0" lac% facilitates the onset of
fatigue because it decreases the metabolic reactions needed to reform
acetylcholine.
) !ffect of drugs:
A. Drugs which stimulate neuro-muscular transmission
1. By direct action: Acetylcholine (exogenous):
It is not used clinically because it is rapidly destroyed by cholinestrase
en.yme. Methacholine, carbacol and nicotine, have the same effect of
acetylcholine but they are not destroyed by cholinestrase en.yme or are
destroyed very slowly. These drugs produce contraction of the muscles which
may persist for many minutes to several hours i.e. produce spasm.
2. By indirect action; anti-cholinestrases:
These drugs increase neuro(muscular transmission by inhibiting the
action of cholinestrase en.yme which normally destroys acetylcholine after
producing its action. Inhibition of cholinestrase en.yme leads to accumulation
of acetylcholine at the motor end plate which causes strong and prolonged
contraction of the muscle. $nti(cholinestrases are of two types4
a) Reversible: These drugs combine temporarily with cholinestrase
en.yme e.g. eserine &physostigmine' and prostigmine &neostigmine'. These
drugs are used in treatment of a disease %nown as myasthenia gravis.
b) Irreversible: These chemical substances combine strongly and
for a long time with cholinestrase en.yme e.g. di-isoprophyl
lurophosphate (!"#). It is a dangerous substance used in war &nerve
gas' which %ills by producing massive inhibition of the cholinestrase
en.yme. This leads to accumulation of acetylcholine causing
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persistent contraction &spasm' of all muscles including the respiratory
muscles. This causes asphyxia and death.
B) Drugs which block neuro-muscular transmission
1. Pre-synaptic block: by inhibiting the release of acetylcholine from the
pre(synaptic terminals. It is produced by4
$emicholiniums: this drug interferes with upta%e of choline and therefore
acetylcholine becomes depleted.
Botulinum toxin: It is an extremely deadly poison produced by bacteria
&clostridium botutinum' present in spoiled food. The toxin interferes with
synthesis or release of acetylcholine. 5oisoning with this toxin results in
muscle paralysis and death.
2. Post-synaptic block: by preventing the action of acetylcholine on the
motor end plate. It is produced by4
Competitive neuro-muscular blockers (e.g. curare) which combines
with the cholinergic receptors in the motor end plate preventing the action
of acetylcholine. $nticholinestrases &e.g. prostigmine' can overcome the
bloc%ing action of curare.
Depolarizing neuro-muscular blockers (e.g. succinylcholine) which
produces initial stimulation of the motor end plate due to depolari.ation,
then bloc%ing by maintaining this state of depolari.ation. So, it produces
initial muscular twitches followed by muscle relaxation.
)euro(muscular bloc%ers are used clinically to produce muscular
relaxation during surgical operation and to reduce movements during
electroconvulsion treatment of psychotic patients.
") !ffect of ions:
- Ca
++
ions help neuro( muscular transmission by causing rupture of the
acetylcholine vesicles. 1ecrease /a
--
ions near the axon terminal will
prevent the release of acetylcholine and therefore decreases transmission.
- Mg
++
ions inhibit neuro(muscular transmission by stabili.ing the
acetylcholine vesicles. ,xcess 6g
--
ions will prevent the release of
acetylcholine and therefore decreases transmission.
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- K
+
ions have anticurare action on the motor end plate.
M#CLE
6uscles are machines for converting stored chemical energy into
mechanical energy &wor%' and heat. 6uscles constitutes 20 of the body
weight &70 s%eletal muscles and 10 smooth muscles and cardiac muscle'.
There are three types of muscles; s%eletal muscles, smooth muscles and
cardiac muscle. They differ in structure &histologically' in location
&anatomically', in functions &physiologically' and in innervations
&neurologically'.
/ele)al -,scles &Somatic, voluntary or striated muscles'
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These muscles are usually attached to the s%eleton &s%eletal muscles'.
Their contraction moves the body &soma' or part of it &somatic muscles'.
/ontraction of these muscles is under voluntary control &voluntary muscles'.
These muscles appear striated under the microscope &striated muscles'.
Functions of the skeletal muscles:
1. They move the body as a whole or part of it e.g. one limb.
". They maintain the body posture by their tonic contraction and muscle tone.
8. 9eat production from s%eletal muscles represents about 20 of the
metabolic rate during rest and increased very much during muscular
exercise. The activity of s%eletal muscles play a very important role in the
control of body temperature.
Functional histology:
)early all s%eletal muscles are attached to bones by means of tendons. $
tendon is composed of dense, white, fibrous &inelastic' connective tissue fibers,
surrounded by loose connective tissue. The fibers of the tendon are fixed to
sarcolemma of the muscle fibers. The connective tissue around the tendon
continues around the muscle to from a sheath %nown as epimysium &epi :
above, my : muscle'. 3rom the outer sheath, connective tissue extends into the
muscle dividing it into fasiculi. ,ach fasiculus is surrounded by its own sheath
%nown as perimysium &peri : around'. The muscle fasiculus is composed of
many muscle fibers &myofibers' surrounded by connective tissue called
endomysium. The endomysium is continuous with the sarcolemma, which is a
thin sheath formed of glycoprotein.
The tight connection between the cell membranes and the surrounding
connective tissue structures ma%e the force developed by the muscle contraction
to be transmitted effectively to the tendons.
The muscle fiber myofiber):
S%eletal muscle is made up of thousands of muscle fibers. The muscle
fiber is the structural unit of the s%eletal muscle. It is an elongated,
multinucleated cell. The muscle fiber is about 10(100 m in diameter and vary
with the length of the muscle. In many muscles, the fibers run from one end to
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the other. 9owever, in other muscles &large muscles' the muscle fibers run
obli;uely and inserted in the connective tissue sheath which surrounds the
muscle.
The muscle fiber is surround by two membranes, the outer is called the
sarcolemma and the inner is the plasma membrane &true cell membrane'.
Tubular extensions of the sarcolemma called transverse tubules &T tubules'
extend deep into the muscle fiber &at the *unction of the $ and I bands'. The
lumen of the T tubules is continuous with the extracellular fluid around the
muscle fibers. The T tubules have the following functions.
1. They increase the surface area of the sarcolemma many folds.
". They help in movement of ions and other substances into and out of the cell.
8. They allow the depolari.ation wave to pass rapidly inside the muscle fiber to
activate deep myofibrils.
The muscle fiber &myofiber' consists of several hundred myofibrils &fibril
: little fiber' which are surrounded by a cytoplasm %nown as the sarcoplasm.
The sarcoplasm contains the usual cytoplasmic organelles; sarcosomes
&mitochondria', sarcoplasmic &endoplasmic' reticulum which extends between
the myofibrils, <olgi apparatus, ribosomes and glycogen granules. The
sarcosomes are located beneath the plasma membrane and also between and
parallel to the myofibrils.
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Sarcoplasmic reticulum and T tubules.
The sarcoplasmic reticulum is a networ% of anastomosing longitudinal
tubules which run parallel to the myofibrils. These longitudinal tubules extend
the length of the sarcomere and are closed at each end. The dilated ends of the
tubules are called the terminal cisternae. $ group of the T tubule and two
terminal cisternae on either sides is called a triad. The sarcoplasmic reticulum
has the following functions4
1.It helps in longitudinal distribution of fluids, ions and substances
synthesi.ed within the sarcoplasm or mitochondria.
".Terminal cisternae releases calcium ions during muscle contraction and
store it during muscle relaxation.
The myofibril:
The myofibrils are about 1 m in diameter and extend from one end of the
muscle fiber to the other giving the muscle fiber its longitudinal striation. The
myofibrils are divided into functional units called sarcomers &little muscles' by
transverse sheets of protein called = lines or discs.
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The muscle fiber contains myofibrils which are composed of sarcomeres
,ach myofibril is composed of filaments &myofilaments', thic% and thin
filaments formed of contractile proteins. The thic% filaments contain the
contractile protein myosin while the thin filaments contain the contractile
protein actin as well as two other proteins, troponin and tropomyosin.
The thic% and thin filaments are arranged in a special manner causing the
myofibrils to have alternate light and dar% bands. These bands give the s%eletal
muscle fiber its characteristic transverse striation under the light microscope.
The dar% bands are called $ bands &$nisotropic', where as the light bands are
called I bands &Isotropic'. = lines &discs' cross the center of each I band and
divide the myofibril into smaller units &sarcomeres; a sarcomere is the part of
the myofibril present between the " = discs'.
The thic% filaments are located in the middle of each sarcomere, producing
the dar% $ band. In contrast, each sarcomere contains two sets of thin filaments,
one at each end. 0ne end of each thin filament is attached to the = disc, where
the other end overlaps a part of the thic% filaments. The I band contains only the
thin filaments that do not overlap the thic% filaments. The = disc present in the
middle of the I band. The function of the = disc is to connect the ends of the
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thin filaments from one myofibril to another attaching the myofibrils to each
other across the muscle fiber.
The 9 .one is a relatively lighter .one in the center of the $ band where
the thic% and thin filaments do not overlap. It corresponds to the space between
the ends of the thin filaments. In the center of the 9 .one, there is a narrow dar%
line, %nown as the 6 line. It is produced by proteins that bind all the thic%
filaments in a sarcomere together. Thus, neither the thic% nor the thin filaments
are free floating, since the thin filaments are attached to the = disc and the thic%
filaments are lin%ed together by the 6 line.
The space between ad*acent thic% and thin filaments is bridged by
pro*ections %nown as cross(bridges. These are parts of myosin molecules that
extend from the surface of the thic% filaments towards the thin filaments. The
head of cross(bridges act as $T5ase and contain a binding site for actin and
another binding site for $T5. 1uring contraction, these cross(bridges ma%e
contact with the thin filaments and exert force on them.
!"citation contraction cou#ling: &mechanism of muscle contraction'4
It is the process by which an action potential initiates the muscle
contraction. ,xcitation contraction coupling involves the following steps4
$. %ro#agation of the action #otential an& release of 'a
((
ions:
5ropagation of the action potential in the motor nerve leads to production
of an end plate potential which results in generation of an action potential at the
ad*acent areas of the motor end plate. This action potential spreads on both
sides of the motor end plate and excites the whole muscle fiber. The action
potential spreads along the T tubules which extend deep into the muscle fiber
causing release of /a
--
ions from the terminal cisternae &calcium(filled sacs' of
the sarcoplasmic reticulum. The released /a
--
ions diffuse rapidly to the region
of the thic% and thin filaments.
). Bin&ing of the cross-bri&ges between the thick myosin) an& thin actin)
filaments:
Note: The thin filament is formed of two chains of actin molecules which wind
around each other. In each actin molecule there is a binding site for myosin.
These binding sites are covered by tropomyosin &a thin filament protein which
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coils around the actin chain'. The position of tropomyosin is controlled by
another protein %nown as troponin. The troponin molecule contains binding
sites for /a
--
ions &troponin /' and tropomyosin &traponin T'.
The action potential leads to release of /a
--
ions &first step' which
combine with traponin molecules. /ombination of /a
--
ions with traponin on
the thin filament causes the tropomyosin to move away from its bloc%ing
position and thus exposing the binding sites present on actin molecules. /ross
bridges from the thic% &myosin' filaments combine with the binding sites on the
actin.
N.B. 6yosin is a complex protein consisting of a head &the cross(bridge' and a
long tail
Action potential leads to release of a
!!
*. 'ross-bri&ge cycling which results in sli&ing of the thin filaments across the
thick myosin) filaments:
yclin" of cross-brid"es occurs by the followin" steps:
a. Binding: /ross(bridges on the thic% filament bind to actin.
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b.Bending: !inding of the cross bridges leads to release of energy stored in
myosin &$T5 by $T5ase' producing angular movement of the cross bridges
i.e. bending of the crossbridges and sliding of the thin filaments across the
thic% filaments.
c.Detachment: 1etachment of the cross(bridges from the thin filaments which
needs energy derived also from $T5.
d.Return to original position: The cross bridge returns to its original position
and another cycle can occur by binding to another actin molecule and so on.
/ross(bridge cycling occurs so long as /a
--
ions combine with troponin.
This leads to sliding of the thin filaments towards the center of the sarcomere
approximating the = lines &discs' from each other &the sarcomers become
shorter'. The width of the I bands decrease and the 9 .ones become narrower
but the width of the $ bands do not change.
ross-brid"e cyclin".
+. ,ela"ation occurs when 'a
((
ions are trans#orte& into the sarco#lasmic
reticulum by an acti-e #rocess using AT% an& 'a-AT%ase.
The active /a
--
pump is located in the membranes of the sarcoplasmic
reticulum. >emoval of /a
--
ions ma%es troponin to return to its original state
which causes trapomyosin to move bac% and cover the binding sites on actin.
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Thus, the cross bridge cycles stop causing the thin filaments to slide bac% again
to their original position and the sarcomere to return to their original length.
'hanges occurring as a result of muscle contraction:
.. !lectrical changes:
Initiation and conduction of action potentials in the s%eletal muscles are
similar to that produced in the nerve fibers except for ;uantitative differences in
timing and magnitude4
( >esting membrane potential in the s%eletal muscle fibers is ?@0 m.v &in
the nerve fibers ?A0 m.v'.
( In the s%eletal muscles, the firing level is reached at (20 m.v. i.e. after 70
m.v. depolari.ation &in the nerve it is at (22 m.v. i.e. after 12 m.v.
depolari.ation'.
( The magnitude of the spi%e potential in the s%eletal muscles is 180 m.v. ,
from ?@0 m.v. to -70 m.v. &in the thic% myelinated nerve fibers it is 102
m.v., from ?A0 m.v. to - 82 m.v.'.
( 1uration of the action potential in the s%eletal muscles is 8(2 m. sec &in
the thic% myelinated nerve fibers 0.2 ? 1 m.sec'.
( The duration of the negative and positive after potentials are relatively
longer in s%eletal muscles than in nerve fibers.
( The velocity of conduction of the action potential on the surface of the
muscle fibers is 8(2 metersBsec &in the thic% myelinated nerve fibers it
reaches up to 1"0 metBsec'.
... !"citability changes:
The excitability changes which occur in the muscle are identical to those
which occur in the nerve. Thus, once the action potential is produced in the
muscle, the excitability passes in the following phases4 $bsolute refractory
period, relative refractory period, supernormal phase of excitability, subnormal
phase of excitability.
.... Metabolic chemical) changes:
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A) !uring contraction: ,nergy of contraction is derived from $T5 which is
considered the immediate and only source of energy in this process. The head of
myosin &cross bridges' contain $T5ase en.yme which catalyses the hydrolysis
of $T5. ATP ADP + P (phosphoric acid) + Energy.
Metabolic reaction durin" contraction.
$T5 is rapidly reformed from $15 by the addition of phosphate group
from creatine phosphate &/r~5' &a high energy phosphate compound'. $T5 and
/r~5 represent the stored energy which can be utili.ed rapidly by the muscle.
The high energy phosphate storage in the muscle is sufficient to allow the
muscle to contract only 20(100 times.
To maintain muscle contraction, a steady supply of energy is derived from
the following sources4
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C Anaerobic o#idation of "lucose $or muscle "lyco"en%:
Glucose ( ms glycogen )
s' &<lycolysi
oxidation $naerobic
2 Pyruvic. Acids + 2ATP
1uring sever exercise, when the muscle is doing wor% at faster rate than
the blood can supply 0
"
and nutrients, the muscle depends on local glycogen
stores and anaerobic glycolysis to meet its energy re;uirements. The pyruvic
acid produced is converted into lactic acid which diffuses out of the muscle and
accumulate in the blood.
The advantage of anaerobic glycolysis is that it is able to supply $T5 at a
high rate and within a short time.
The disadvantage of anaerobic glycolysis is that it provides only small
amounts of high energy phosphate & " $T5 molecules from each molecule of
glucose'. So, anaerobic glycolysis is rapid but not economic.
C Aerobic o#idation of "lucose and free acids:
BI. Glucose + !
2

cycle' s &+rebD
oxidation $erobic
"!
2
+ #
"
! + $%ATP
&ree 'a((y acids + !
2

oxidation $erobic
"!
2
+ #
2
! + ATP
$t low or moderate levels of activity, $T5 is produced by the aerobic
oxidation of blood glucose or free fatty acids &carried by the blood from the
adipose tissues'. $erobic oxidation of glucose or fatty acid produces great
amount of high energy phosphate &8E $T5 for each molecule of glucose', but
the process is relatively slow.
6ost muscles contain a mixture of cells, some adapted to use anaerobic
glycolysis which can supply $T5 very rapidly &but not economic', and others
adapted to use aerobic metabolism &economic' which is relatively delayed.
C In exhausted muscles, there is an emergency mechanism for the supply of
$T5. This is done by combining two $15 molecules to reform one $T5
molecule and one $65 &$denosine 6ono(phosphate' molecule.
ADP + ADP ATP + A)P
B) !uring reco%ery:
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$t the end of muscular activity, the energy stores in the muscle &$T5, /r(5
and muscle glycogen' are depleted and lactic acid is increased in blood.
>ecovery occurs by removal of lactic acid and regeneration of the energy
stores.
a' 5art of the lactic acid is oxidi.ed into /0
"
and 9
"
0. The energy produced
from this oxidation is used for reformation of $T5 and by turn /r(5.
*ac(ic acid
0xidation
Pyruvic acid "!
2
+ #
2
! + ATP
ATP - crea(ine "r+P - ADP
b' The other part of the lactic acid diffuses to the blood stream and then to the
liver where it is converted into blood glucose &through the /ori cycle which
is the reverse of glycolysis'. 6uscles ta%e glucose from the blood stream and
changes it into muscle glycogen.
$t the end of recovery the energy stores in the muscle &$T5, /r~5 and
muscle glycogen' are reformed again, and the lactic acid is removed.
Metabolic reactions durin" reco&ery
./. Thermal changes:
1uring contraction, the heat production in the muscle is mar%edly
increased &about 100(1000 times' compared with the heat production during
rest. 1uring contraction, 70(20 of the energy liberated as a result of
hydrolysis of $T5 is converted into wor%. The remaining 20(F0 of the energy
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is liberated as heat at the onset of and during contraction of the muscle. The
heat production from the muscle during contraction occurs in two phases4
A) Initial eat! which includes4
1. Activation heat:
It is a very rapid heat production which starts before any shortening has
occurred. It results from release of /a
--
from the terminal cisternae, binding of
/a
--
to troponin protein, movements of cross(bridges towards the binding sites
on the thin filaments, and active reupta%e of /a
--
by the sarcoplasmic
reticulum which re;uires $T5 and starts immediately after /a
--
release.
2. Shortening heat:
The heat production during isotonic contraction &the muscle shorten' is
greater than the heat production during isometric contraction &contraction
without shortening'. The difference represents the heat produced by the
process of shortening &cross(bridge cycling'. Shortening heat is proportional
to the degree of shortening.
3. Work heat:
If the muscle performs wor%, additional heat is liberated which is
proportional to the wor% done.
") Dela#e$ (recover#) eat!
It is the heat liberated from the muscle after its relaxation. 1elayed heat
results from the metabolic reactions needed to reform the energy stores in the
muscle &$T5, /r(5 and muscle glycogen' and to remove lactic acid. 1elayed
heat is nearly e;uals to the initial heat, and it continues for about 80 minutes
after the end of muscle contraction.
/. Mechanical changes:
There are two types of muscle contraction:
1. Isotonic (same tension) contraction:
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This type of contraction occurs when the muscle contracts against a light
or moderate load. This contraction leads to shortening of the muscle and
movement of the load. Thus a wor% is done &wor% : weight of the load x
distance of movement'. In this type of contraction, the mechanical efficiency of
the muscle &percentage ratio of the wor% done to the total energy expenditure' is
maximum &70(20'. The tension inside the muscle increases at first, then
maintained constant during the ma*or part of contraction &isotonic'
Force velocity relationship:
#hen the muscle contracts isotonically &against a movable load', the
velocity of shortening is inversely proportional to the weight of the load. If the
muscle is unloaded, it shortens with maximum velocity. $s the weight of the
load increases, the velocity of shortening decreases. #hen the load reaches a
maximum, the muscle contracts without shortening i.e. contracts isometrically.
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'orce &elocity relationship
2. Isometric (same length) contraction:
This type of contraction occurs when the muscle contacts against a heavy
load. The muscle does not shorten i.e. contracts without change in length
&isometric', and the load does not move. So, no wor% is done and the
mechanical efficiency is .ero i.e. all the energy is converted to waste heat. The
tension inside the muscle is mar%edly increased .
(sotonic and isometric contraction
Mechanism of isometric contraction:
The muscle is supposed to be composed of " components, a contractile
components &sarcomers' and elastic components; one in series with the
contractile components, and a second elastic element in parallel with the two
components. The parallel elastic element present in the sarcolemma and the
series elastic element may be present in the tendon, connective tissues or in the
corssbridges &in the hinge regions of the myosin'.
#hen the muscle contracts against a heavy load &isometric contraction',
the contractile components shorten, in the same time the elastic components are
stretched to the same degree. So, the length of the muscle remains constant, but
its tension is mar%edly increased.
N.B. The muscles in body can contract both isometrically and isotonically, but
most contractions are actually a mixture of the two. ,xample, during wal%ing or
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running, the muscles of the leg contract isometrically to %eep the limbs stiff
when the leg hits the ground and isotonically to move the limb.
Length tension relationship:
The tension developed during the isometric contraction depends on the
length of the muscle during experiments. $ maximum tension is obtained when
the length of the muscle is nearly e;uals to the resting length of the muscle in
the body &optimal length'. The tension decreases when the length of the muscle
is longer or shorter than the normal body length &optimal length' $t optimal
length &when the sarcomere length is ".0("." m' there is a maximum number
of cross bridges connecting the thic% and thin filaments. $t lengths longer or
shorter than the optimal length the degree of overlap between the thic% and thin
filaments decreases and the number of cross(bridge between the thic% and thin
filaments also decreased leading to decreased contraction i.e. decreased tension.
!ffects of stimulation of skeletal muscle by a single stimulus:
The response of the muscle depends on:
A) Intensity of the stimulus:
( Subminiml &subthreshold' stimuli4 are ineffective i.e. produce no
contraction.
( 6inimal &threshold' stimulus4 produces wea% contraction which results from
stimulation of the most excitable muscle fibers.
23
( Superminimal &superthreshold' stimuli4 produce contractions which increase
in magnitude according to the intensity of the superminimal stimulus. These
stimuli produce contraction of more muscle fibers.
( 6aximal stimulus produces maximal contraction because all muscle fibers
are stimulated.
( Supermaximal stimuli, produce no further increase in magnitude of
contraction.
Simple muscle twitch:
$ single maximum stimulus produces a single brief contraction followed by
relaxation %nown as simple muscle twitch. It consists of the following4
Simple muscle twitch
24
1. Latent period:
It is the time between stimulation of the nerve and beginning of
contraction.
2. Contraction phase:
1uring this phase, the muscle shorten and performs wor% &move the lever'.
3. Relaxation phase:
1uring this phase the muscle relaxes and returns to its original length.
B) Conditions of the muscle which affect the response:
(Factors affecting the simple muscle twitch)
$) Ty#e of the muscle:
S%eletal muscles contain mainly two types of muscle fibers.
a% Slow $red% muscle fibers $type (%:
These muscle are adapted for long slow contractions which maintain the
body posture &support the body against gravity' e.g. bac% muscles, soleus
muscle etc. These muscles have a relatively longer latent period, contract
slowly and relax slowly. The duration of the simple muscle twitch is about 100
m. sec
25
)uration of S.M.T. of different types of muscles
These muscles are red because they contain the respiratory pigment
myoglobin which facilitates the upta%e of 0
"
from the blood stream. These
muscles are composed of muscle fibers which are of small diameter, contain
much mitochondria &aerobic oxidation' and surrounded by numerous blood
capillaries &red fibers'. Slow &red' muscles do not show fatigue because4
( They are slowly contracting i.e. use $T5 at a slow rate.
( These muscles are richly supplied with blood which is able to supple them
with 0
"
and nutrients &glucose and free fatty acids'.
( These muscles are adapted to use aerobic oxidation &contain much
mitochondria, myoglobin and blood capillaries' which provides much
energy &8E $T5 molecules for each molecule of glucose'.
b% 'ast $pale% muscle fibers $type ((%:
These muscles are adapted for fine and rapid movements e.g. extra ocular
muscles. These muscles have a short latent period, contract rapidly and relax
rapidly. The duration of the simple muscle twitch is less than 10 m. sec.
These muscles are composed of muscle fibers which are larger in si.e and
contain much more sarcoplasmic reliculum and glycogen granules. The
myoglobin is absent and there are few blood capillaries &pale fibers' and few
mitochondria.
3ast &pale' muscles are adapted to use anaerobic glycolysis &absent
myoglobin, few mitochondria, few blood capillaries and more sarcoplasmic
26
reticulum and glycogent granules'. So, these muscles are able to produce $T5
rapidly and at high rates but ;uic%ly fatigued once their glycogen stores are
depleted.
c% A third type of muscle fibers $intermediate type* fast o#idati&e% are present.
These fibers share the characteristics with each of the other two types. They
have high $T5ase activity li%e the fast &anaerobic' fibers and high oxidative
capacity li%e the slow &aerobic' fibers. They contract more rapidly than the slow
fibers and can maintain contraction for a longer period of time than the fast
fibers.
6ost muscles of the body are composed of a mixture of the three types of
muscle fibers e.g. gastrocnemius muscle &duration of simple muscle twitch 80
m. sec'. The muscles which react very rapidly are composed mainly of the fast
fibers while the muscles which maintain contraction for long periods of time
without fatigue are composed mainly of the slow fibers.
Types of muscle fibers: +ale fast and slow red fibers.
)) Tem#erature of the muscle:
#arming of a muscle leads to a stronger contraction than normal, together
with shortening of all phases of the simple muscle twitch. The effects of
warming are due to acceleration of the metabolic reactions needed to provide
energy for muscle contraction. $lso, warming decreases the viscosity of the
muscle and therefore facilitates the process of contraction. 1uring muscular
exercise the muscle temperature rises which ma%es contraction stronger and
more rapid. /ooling of the muscle produces the opposite effects.
27
,ffect of temperature ca S.M.T $- . warm/ N . normal/ . cold
*) Fatigue of the muscle:
>apid and repeated simulation of the muscle leads to muscle fatigue which is
manifested by decrease in strength of contraction and prolongation of all phases
of the simple muscle twitch specially the relaxation phase. >elaxation becomes
incomplete i.e. contracture.
,ffect of fati"ue on S.M.T.
/ontracture is a state of sustained muscle contraction which occurs when the
muscle become extremely fatigued. It is due to depletion of $T5 which is
important for muscle relaxation.
In isolated muscles, fatigue occurs rapidl because:
( 3atigue of the excitation contraction coupling mechanism &fatigue of
neuromuscular transmission, changes in the membrane permeability and
failure of cross(bridge cycling due to decreased $T5'.
( 1ecreased active transport of /a
--
ions into the sarcoplasmic reticulum.
( 1ecreased energy stores inside the muscle &$T5, /r(5 and glycogen'.
( $ccumulation of metabolites e.g. /0
"
and lactic acid.
( 1ecreased 0
"
supply.
( 1ecreased p9 of the muscle cells.
28
( ,lectrolyte disturbance.
Inside the bod, muscle fatigue is delaed because:
( The circulatory system plays a very important role in supplying the muscle
with 0
"
and nutrients and in removing the metabolites from the muscle.
( The /)S regulates the muscle contraction so that not all the muscle fibers
are contracted at the same time, but instead, there is alternation between
contracted and relaxed muscle fibers.
( 9ormones &e.g. adrenaline, nor(adrenaline, glucocorticoids, thyroxin and
insulin' delay onset of fatigue because these hormones regulate the
metabolic rate, glycogen stores, blood pressure and excitability of the
nervous system.
+) .nitial lesngth of the muscle:
The strength of the muscle contraction is directly proportional to the initial
length of the muscle, within limit. This is %nown as StarlingGs law which is
applied also to the cardiac muscle and smooth muscles.
If the muscle is stretched, its initial length is increased and the resulting
contractions are increased. If the muscle is over stretched, the muscle
contraction becomes wea%er.
This is proved by muscle loading. If the weight attached to the tendon of the
muscle is supported during relaxation and does not pull on the muscle except
when the muscle starts to shorten, the contraction is called after loaded i.e. the
muscle is loaded after the contraction starts. 0n the other hand, when the load
pulls the muscle during relaxation and increases its length, the contraction is
called preloaded. $ preloaded muscle gives stronger contraction than after
loaded muscle provided the weight does not overstretch the muscle.
29
ontraction of preloaded muscle is stron"er than after loaded muscle.
0) 1i2e of the muscle:
The strength of the muscle is determined mainly by its si.e. Thus, the
athlete who has hypertrophied his muscles through an exercise training program
will have increased muscle strength because of increased muscle si.e. The
maximal contractile force is ".2 ? 8.2 +g. B cm
"
of muscle cross(sectional area.
3) Age of the muscle:
The maximal strength of the muscles decreases with increasing age. It is
due to an unavoidable effect of aging and the typical decrease in physical
activity that often accompanies getting olderH. It is apparent that strength
training remains highly effective in maintaining muscular strength throughout
life. 9owever, after about age F0, strength levels fall more rapidly, independent
of training. This is probably influenced by the mar%ed hormonal changes. !oth
testosterone and growth hormone appear to decline more dramatically after
about age F0. >eduction in the circulating concentration of these hormones will
result in a shift in the balance between muscle protein synthesis &anabolism' and
protein brea%down &catabolism'. The decreased strength is due to atrophy of
muscle fibers. It is important to notice that with strength training, the maximal
strength of a F0 year old can exceed that of his untrained sonsI $nd, several
30
studies have demonstrated that strength gains are possible even at @0 years old.
So it is never too late to begin a strength training program.
!ffects of stimulation skeletal muscle by two successi-e stimuli:
The response of the muscle to the two successive stimuli depends on the
time interval between the two stimuli.
(If the second stimulus falls during the latent period of the first twitch, it will
produce no response because the second stimulus falls during the absolute
refractory period of the first stimulus.
(If the second stimulus falls during the contraction phase of the first twitch,
the muscle responds by more contraction giving a stronger contraction
&higher twitch' with more prolonged duration.
(If the second stimulus falls during the relaxation phase of the first twitch,
the muscle will contract again given another twitch i.e. a curve with two
pea%s.
(If the second stimulus falls immediately after the end of relaxation phase of
the first twitch, the muscle will contact again giving another twitch which is
bigger than the first twitch. The second stimulus finds the muscle in a better
physiological condition &more warm and more /a
--
ions are present inside
the muscle fiber.
,ffect of two successi&e stimuli
!ffects of stimulation of skeletal muscle by se-eral successi-e stimuli:
The response of the muscle to several successive stimuli depends on the
fre;uency of stimulation4
31
,ffect of se&eral successi&e stimuli.
If the fre;uency of stimulation is low, so that the stimuli fall immediately
after the relaxation phases of the preceding twitches, separate twitches will be
obtained, the first few contractions gradually increase in strength. This
condition is %nown as the stair case penomenon. The cause of this
32
phenomenon is that the second stimulus finds the muscle in a better
physiological condition &more warm, and more /a
--
ions are present inside the
muscle fibers'. The third and fourth stimuli find the muscle in a more and more
better conditions producing increasing contraction up to a certain limit where
there is no further increase in contractions.
If the fre;uency of simulation is increased so that the stimuli fall during the
relaxation phases of the preceding twitches, colonus or incomplete tetanus is
obtained. /olonus means rapid repeated contractions of the muscle.
If the fre;uency of stimulation is further increased, so that the stimuli full
during the contraction phases of the preceding twitches, a complete tetanus is
obtained. Tetanus means a continuous contraction which results from fusion of
successive contractions produced by the rapid successive stimulation. These
stimuli cause persistent release of /a
--
ions which lead to continuous
contractions. The tension developed during a complete tetanus is about 7 times
that developed by a simple muscle twitch. Tetanus is the common type of
muscle contraction which occurs in the human body.
The fre;uency of stimulation needed to produce tetanus depends on the
duration of the simple muscle twitch. It is around "0(F0 times per second for
most s%eletal muscles. The longer the duration of the twitch, the lower the
fre;uency of stimuli needed.
The minimal fre0uency needed to produce complete tetanus depends on:
%& '#pe o( te muscle! Slow &red' muscle which have a longer
contraction phase needs a less fre;uency of stimulation to produce
tetanus.
)& All (actors tat lengten te contraction pase lower the minimal
fre;uency needed to produce tetanus e.g. cooling, fatigue, decrease 0
"

supply, decrease blood supply and decrease /a
--
ions.
*- Anticolinestrases (e&g& prostigmine) prolong the contraction phase by
preventing hydrolysis of acetylcholine. Stimulation of the motor nerve leads
to accumulation of acetylcholine at the motor end plate producing tetanus.
33
&he (ower o* )he -,scle.
The power of the muscle is a measure of the amount of wor% which the
muscle can perform in a given period of time. This is determined by4
( The strength of muscle contraction.
( The velocity of muscle contraction.
( The number of muscle contractions in each minute.
The muscle power is measured in +ilogram(meter & +g(m' B minute. $
muscle which can lift a %ilogram weight to a height of 1 meter in 1 minute is
said to have a power of 1 +g(mBmin. The maximum power can be done by all
muscles in the body of a highly trained athlete with all the muscles wor%ing
together is the following4
( 3irst 10 to 12 seconds A000 +g(mBmin.
( )ext 1 minute 7000 +g(mBmin.
( )ext half hour 1A00 +g(mBmin.
Thus a person has the capability of an extreme power surge for a short
period of time, such as during a 100 meter dash which can be completed within
the first 10 seconds, where as for long(term endurance events the power output
of the muscles is only one fourth that produced during the initial power surge.
E+d,ra+ce i+ -,sc,lar exercise.
,ndurance is the final measure of muscle performance. This depends on
the nutritive support for the muscle ? more than anything else ? on the amount
of glycogen stored in the muscle before the start of exercise. $ person on high
carbohydrate diet stores far more glycogen in muscles than a person on either a
mixed diet or a high fat diet. So, endurance is greatly enhanced by a high
carbohydrate diet. #hen athletes run at speeds typical for marathon race, their
endurance is measured by the time that they can sustain the race until complete
exhaustion is approximately the following4
J 9igh carbohydrate diet "70 minutes.
J 6ixed diet 1"0 minutes.
34
J 9igh fat diet E2 minutes.
The corresponding amounts of glycogen stored in the muscles are the
following4
C 9igh carbohydrate diet 88 grams B +g. of muscle.
C 6ixed diet 1A.2 grams B +g. of muscle.
C 9igh fat diet F grams B +g. of muscle.
E+ergy ys)e-s i+ (or) a+d Exercise.
The same basic metabolic systems are present in muscles as in all other
parts of the body. 9owever, special ;uantitative measure of the activities of the
three metabolic systems are important in understanding the limits of muscular
activity. These are4
35
1-Phosphagen system: ( ATP and Creatine-Phosphate )
& Adenosine 'riphosphate ( A'# ):
The basic source of energy for muscle contraction is $T5, which has the
following formula4 $denosine(508 K 508 K 508 . The bonds attaching the "
phosphate radicals are high energy phosphate bonds. ,ach of these bonds stores
about 11,000 calories of energy per mole of $T5. >emoval of first phosphate
converts the $T5 into $15 & adenosine diphosphate ', and removal of the
second coverts this $15 into $65 & adenosine monophosphate '.
Lnfortunately, the amount of $T5 present in the muscles is sufficient to
sustain maximal muscle power for only 2 or F seconds, may be enough for a 20
meter dash. Therefore, it is essential that new $T5 be formed continuously.
This is done through the /reatine(5hosphate.
36
& (reatine-#hosphate:
It is a chemical compound which has a high energy phosphate bond, with
the following formula4 /reatine K 508. The high energy phosphate bond of
/reatine(5hosphate has more energy than the bond of $T5. Therefore, the
/reatine(5hosphate can provide enough energy to reform $T5. 6uscles contain
" ? 8 times as much /reatine(5hosphate as $T5.
Transfer of energy from /reatine(5hosphate to $T5 occurs within a small
fraction of a second. So, all the energy stored in /reatine(5hosphate is readily
available for muscle contraction, *ust as is the energy stored in $T5.
$T5 and /reatine(5hosphate can provide maximal muscle power for a
period of 10 ? 12 seconds, both are enough for 100 meter run. Thus, the energy
from the 5hosphagen system is used for maximal short brusts of muscle power.
2-Anaerobic system: ( Glycogen lactic acid system )
The stored glycogen in the muscle is hydroly.ed into glucose and the
glucose then utili.ed for energy. <lucose is split into " pyruvic acids, and the
energy is released to form " $T5 molecules.
Glucose ( ms glycogen )
s' &<lycolysi
oxidation $naerobic
2 Pyruvic. Acids + 2ATP
1uring sever exercise, when the muscle is doing wor% at faster rate than
the blood can supply 0
"
and nutrients, the muscle depends on local glycogen
stores and anaerobic glycolysis to meet its energy re;uirements. The pyruvic
acid produced is converted into lactic acid which diffuses out of the muscle and
accumulate in the blood.
The advantage of anaerobic glycolysis is that it is able to supply $T5 at a
high rate and within a short time. The disadvantage of anaerobic glycolysis is
that it provides only small amounts of high energy phosphate & " $T5
molecules from each molecule of glucose'. So, anaerobic glycolysis is rapid but
not economic.
#hen there is insufficient 0", most of pyruvic acid is converted into lactic
acid, which then diffuse out of the muscle into the interstitial fluid and blood.
$naerobic glycolysis can form $T5 molecules about ".2 times as rapidly
as can the aerobic oxidation of glucose. It can provide 80 to 70 seconds for
37
maximal muscle activity in comparison of 10 to 12 seconds provided by the
5hosphagen system.
3-Aerobic system:
$erobic oxidation of glucose and fatty acids leads to release of excess
amounts of energy which are used to reform $T5.
BI. Glucose + !
2

cycle' s &+rebD
oxidation $erobic
"!
2
+ #
"
! + $%ATP
&ree 'a((y acids + !
2

oxidation $erobic
"!
2
+ #
2
! + ATP
$t low or moderate levels of activity, $T5 is produced by the aerobic
oxidation of blood glucose or free fatty acids &carried by the blood from the
adipose tissues'. $erobic oxidation of glucose or fatty acid produces great
amount of high energy phosphate &8E $T5 for each molecule of glucose', but
the process is relatively slow.
6ost muscles contain a mixture of cells, some adapted to use anaerobic
glycolysis which can supply $T5 very rapidly & but not economic ', and others
adapted to use aerobic metabolism & economic ' which is relatively delayed.
In comparing te aerobic, anaerobic an$ +ospagen s#stems, te
relative ma,imal rates o( A'+ utilize$ are te (ollo-ing!
- Aerobic s#stem 1 6 of $T5 B min.
- Anaerobic s#stem ".2 6 $T5 B min.
- +ospagen s#stem 7 6 $T5 B min.
.n te oter an$, -en comparing te s#stems (or en$urance, te
relative values are te (ollo-ing!
- +ospagen s#stem 10 ? 12 seconds.
- Anaerobic s#stem 80 ? 70 seconds.
- Aerobic s#stem unlimited time & as long as nutrients last '
Thus, 5hosphagen system is utili.ed by the muscle for power surges,
anaerobic system gives the muscle extra power during intermediate races & as
"00 to E00 meter runs ', and aerobic system is re;uired for prolonged athletic
activity.
38
/nerg# s#stems use$ in various sports!
C 5hosphagen system4 100 meter dash, *umping, weight lifting, and diving.
C 5hosphagen and anaerobic systems4 "00 meter dash.
C $naerobic system mainly4 700 meter dash, 100 meter swim, E00 ? 1,200
meter dash, "00 ? 700 meter swim, and boxing.
C $erobic system4 10,000 meter s%ating, marathon run, and Mogging & 7"."
+m.'
+er(ormance in atletic events is determined by how rapidly the athlete
can recover strength between surges of activity, and in general this means how
rapidly the energy systems can recover.
E**ec)s o* exercise o+ s/ele)al -,scles.
3orceful muscular activity over a prolonged period causes muscle to
increase in si.e as the number of myofibrils within the muscle fibers increases.
Increase in muscle si.e, called hypertrophy, occurs only if the muscle contracts
to at least A2 of its maximum tension.
5rolonged muscular exercise improves muscular strength, muscular
endurance, and flexibility. Muscular strengt is the force a muscle can exert
against a resistance in one maximal effort. Muscular en$urance is *udged by
the ability of a muscle to contract repeatedly or sustained a contraction for an
extended period. 0le,ibilit# is tested by observating the range of motion about
a *oint.
$s muscular strength improves, the overall si.e of the muscle, as well as
the number of muscle fibers and myofibrils in the muscle, increases. The total
amount of protein, the number of capillaries, and the amount of connective
tissue, including tissue found in tendons and ligaments, also increase. 5hysical
training with weights can improve muscular strength and endurance in all
adults, regardless of their age. 0ver time, increase muscle strength promotes
strong bones.
6uscles which are not used or which are used for only very wea%
contractions decrease in si.e, or atrophy. $trophy can occur when a limb is
placed in a cast or when the nerve supply of the muscle is damaged. If nerve
39
stimulation is not restored, muscle fibers are gradually replaced by fibrous
tissue.
40