5

SE TO
CA RD IO VA SC UL AR RE SP ON
EX ER CI SE AN D TR AI NI NG

An Ove rvie w
and a greater supply of
The longer duration of activities dem
s. This demand is fulfilled
pxygen to the working tissues and cell
s system constitutes the
by the cardiovascular system. Thi
ch serve several functions.
heart, blood vessels and the blood whi
n other than the supply of
J The cardiovascular system's functio
demanded nutrients to the
oxygen, includes the supply of the
hormones to the ir targ et
cells of various organs, carrying the
l metabolic waste products
tissue or organ, remo'(al of the severa
is in oth er par ts of the body.
and thus sus tain ing the homeostas
on the cha nge s in the
In this chapter, we will be focussing
ult of exe rcis e and trai nin g.
abo ve functioning that occ ur as a res
the eff ect s of two ma jor if
A(s o, we, wo uld be exp lor ing
which dem and s trem end ous
classification of spo rt activities. On e
and s trem end ous end ura nce
stre ngt h and the oth er wh ich dem
oth er wo rds , we will be goi ng
on the car dio vas cul ar sys tem . In
bro ugh t abo ut as a res ult of
thro ugh the cha nge s in this sys tem
stre ngt h and end ura nce trai nin g.
chapter are as follows:
The major aspects discussed in this

the car div asc ula r

• Effect of exe rcis e and tra inin g on
parameters.

•· Cardiac hy,pertrophy.
 .
11 5 ~J:
I
•
158
Ca rd, ov as cu /ar
114 Ex erc ise Ph ys Re sp on se to
iol og y f;X erc
As a result of ex
oxygen supply,
erc ise , the re is
an inc rea se in or
a gre ate r utrlrs the de ma nd of ==
an inc rea se d ation of the es tnl ~ fl•
me tab oli c rat e se nti al nu trie nts
accumulation of an d a re su lta nt ,
the ac tiv e me tab inc re as e in the
muscles. Pu t tog oli c wa ste pr od L,i tre S
eth er, all the se uc ts in the ac tiv == ~ -
ca rdi ov as cu lar ch an ge s lay a e tn lfl •
sy ste m wh ich str es s up on the
ful fill s thi s inc .
the mo st eff ici re as ed de ma nd s in
en t ma nn er. During Rest \
. . .-n
We wo uld be em
The resting card . t .s proJ<"" a.te\Y be tw eert" 4
iac outpu 1 ap
ph as izi ng on the
ma in ca rd iov as to 6
or pa ram ete rs
to se e its ex er cis e an d tra ini
cu lar fac tor s L. min-' in the
supine pos1t1on-
. a fa ll fro rn •
5 to 4 L- .,, ,n.,
0~
ng re sp on se . after the subject au t it m y t
as um es an up rig th e re as on be
• Ca rd iac Ou tpu ht po s u ~; ;n d \0 9
•
: pooling of blood
in the 1owe.r e~rer .
n1
Ro da hl , 19 87 ). ~\
He er t Ra te The absolut 11 es (AS ·' s w, th th e bo dY
• siz e and en due value fo r th e ca rd ia c ou tp
Stroke Volume ra nc e tr> tin in g. ut va ne
components, th As m al es ha
•Re dis tri bu tio n ey ar e eJ<pec ve la rg er bo
of Bl oo d Fl ow compared to fe ted to po ss es dY
a la rg er he ar

!j
• Blood Pr es su males. Ch ild re t as
re compared to th n' s he ar t si ze
e ad ul t he ar t. is al so sr na lle
• The Bl oo d Th er ef or e, in r w he n
the cardiac outp no rrn al ac tiv e
ut is ar ou nd 6 L. rn en ,
• Ca rd iac Hy pe than th ei r fe m al rn io -', wh ic h is ab ou
rtr op hy e co un te rp ar ts t 10 % gr ea te r
cardiac ou tp ut of th e sa rn e bo
in cr ea se s ap pr dy si ze . Th us
EF FE CT S OF ox irn at el y lin ea , th e
EX ER CI SE AN in body su rfa ce rly w ith an in cr
O TR AI NI NG ON ar ea (C la rk e, ea se
CARDIOVASC 19 75 ).
ULAR PARAME Du rin g re st th er
TERS e is a lit tle di ffe
whe~ tra in ed an re nc e in th e ca
Ca rd ic Output d un tra in ed su rd ia c ou tp ut
. bj ec ts ar e co ,
cardiac ou tp ut • 1n ca n e rn pa re d. A re
Card of 5 L m· at ta in ed 1f st in g
iac ou tp ut is the . -1 b th e he ar t ra te 1s
amount of blood b mm 1 an d th e st ro ke vo lu m e 77 m l (i• • 65
in one minute. In
other wcrds, it is pumped by the he
art 5. 00 5 ·Lm in •') . e 65 x 75 - •
and heart rate. the product of str 50 05 m l -
oke volume • • ·•
- •-
·-'
Mathematically, D ur in g Exercise
it can be expres
sed as follows:
~, Cardiac output =
Heart rate
X Stroke volume.
Cardiac output in
creases directly
with in cr ea si ng
(Q)L. min.-1 intensity. The incr ex er c, se
ease may be ab
= (HR)b. min.-1
(SV)Ml.bt.-1. cardiac output fo
r an untrained m
ou t- 4 to 5 to\ds. T he
m ax ,m a\ ' I
25 L. min-1 and in a\e may ra ng e
be tw ee n 20 to
be at •ml blood who have lower
an untrained fem
a\e it may be ar
ou nd "\ 5 L. m ,n
..._ - - I

mm. X work and \ower ·'

I

b e~ aerobic ca pa ci ....
On the contrary t,e s.
, the maxima\
male has been ca rd ia c ou tp ut
recorded as 30 in th e tr ai ne d
L. m in :'. W he re
as , to r a h,gh
\~

..
 -- .,
.
115 ~
.,.

116 Exercise Physiolog y

trained enduran ce athlete, with exceptio nally high aerobic
· ~ capaciti es, 40 L. min- 1 of maxima l cardiac output has been
u recorde d (Fox Bowers. Foss, 1993 ).Therefo re, it is seen that
the greater the maxima l cardiac output, the greater the maximal
~o 6 aerobic power (V02 max.) or vice versa {Ekblom , Hermans en,
1968).
lin-'
ing Therefo re, there is an increase in the cardiac output with an*
r)- increase in the oxygen intake, but not linearly, if a range from
I - rest value to maxima l is conside red.
rY
An increas e in the maxima l cardiac output reflects the
accomp anying increase in both the heart rate and stroke volume.
Therefo re, in order to achieve a maxima l cardiac output of 30
L.min-' the heart rate may be increas ed to 195 b. min- 1 and the
stroke volume may be doubled to 154 ml. (i.e., 195 X154 = 30 L.
min-') ..
Therefo re, during the initial phase ofexercise , ~n increase in
both the heart rate and stroke volume results in an increase d
cardiac output. But when the exercis e intensit y exceeds 40 to
60% of the individu al's capacity , the stroke volume either remains
unchan ged or starts increas ing at a much slower rate. In other
words, the stroke volume does not necessa rily increase followin
• g
I
a subma ximal level of exercis e. Therefo re, the increas e in the
cardiac output takes place due to an increas e in the heart rate.
Effect of Training on the Cardiac Output
• The Restin g Cardiac Outpu t
There is not much of a change in the resting cardiac output
when trained and untrain ed subjec ts are compar ed. Mussho
ff
indicat es a higher a -vo differen ce which reflects they would
2 vo ditt. a\so increas es by 50%. tAstrand, '\977 and Sa\t,n, '\969).
have a smalle r cardiac output at rest i.e, with incre_ased ability
Carc1iovascular Response to Exercise & Training
"\ "\ 7
• Changes during Steady State Submax \ma\ Exerc\se
Followin g Training
The cardiac output during submaxima\ exercise at a given
rate of work does not change as a resu\t of training. We\\ trained
endurance athletes achieve the same cardiac output as in \he
case of untrained subiec\s. \t may be re\ated to the wpe,
intensity and duration of the training program invo\ved.
• Change s during Maximal Exercise
The maximal cardiac output increases with training. "The
maximal cardiac output and the max V0 are direct\')' related.
2
The maximal cardiac output is a factor determining the max
V0 2 . The highest cardiac output is seen in high\')' trained
endurance athletes.(Ekb\om and Hermansen, "\968).
As mentioned ear\ier, the cardiac output is the product o\
heart rate and stroke volume. As the maxima\ heart rate a\ter a
training program is either unchanged or s\\ght\y decreased,
therefore the increased cardiac output io\\owing training is main\y
due to an increase in the stroke vo\ume.
• Endurance Performance
An increase in the stroke vo\urne and card\ac output \o\\owing
training enhanc es the enduran ce penorrnance. Two \actors
contributes,to such a change. One ,s the ,ncreased b\ood vo\urne
and the other is the ,ncrease d rnyocard,a\ contract\\\\~ ~Sa\t,n
et.a\., 1968) (Schener, 973). The rnyocard,a\ contrac\\\\\'1 means
the slrength o1 ventricu \ar contrac\\on. Fo\\ow\ng endurance
training in a sedanta ry adu\t, the \J0 max ,s ,ncreased b~ 50%
2
which is re\ated to an increas ed mrudma\ card,ac ou\pu\.1 he a-
2

of tissue to extrac t oxygen from circula tion, less blood volume Most of the increas e in the \J0 max observe d ,n the\\\, '/Oung
. 2
and o\der rna\es \S due to a greater rnax,rna\ card,ac output
is require d.
f, Therefo re, it can be rnent,on ed that the ,rn?rO\Jemen\ \n max\ma\
cardiac output due· to endura nce tra,n,ng ,s as ,m??r\a n\ a~ an~

' other change ,n the rnax,ma \ card,o\Jascu\ar \unc\,on and\\ ma~

..
:!.~~
·,~,..t;:-"');
.. ..;.__;_,=
.. ~?"- -
 11 9
carcfiov•sc"'" £_xerc/se & ,ra
'A P in in g 1:
" 10
Exorcise Ph such sirnnar 95 0 56 • d th ro u9 h n in cr ea
rate and a de sults are achieve e !h ' • a.
1 tB ysiology re
. . se d t, ea rt
be the on , L' s1gn1ficnnt cn on ob se rv ed in creased sirol< e
J
(fi ow ell 19 i5
ge so m e subjec
ts. e vo lU ~ ·,nre fe!Tla1es i,a ve a 1ower (
), e ph ys io lo gi
. - stroke voiurne ca l factors:
b"c endursnc
e training, the which is rna1nlY
Follo,\.,~ng, 8 8
, ,: :
.
maximal card
• due o
output f>p:ca I)
from the untra iac • sm al le r ft
8 ined values of
24 L.min _, rn adu" males an
d fro
22 L.min•' ~o • Lo we r btte ve nt le
ood vo turic
young adult fem }rotJ09 •
" m 16 L. min-' rn e
ales. (Astrand to 18 L.miff' ,n · nd \ess w e \\
and Aodahl 19 A "e '"o e fern c on di tio ne
This training ind
uced increas
69 ). - .v1::1, .... :::,- ale is 1ess ac
11ve a d
,snot due to an e in the maxim
increase in m al cardi~c.ou
there is a decre aximal heart tput
ase in maxim rate after trainr H EA
as mentioned al heart rate af ng. As \hAT RArn
e nu TE
ber of cardia
earlier, the gr ter training, th c co nt ra ct io
be the result eater maxim erefore, he ar t rate. n, ns in on e m
of a greater al cardiac ou e nurnber of co in ut e is ca lle
volume before stroke volum tput m ay The rate ntractiOns rang d
training of 11 e. The maximal and intensity es fro m 60 to 80
an d females, 0 and 80ml. stroke exercise, long of th e ca rd ia b. rn in .-'
respectively, in young adul term training, c co nt ra ct io
ty pi ca t males 1;1ge, di se as ns is af fe ct
after several
months of tra
lly increases
to 122 an d 96 temperature e, st re ss , en ed bY
ining. (Saltin ml. etc. Howe-,e vi ro nm en ta
, 1969). a norrnal ne r 12 b. (Tlin.-' l
Strength Trai ar t rate, ho is ge ne ra llY
ning an d Ca recorded in th w ev er , a 1o co ns id er ed
rdiac O ut pu wer re st in g as
Soviet resear t Ad ap ta tio n e tra in ed in n e a rt ra te is
ch indicates di vi du al . w e
increase 1.5 th at weight lift sh al l be di
- 2 times ab er's cardiac sa m e in tra sc us si ng th
exercise activ ove the restin ou tp ut in in g as pe e
g values durin ct s.
ity. (Stone et g strength
weight lifters . al ., 1991). The R eg ul at io n of I
increases up cardiac ou tp
volume in cr to 30 L. m in -1 ut of The heart's H ea rt R at e
ea si ng up to after exercis
e with stroke fu nc tio ni ng
15 0- 20 0 ml. 1 is re gu la te d
untrained su
bjects sh ow b- • At the factors w hi ch or co nt ro lle ' •
I

no significan sa m e tim e ar e m en tio ne d b y se ve ra

during st re ng t change in ca d be lo w : '
th tra in in g ac rd ia c ou tp ut I '
tiv ity (Stone
Bodybuilder et. al., 1991 N eu ra l Fa ct
s sh ow a si gn ). or s '
stroke volum ifi ca nt ly gr ea The heart is su
e, but no t th te r cardiac ou th f c
pplied with th
e• sympa e 1 n e rv e s (ca rd ia c
1

e he ar t rate tp ut an d
power lifters when co m oa accelerator) an
during sets of re d to th e
of on e repe th e ba ck squat at va autonomic ne d pa ra sympa 5 a subd1v • 1s
• 1o
• n f th
tition m ax im
um to vo lit io
rious pe rc en
ta ge s rv ou s sy st em thetic ne rv e , o e \
1989). na l fa tig ue .(M ar e st im ul at . W he n th e pa ra sy • l 1
ur ra y et. al., ed th ey se rn pa th
cr et e ca te ~ t, c n e ~ e s
However, th adrenaline an ch o la m in e
e ab ov e st ud d norepineph s ( e p tn e p
hnne/
training m ay ie s do su gg
es t th at th e endings of the rin e/ noradrenaH '
le ad to ad ap
ta tio ns th at st re ng th heart. These ne) o n th e ~I
ou tp ut du rin al lo ws an el heart rate. On ch em ic al su bs ta nc n e rv e I

g st re ng th tra ev at ed ca rd the contrary, es in cr ea se

in in g ac tiv ity ia c
• Females
. (vagus nerves w he n th e p a ra sy m th e 6
) are stimulat p a th e tic n e ~.
ed, th ey se cr rv es
,. Giv~n
decreases the et e ac et y\ ch
o\ in e w h ic h
sa m e ra te of heart rate. l.,:.
ou tp ut rs s1m1 wo rk , th e tra
lar to th at of in ed fe m al es The sympath

::r
he r m al e tra ca rd ia c etic and p a
in ed co un te
rp ar t. H ow ev
er
controlled b~ th
e nerve centre
ra sy m p a th e
tic n e rv e
ac ti vi ty is
- •l
Thes~ cardia s in th e br ai n
c control ce nt m ai nl y, in th
e m e d u '\a .
:,:y
I

emotions, bloo re is st im ul at
d pressure, ed b y fa ct o
ar te ri al pH et rs such as
c.
·~- ·~~---.:.
\.
•• '
•

Iii
 119

reased heart
~.
. have a lower
~-
igical factors:
¾. 120 Exercise Physiolog y
Therefo re, the major increas e in the exercise heart rate
is
due to the inhibitio n of the normal parasym pathetic (decrea Cardiovascular Response to Exercise & Training
sed
1nditioned heart rate) activity ; there is an increas ed activity ,2,
of the Exercis e Heart Rate
sympat hetic nerves during exercise . Howeve r, the decreas
ed
parasym patheti c nerve activity is more significant. Studies have detected a taster heart beat instant\v at the
Hormo nal Factors start of an exercise . This first heart beat aft.er the exercise
is
faster than the preceed ing ones. Such a fast heart beat ma'i
f is called
f b.,nin.-l The catecho lamines (epinephrine and norepinephrine) and the
probably , be caused by a nerve rei\ex part\'i originati ng tram
the
various proprioc eptors {musc\e spind\es , ioint receptor s etc.).
rctedb y thyroid hormon es circulat ing in the blood increas e the heart
rate. Therefo re, as the muscul ar contrac tion starts and
the
rmenta l The catecho lamines have a more significa nt role in the increase corresp onding joints are put into action. the impu\se s
of the heart rate. are
ired as transmi tted in the muscle spind\es and ioint receptor s: these
te is Intrins ic Factor s impulse s pass further to the spina\ cord and to the cardiac
the regulati ng centre of the brain. Such muscle /joint mechan
o
Factors such as the temper ature variatio n, stretch and the reflexes cause the parasym pathetic nerves to be inhibited and
electro lyte balanc e influen ce the heart's activity directly without a corresp onding increase in the heart rate occurs.
~ -
the interfer ence of the neural and the hormon al factors There are few other factors which int\uenc e an increase
e.g., in
heat increas es the heart rate; cold decrea ses the heart
~a''
l
rate. the exercise heart rate. They are:
The increas ed filling of the heart chambe rs with blood stretche
s •
the SA node of the heart. This stimula tion of the SA Control by Higher Centres oi the Brain
node
increas es the heart rate. Variatio n in the electro lyte balance • Muscle Chemor eceptor Re\\exes
of
sodium and potass ium may either decrea se or increas • Circulat ing Hormon es
e the
heart rate. • Intrinsic Factors
~ ~ ; .

The Pre-Ex ercise Heart Rate -',.

Contro l by Higher Centres oi the Brain
Before we start our exercise or competition, the pre exercise
During a.voluntary muscu\ar movement, the motor areas o\
heart rate increa se well above the resting values. This is also
the cortex of the brain are stimu\ated, which transmits the
referre d as antici patory respon se. The reason for such an
~. increa se is the increa sed sympa thetic nerve activity and
a
impulse s to the active musc\es and a\so to the card,ac regu\atof'i
centres of the medu\\a in the brain.Thus, the sym?athetic neNes
decrea sed parasy mpath etic tone. The other factors mentioned
. - are excitate d and the parasympathetic nerves am inhib,ted.This
earlier in the contro l of heart rate may also influence such results in an increased heart rate during exerdse. tPetro, \-\o\\and
an u
anticip atory rise. Such a situatio n is most prevalent during
s
.
a and Bouman, 1970).
highly compe titive situati on. Therefore, it is sugges ted that
the
pre exerci se heart rate should not be used to determ ine Muscle Chemo-Receptors
the
resting heart rate. During muscu\ar contract,on severa\ chem\ca\s \µo\ass,um,
\actic acid etc.) \eave the ,ntrace\\u\ar sµace and accumu\a\e \n
the tissue Huid. 1he potass,u_rn \eakage horn \he musc\e ce\\s
may stimu\ate the \ree nerve "bre end,ngs \n \he 'o\ood \Jesse\s

I
 '\2 3
car<Jlo•••cul•'
.
56
,rainin9
&
fl• Pon ss to [;)(Brei
5 . . crease in
Exercise Ph th er e ,s an t1,e r,eart ra te .(
12 2
ec tiv e tis su
ys iol og y
onlY possib ,n fo x, "\ '2.4
e of the m us
orrv
ne rhee c Onn
• se
fibre m ay cl e. Fo llo wi sowers an le whengg3)
nd si gn al s to th e ng th at , th es e ch ngin9d fo1', 1 all )(.•l"
\C
th e brain wh
ich m ay in
cr ea se th e
• c
ca rd ia co nt ro l ce nt durin · 9 su b•-' "' a ""a\ e, ,c er CI• Se
The la ck of he ar t ra te ( re s o f ,,.
ne rv e en di ng
ox yg en (h yp
ox ia ) in tis su Pe tro fs ky , 19 81 ). 8
urinQ su b "' . I I
"" '" '" eve ls of e) (e rc is e w ne n tn e rate ol wo \'
es m ay al so h r\<.
d at a co ns ta nt 1evel, t, ,e he ar t rate in cr ea se s
. to in cr ea se st im ul at e th is maintaine ' \
se en du rin g th e he ar t ra e
se ve re st at
ic co nt ra ct io
te . Su ch a
si tu at io n is rapiOdlY til l it ," '·s''
pl ateau
a\mast
re ac he s a \ateaU- "'
P ,n u s, t "'d ', st is reterred as tr>e
in ad eq ua te n (is om et ric ) th at m
oxygen supp ay stesdY state te
ly in the w ca us e i,e at
opti111al heart art rs ·. in tnB ca rd e ne ar t ra te ,s
orking tissue. s eC >
, •
Honnonal Fa rate tor sat1slY io va sc ul ar de
• th e
ctors that specific ra g l tr ie r in m an d at
During prolon
ged duration te of work- vv cr ea se in tn
e e,<ercise
s,
heart rate ab heavy exerci inteneitY, the ,tn ur eW
ove 150 min se, may be heart will appr steadY st at e n
increase in th utes or mor with the oac_ a :e co va lu e w ith in
e level of ep e, there is a 1 IP 2 111in- m in Q m or e
progressive aut with the . t'
thyroid horm
one th yr ox in
inephrine, no
repinephrine exerciseth e 5 te ad Y st at e \est re nu ou s, a
these ho rm on e in the bloo and also the 1onQer ti111e is h ve •
es in cr ea se d. As discus taken to ac \
the he ar t ra sed earlier ,eve
duration he av te during th ourinQ t,1a,dm
y exercise. e prolonged The heart rate al in
e"crercise·
eases direct
Intrinsic Fa in the e)(erc ly with a co rr
ct or s ise intensity es po nd in g in
By in tri ns ic e)(haustion. Th , until th e su cr ea se
factors, we e n,a,<imallY bi ec t re ac he
that m ay in cr mean th os e VO, and hear at ta in ab le va s a p o in t o
ea se th e he factors with
in the he ar t t rate are fi)(e lu es io r ca rd i
is th e in cr ea ar t rate durin d for everY in ia c ou tp ut ,
se d ra te of fir g exercise. Th di vi du al d u
it is st re tc he in g of the sino e first fa ct or even in an ad ri n g e,<ercise,
d w he n m or atrial node (S ve rs ed si tu
he ar t du rin e bl oo d retu A node) as at io n.
g rh yt hm ic rns to th e rig
ex er ci se . Th e ht side of th
te m pe ra tu re
of th e he ar se co nd fa ct e Effects of Tr
t. D ur in g st or is th e aining o n H
te m pe ra tu re re nu ou s ex ea rt R at e
of the he ar t er ci se when
po te nt ia l in rises, it ca us th e
th e he ar t w es an increa ou ri n9 Res
hi ch st im ul se in the actio T he re ist a
at es th n de cr ea se in
1984). e he ar t rate th e re st in g
(Lamb, established h e a rt ra te
I

After having fo llo w in g a w h ic h is

discussed al resting he ar tr ai ni ng p ro
the heart du l those factor t rate is al so g ra m m e . T
ring exercise s which may ca lle d th e h e d e cr e a
, we would se influence is very co m re s ti n g b ra se d
e the respon m on ly se en d y c a rd ia .
.rate to exer
cise. se of heart in th e ca se T h is
Studies re ve o i tr a in e d
in d iv id u a ls
It is evident
that the hear al s th at th e .
t rate increase a result o i lo re st in g b ra
to the intens ng te rm st re d yc a rd ia ta
the work load
ity of exercise
and oxygen
or the VO (in
2
s rapidly in pr
tensity of ex
er
oportion
cise or
th e su bj ec
t is g re a te
n u o u s tr a in in
r, th e n th
g . Ii th e fi
ll. es p la ce
tn e ss \e ve \
as 1
bo th trained up take are both br ad yc ar di a e m a g n it u o!
and untrained directly rela pr od uc ed d d e o l th e
subjects • te d) in u e to tr a in in re s ti n g
induce th e tr g is le ss . T h
Usually, the ai ni ng b ra d e !a c to rs w
stroke volum yc a rd ia a t re h ic h
workloads, e becomes m were discus st in cl u d e s
therefore a aximal at su sed ear\ier. th e \a ct o rs
further increa bmaximal T h e se are w h ic h
se in the ca
rdiac output as lo\\ows:
is

•
1
 123
K-
!<Fox,

124
' ~
1
rk
(a) Exercise Physiology.
•
An increased parasympathetic influence
(b)
~t A decreased sympathetic influence Cardiovascular Response to Exercise & Training ''25
(c)
Submaxlmal Exercise Heart Rates
A combination at the parasympathetic and sympathetic
influence.
Foll~wing trai_ning, the heart rate decreases during
-~ submax,mal exercise. The decrease in the exercise heart rate
• It may be recalled that when the parasympathetic nerves are may be caused by an increased parasympathetic acfo,ity.Training
stimulated it decreases the heart rate; whereas, the sympathetic causes a reduction in the plasma epinephrine and norepinephrine
nerves when strmu/ated increase the heart rate. Therefore, the at submaximal work loads, but such decrease in the hormones
is not closely related to the decreased exercise heart rates.

:;:
resting bradycard1a due to training can be induced if the
parasympathetic nerves which decrease the heart rat~ are
stimulated; and the sympathetic nerves (which increases the
heart rate) may be inhibited which may be dominated then, by
the pj:irasympathetic influence. Also, a combination of these two
finally, could produce training bradycardia at rest. The intrinsic
rate of atrial pacemaker or the SA node influence also contribute
to training bradycardia at rest. Following training, the increased
parasympathetic influence predominate the intrinsic firing rate
of the SA node. The slowing of the intrinsic rate of the SA node
may be, related to an increase in the acety/choline quantity in
the atrial tissue and a decreased senstivity of the cardiac tissues
to the epinephrine and norepinephrine following training.
.'
Highly strength-trained athletes hav: average (Fleck, 1988)
or lower than average resting heart rate (Stone, 1991 ).
Major cardiovascular adaptations that take place due to
endurance training do not appear to be sex specific.The resting
heart rate can be reduced to 50b. min- 1 or less. Several female
distance runners have had heart rates below 36 b. min-1 which
indicates a significant training response and also correspond to
an exceptionally high stroke volume. Sidney and Shephard (1973)
I~
have observed a relatively high resting heart rate of cannoeists:
1 Here the cardiac output was greater and the stro~e vo\urne
they reported 7·1 b. Min- 1 in juniors, and 60 and 67 beats Min- in
men and women respectively.
j
(Winder, Hagberg, et a\.,1978).
However, few factors or situations may lead to an increase
in the submaximal exercise heart rates, without being
accompanied by a reduction in the sub\ects \J0 max. as
2
mentioned below :
• Dehydration during heavy exercise or during heat
exposure - prolonged exercise in a hot environment
increases the heart rate than exercise at \ow room
temperature.
• Emotional factors, nervousness and apprehensions ma'J
also iniluence the heart rate at rest and during \ight and
moderate exerdse intensity.
• Exercise involving a lesser musc\e mass than in\lo\\led
in running. A higher heart rate is reported whi\e exerdsing
with arms when compared \o exerdsing with the \egs.
Such a change in the heart rate is brought about due to
changes in stroke vo\ume tdecreased), \n order to
maintain the cardiac output tSt~nberg and ~strand,
1987).
• Exercise atter alcohol \ntake - Stud,es re?ort dur\ng
subrnax\rnal exerdse, the heart on an average b~atsi 2
to 14 beats- h\gher per m\nute \n a\coho\ ex?enments.
l
was not aHected. The VO 2 a\so was s\\gh\\'1 h\gher.
\,

,c· .~
 126
Exer cise Phys iolog y 127
Card iovas cular Resp onse to
Cha nge s Dur ing Exer cise & Train ing
Max ima l Exe rcis e Foll owi ng Trai ning

-
Tab le 5.1:
Following a training prog ram the
max imal hea rt rate atta ined 128
;5 eith er unch ang ed
or sligh tly dec reas ed. Suc h Stro ke Volu me
dec reas e is
clea rly seen in the case of end
uran ce train ed athl etes (Saltin, Sub jects in Res ting
Max ima l
•
1969). Suc h a dec reas e was (m.l. bt-')
who underwent training for sho
also see n in sed enta ry subj
ects
rt duration. (Fox and Bartels, 1975
sittin g post ure
1 oo to 120 rnl/
•
70 to 90m l/bt.
The fact ors whic h influ enc e
suc h a dec reas e in the max imal
). (a) Untr aine d male
bea t •
hea rt rate follo wing train ing 1 soto 110 ml/
are (Bot /er, et al., 197 3): (b) Trained male 100 to 120 ml/b t.
bea t E
• A dec reas e in the intri nsic
firin g of the SA nod e. High ly train ed male
(c)
• An incr eas e in the para sym
path etic nerv e influ enc e. endu ranc e athle tes
- 2oo ml/b eat or
mor e. G
•
-~
I~
On the con trar y, the dyn ami Untr aine d fema les ao to 1oo ml/
c hea vy stre ngth exe rcis e (d) 50 to 70 ml/b t.
prod uce s a sub stan tial incr eas bea t -,
e in the hea rt rate. (Sto ne, 198 ..
Whi le perf orm ing a two legg 3).
ed pres s to failu re at 95% of (e} Train ed fema les 1 oo to 12o ml/
RPM, in which a vals alva man one 70to 90m \/be at
oev re (wh ich elevates intra thor
pres sure whi ch may limi t ven acic bea t.
ous retu rn and dec reas e card
outp ut) was allo wed , a hea rt iac The stroke volume is lower in F~
rate of 170 b. min -1 was reco
rded
the sitti ng or in the upr igh t
(MacDouga/1, et. al., 1985).
norm ally occurs during the
Moreover, the highest heart rate
posture when compared to the
more blood pools in the extremi
lying pos ition . Thi s is bec aus
e,
~- -4 ~
last repe titio ns of a set to volitiona ties in the upr ight posture, the reb
fatigue.(Stone, 1991 ). l redu"cing the ven ous retu rn to the hea rt. Thi
s res u\ts in a
y 63
decreased stroke volume. .
Stro ke Vol ume -

The stroke volume usually incr I

The amount of bloo d pum ped eas es as the sub1ect pro cee •
\
I

into the aorta with every heart from rest to submaximal work. ds
bea t is kno wn as the stro ke volu But a furt her incr eas e in the stro
me. The resting and max ima l volume doe s not nec ess aril y ke
stro ke volu me for both untraine occ ur as the sub iect pro gre . I
sse s
is pre sen ted in given Table 5.1.
d and trained males and females
(Ek blom , et. al., 1968). It may
from sub max ima l to max ima l
wor k. 9
be note d, the females hav e low It is evid ent tha t the stro ke volu
er stroke volume which is due me bec om es rna xim a\ at a
the ir sma ller hea rt volu me. to submaximal wor k load whe n
the VO ma x rea che s 40% to
the rea fter the stro ke volu me 2 60% ,
sta blis es and the car dia c out
influ enc ed by cha nge s. \t is put is
app lica ble to trai ned as we\
unt rain ed ma le and fem ale sub \ as
iect s. Thu s, the stro ke vo\ um
a prime fact or whi ch det erm ines e ,s
the car dio res pira tory end ura
cap acit y. nce

The fac tors whi ch dire ctly con

tra\ the cha nge in the stro
volu me due to incr eas ing exe ke
t rcis e inte nsi Hes are cited be\
ow :

54-- -

-~
 127

128
,a/
Exer cise Phys iolog y
V). Cardiovascular R
• The End -Dia stol ic Volu me (ED espo nse to Exercise & Trarn,ng '\29
•
d Pres sure . The filling of the blood in h
The Ave rage Aor tic Bloo ncles during diastole, stretches
-~ • the card iac fibre Final\ t v~nt raction
• y, urmg the next powertul cont
• Ven tricu lar Con trac tility . (sys tole
d is pum ped out from the vent ricles into the
) ~o~e bloo
e vo\u me. How ever rece nt
aort a. This incre ases the strok
End -Dia sto lic Vol ume the diasto\ic volu me does not
~esearch ha~ dem onst rated that
the exer cise. Ther efore , an increase in the stroke
incre ase du~mg
to the volu me of bloo d in the volu me durin g exer cise is not that sign ifica nt.
End -Dia sto lic Volu me refe rs
tole . It is also calle d the 'pre load'. an incre ased strok e vo\ume
ven tricl es at the end of a dias us The mec hani sm resp onsi ble for
es the EDV is the rate of veno card ial contracti\\ty.
The mai n fact or whi ch influ enc retu rn will duri ng exer cise is prob ably the myo
an incr eas ed ven ous
retu rn to the hea rt. Bec aus e At resti ng cond ition s, appr oxim
ately 40 to 50% of the bloo d
an incr eas e in EDV , ther eby incr eas ing the stro ke s durin g the dias tole is e\ec ted
or
resu lt in volu me filled in the vent ricle
volu me. vent ricul ar syst ole. The strok e 'Jo\ume ~o \d
pum ped out at ever y 11
by exer ting a mor e stttm ger
Pre ssu re ther efor e be alm ost dou bled
The Ave rag e Aor tic Blo od stro nger vent ricul ar cont racti on is
vent ricu lar cont ract ion. This ugh the
re is also refe rred as the 'after tility, is med iated thro
Ave rag e Aor tic Blo od P,e ssu calle d the myocardial contrac
the horm ona l and neu ral facto rs.
d, the pre ssu re gen erat ed by
load '. For the ejec tion of bloo
!

in the aort a.
r than the pres sure
left ven tricl e sho uld be gre ate
I
to Training
~ I
re incr eas es then less bloo d will Stro ke Volu me Ada ptat ion
Tha t mea ns if the aor tic pre ssu ng
(de crea sed stro ke volu me) . But duri Dur ing Res t
be pum ped or ejec ted king mus cles ,
odil atio n in the wor
exe rcis e, due to the arte rial vas rt is able to Dur ing resting conditions, no sign
iiicant differences exists
red uce d an<;t thus the hea
the pre ssu re in the aor ta is trained and untrained subiects.
in the cardiac output between the
bloo d (inc rea sed stro ke volu me) . observed in the tra,ned
pum p a gre ate r volu me of However , a decreased resting heart rate is
eased heart rate, the stroke
subjects. ~s a result of the decr
Ven tric ula r Con trac tilit y ects in order to maintain the
the volume is greater in the trained subi
sym pat het ic stimulation of normal resting cardiac output.
Bot h the neu ral (inc rea sed the
hea rt) and the hor mo nal (ca
tech olam ines ) factors influences n ,n endurance ath\etes.
iac Lar ger stro ke volu mes are see
stro ke volu me . Bot h the se
me cha nism s incr eas e the card stroke vo\ume when compared
cardial However, fema\es have a \ower
calc ium ava ilab ility to the myo reason for such dmerences are
con trac tilit y thro ugh mo re to thei r ma\e counterparts. The
:
cell. rela ted to the following factors
a\es ret\~cts a sma\\er
• Body size: sma\\er body size of fem
reased
Ho w the Str oke Volume is Inc heart and their corresponding srna
\\ \eft ventnc\es.
an incr ease in the stroke e sma\\ b\ood vo\ume ,,,.J'n\c~
Earlier the main me cha nic s behind • Blood volume: the terna\es hav
Frank-Starling Law. This law ) when com~ared \o \ne\r
volume was thought to be the is related to their sma\\ body size
t:! j inc rea ses in response to an
sta tes tha t the stroke volume male counte·parts.
g the ventricle during diastole.
increase in the volume of blood fillin ·1
a
 •
130
Te sto ste ron e: low er
the pro ba ble reason
.
Exercise Ph ysi olo gy
testosterone levels in
the females is also
car dio vas cul ar Re
tollowlng training is
vo lum e (Sa ltin , 19
.
due o
t Ex erc ise & Tra
spo nse o
inin g
t an inc rea se ,n
h
• the ma xim a\
13 1

str ok e
a,<imal he ar t rat e de •
t
69 ) because1t97e3m cli ne s
• Ac tivi ty lev els : an .
slightly with 1ra1nI ) Ag ain the sa me
av era ge female is · · ng (Po llo ck, ge nd et
we ll con dit ion ed wh less active and less . . •• al lev els of e,<erc•
en compared to her male coun dif fer en ce s ex ist in sp on se to ma xim 1ses.
ter part. re
Th e low er stroke
volume in the trained RE DI ST RI BU TIO N
ma inl y du e to the endurance athlete is OF BL OO D FL OW
ir increased ventricular cavity wh
the filling of lar ge r ich helps in . 85 % of the ca rd
blo od volume du ou nn g resting co nd itio ns a b ou t 80 to
· iac
res ult in an increa ring diastole which ds t~e vis ce ra l or ga
sed str ok e volume. may output 1s dir ec ted tow ns . Th e re ma ini ng
before, an increased Secondly, as discusse ard flo w is dir ec ted tow
myocardial contractilit d ar ds th e mu se es
program results in y following a training 15 % to 20 % o f th e blo o I .
an fr,creased stroke However, du rin g sub
al. , 19 79 ). volume. (Michielli, et. maxir11al an d ma xim
the ac tiv e mu sc les al lev els of ex er cis
e,

J
de ma nd a gr ea ter
Studies de mo ns tra ox yg en co ns um pti on su pp ly of ox yg en . Th e
te a gre ate r ca rdi ac cif the sk ele tal mu sc
thickness in the ath volume and wall ex erc ise is inc rea se les du rin g ex ha us
let es . Therefore, su d by ~O to 20 tim tiv e
ve ntr icu lar siz e wo ch an increase in the de ma nd is ac co mp es . Su ch an inc re
blo od (increaser! str
uld inc rea se the ca
pa cit y of the ejection lis he d thr ou gh an
inc re as ed ca rd iac
as ed 4
ok e vo lum e) that is of (w hic h res ult s in a ou tp ut
athletes. As the sp rin demonstrated in the gre ate r blo od su pp
ter s have a sm all er the blood flo w fro m ly) an d re dis tri bu
he art size and volum the ina cti ve are as tow tio n o1
the ov era ll ca pa cit y e, Th e fac tor s tha t inc ar ds the ac tiv e mu
to pu mp blo od (lo we rea se the ma xim a\ sc \es .
when compared to en r stroke volume) is les ca rd iac ou tpu t is
durance athletes. (Ba s dis cu ss ed . Th e pro a\r ea dY
r-Shlomo, et. al., 1982 ce ss tt:lat he lps in
). flo w fro m the ina th e re dis tri bu tio n
cti ve ar ea s to wa ot b\ oo d
During Su bm ax im rd s th e ac tiv e ar
al Exercise me nti on ed be low : ea s ar e
Fo l/o win g tra ini ng , • Re fle x va so dil ati
the str ok e vo lum e on of the ar ter io\
su bm ax im al ex erc inc rea se s, du rin g a es wh ich su pp \y
ise at a giv en wo rkl the ac tiv e sk ele tal bl oo d to
Co he n, 1975). Th e oa d. (Fox, Kenzie an d ml'..iscles. Th is re
rea so n for su ch an su lts in a gr ea te
inc rea se is the sa me as su pp ly to ac tiv e sk r b\ oo d
me nti on ed ea rlie r ele tal mu sc les .
i.e ., the inc rea se d
inc rea se d my oc ard ve ntr icu lar siz e an • Reflex_ va so co ns
ial co ntr ac tili ty. Th d an tri cti on of th e ar te
the prime co mp on en e str ok e vo lum e is to the inactive areas. rio les wh ich su pp
on e of ly bl oo d
ts of the ae rob ic sy
ste m. At a giv en wo This re
sults in re du ce d b\ oo
load sa y 50 % of V0
ma x, fem ale s ten d rk the inactive areas. d su pp \y to
ou tpu t, str ok e volum
2 to ha ve a low er ca rdi
e an d ox yg en co ns ac
um pti on an d sli gh • Increased metabolism
higher heart rat e tha tly ca us es an in cr ea se
n their ma le co un ter accumulation, local in la ct ic ac id ,
pa rt. temperature, CO
Such local changes 2 an d ox yg en de fic it.
Du rin g Maximal Ex within the m us cle s
ercise tri gg er va so di \a tio n
through autoregulatio
n, th er eb y in cr ea sin
The maximal str ok e the local capillaries. g th e b\ oo d f\o w to
volume is inc rea se d
Su ch inc re as es ar fol low ing tra ini ng .
e du e to the inc rea
myocardial contractili se d ve ntr icl e siz e an d
ty. Th e gr ea ter ma xim
al ca rdi ac ou tpu t

-~

l
 137

ia/ stro ke ~ J

dec line s
gen der 132
·ise s.
Exer cise Phys iolog y
Cor ona ry Circ ulat ion
133
Exe,c lse & T,aln;ng
Csrr1mvascu1ar Response lo
card iac mus cles demand an
i~
With stre nuo us exe rcis e, the unt of blOOd ejected from the left
[rdia c dem and is satisfied through In other words, the increased amo
incr eas ed sup ply of oxy gen . This first pass from the right ventricle
five ventricle during exercise, should
ring coro nary arte ries i.e., about in the cardiac output clearly
an incr eas ed bloo d flow in the to the lungs. Ther efore , an increase
~_,es. ls. The hea rt norm ally extr acts 70- ase in the pulmonary blood flow. 1'he
time s abo ve the rest ing leve states proportionate incre

I
/Se,

rhe
80% of the oxy gen from
is why an incr eas ed bloo d
the bloo d in the coro nary arte ries
flow tow ards the
nec ess ity. The incr eas ed bloo
d flow in the card
hea
iac
rt
mus
mus
cles
. That
cles is a
take s
pulmonary circulation has to acco
•Bloo d Flow to the Adipose
Tiss ue
modate the entire cardiac output.

(fat) tissue lying beneath the

(Ve tole . Dur ing the ven tricu lar syst ole The blood flow to the adipose
plac e dur ing ven tricu lar dias eys increases significantly durin
g
fd aps es. Foll owi ng train ing,
duri ng skin and surr oun ding the kidn 400% in the blood
the cor ona ry ves sels coll num ber of times. prol ong ed exercise . An incre ase by abou t
ut hea rt bea ts less eath the skin and an increase
of
!, sub max ima / exe rcis e, the
Thi s give s mor e res t to the
hea rt and furt her aids in incr eas ed
eph rine
flow to the adip ose tissu e ben
700 % in the blood flow to the adip ose tissu es around the kidneys
epin

:::
one s
bloo d flow to the car diac mus
e/es . The horm lts are significant as they enhance
coro nary was dem onst rate d. Suc h resu
cau ses vas odil atio n of the acid s from its storage form of tat
and nor epin eph rine whi ch the tran sfer of free fatty
ed cor ona ry bloo d flow . cles specially during prolonged
arte ries help s in an incr eas (trig lyce ride s) to the activ e mus
incr ease utilisation of free fatty
Dur ing exe rcis e. In othe r wor ds, an
istr ibu tion of Blo od Flow rgy occu rs especia\\y during prolonged
Tab le 5.2: Sum mar y of Red acid s or the sup ply of ene \d
free fatty acids utilisation wou
Exe rcis e. dura tion exe rcis e. A grea ter ld he\p in
metabo\ica\ \y whic h wou
Reg ions /Org ans Res t Sub max ima/ Max imal mea n less glyc oge n use d brea kdow n
It may be reca \\ed that
Exe rcis e Exe rcise dela ying the ons et of fatig ue. a fact or
ic acid acc umu latio n,
(ml. min - 1) (ml. min- 1) (ml.m in-') of glyc oge n resu lts in lact
for fatig ue.
' resp ons ible
120 0 4500 12,5 00
(1) Mus cle ........

750
Visceral Blood Flow
(2) Hea rt 250 350
is a greater blood How to the
750 750 During· resting condition, there
(3) Brai n 750
\iver. These organs extracts
visc era suc h as the kidney and
I ~ 500 1500 1900
the circulating blood. The main·
(4) Skin limited amo unt of oxygen from
900 600 is transportation and excretion
(5) Kidn ey 1100 function of this regional blood flow i
, rat~er than the removal oi C<u
140 0 1100 600 of the metabolic waste products
(6) Abd ome n
400 and 0 2 supply.
600 400
(7) Mis cell ane ous d !low to the live:, spleen,
17500 Du;ing strenuous exercise the bloo
9500 reduced by upto 80 Vo. Th,s l's
stomach intestine and kidneys is
580 0
Total Car diac Out put
•
sympathetic nerves on th~ b\o :d
probably' caused by the role ot
constncts t e
\ in these organs. 1hese nerves,
Pulmonary Blood Flow ~~: :;~e :~~ fs~ h;re by, lesser
blood flow to thes areas occu1.
ia

eas ed blood flow to the lungs.

During exercise, there is an incr
g increased in the cardiac output.
This is fallowed by a correspondin "'

•
'• .;;,
 I
134 Exercise Physio logy
Ca rdiovasc u/ar Respo nse to Exerci se &
However, while exercising for longer duration Trainin g
in the heat, the . incre ases
visceral flow is drastically reduced, sometimes . blood tloW
D unng a submaximal exercise, the skin d ne
to about 113rd ThiS is 0
of the resting value, with a corresponding increa about four to seven times above the resting value
se in oxygen · s.) rid therebY
extraction. Such a change results in the widen in order to transfer the excess heat (Ander~o n 1968 a • 136
ing of the arteri o- · ta1rnng
· · the ' waver, thiS 15
venous oxygen difference (a-VO diff.) (Rowe main internal core body temp erature. Ho • e
2 ll, 1986 and Wade, . The actr..t
1962). The excretory function of the kidneys is not the case during prolonged strenu ous exerc ise.
reduced resulting ome of the ret
in an increase in the serum concentration muscles demand a greater blood flow, th erefo
of urea especially re, ; e musc les br·
observed during the mara thon race. The drasti increased skin blood flow is shifte d towar d~ th
c reduction (due e ac iv
to exposure to heat stress) in the renal blood (Rowell, 1969). b\!
flow at times leads . . . of the blood f\oW to Ci
to pathological conse quenc es including renal The hypothalamus helps in redist ributio
damage.
With prolo nged durat ion exercise, the liver the skin to remove excess heat. Dun~ ·
n .
erc,se the •in creas ed d
can function with g ex 'h otha\ arnus
only 20% of its norm al blood flow. Altho ugh, temperature of the circulating blood stimu lates th
the liver and the . . . e yp t·rnu\ ated t
h
gut norm ally receiv e aroun d 1/4th of the total while passing through 1t. The hypot a Iam us is also
. .
s1
h at
cardia c outpu t of by the increased skin temp eratu re d unng • xerc1se in e • The
5 L.min-1, only 10-25 % of the availa ble oxyge e
n is extra cted by · ·
hypothalamus then stimu lates the nerve s to the b\oo d ves se\s
them from the blood . The exten t of vasoc . Thes e nerve s re \ax
onstr iction to these of the skin throu gh the mequ lla of the brain
organ s depe nds on the sever ity of exerc ise .
in a given individual the smoo th musc les lining the blood vess I whic h caus e
(Rowell, 1969). es

"~
vasodilation thus result ing in an incre ased
blood flow.
The exten t of the circul ation to the intern
al organ s depen ds Cereb ral Blood Flow
on the athle te's capa city and how much
durin g comp etitio n.
strain he under goes
Blood flow to the brain is influe nced by chan
@·
ges in the mean
syste mic bi°ood press ure. Durin g mode rate
The proba ble facto rs behin d this mech endu rance exerc ise,
nerve reflex path origin ating iri the activ
recep tors in these musc les may be stimu
anism may be due
e musc les. Certa in
the systo lic blood press ure progr essiv ely
.
is a little change in the diasto lic press ure, .
incre ases and there
.
which tends to_ incre ase
lated by a chem ical, the cereb ral blood flow. Wher eas, durin g
for e.g., lactic acid, the meta bolic end exha ustiv e exerc ise _in
produ cts of stren ous extre me heat the systo lic blood press ure ~··~ .~
exerc ise. Howe ver, it need s furthe r confi starts decre asing whic h
rmati on (Row ell, 1969) . is assoc iated with a reduc ed cereb ral blood
flow. This may resu\ t
Skin Blood Flow in the impa irmen t of cons cious ness : The
subie ct may beco me
confu sed or may comm it techn ica\ ~rror
Skin blood flow is a/so referr ed to as the s (e.g. , the mara thon -·~ . '
cutan eous blood runne r who turns in the wron g direc tion on
flow. Durin g restin g cond itions in a warm enter ing the stadi um),
envir onme nt, there is a and is more prone to injury .
, rise in the skin b/Jod flow abou t 5 to 6
1-.min.-1 The purpo se of
5uch local blood flow is to carry away t 1e exces If the blood flow is redu c~d to the
m~to r corte x and
s heat forme d
and not for the trans porta tion uf CO and cereb ellum , it may resul t in the deter iorat
2 0 2
• As in the case of ion of coor dina tion and
the visce ral blood flow, only a smal l amou postu r?I contr ol with an ineffi cient , stag
nt of oxyg en is gerin g gait prog ress ,ng
extra cted from the circu lating blood to
the skin. to final colla pse.

• • I .,
I

~_\\-,
'-r (
,:
I ':,

\;/.,..,
.:
l
 r,::,_

.~ 136 , n
Exercise & Trainmg
&et cise Phys iolog y C.rdlovascu/ar Response to,
-~ us sel -Th e arteriolar
the rapi d reco very as the veno diam eter ot the blCICld Ves
Sup ine lyin g may ass ist in sure is requ ired in the fc)
the neural, horm onal and
ret~ rn is enh_ ance d and a lowe
r blOOd pres diam eter is influ ence d Illy
ity of the eter of.the blood vessel
con trary , ther e is a prob abil chemical factors. Whe n the diam
bra, n perf usio n. On the t duri ng exer cise . Such ocon stric tion) , there is an increase in the
ng con stan decr ease s (vas
-~ bloo d flow to the brai n rem aini muc h sels. with sma ller diameter
t exe rcis es whe re ther e is not resis tanc e to flow. Blomd. v.es.
cas es may be evid ent in ligh bloo d pres sure . will have an.increas.ed •frict ion with mreater port ion ot the
of an incr eas e in sys tem ic
the vessels-When the blood
blood comingiin contactiwith
in diameter, the resistance
.~ Hem ody nam ics vess els (vas odila te) incre ase
to flow decr ease s.
redi strib utio n of the bloo d flow
Afte r hav ing disc uss ed the phy sica l
ism , we will be disc uss ing the BLO OD PRE SSt !lRE
and its und erly ing mec han ed hem ody nam ics. bloo d on the wal \aat the bloo
d
flow , a stud y call The pres sure -exe rted by the
law s that con trol the bloo d uss ing is -. It has two limit s i.e., the
ic fact ors, we wou ld be disc \tes sels is calle d bloo d pres
sure
Two imp orta nt hem ody nam the resi stan ce pressure and :the lowe r limit
calle d
ssu re and incr eas e in upp er limit calle d sys tolic
an incr eas e in the bloo d pre flow and card iac . Sys toli c pres sure . is reco rded whe n
thes e fact ors to bloo d the dias tolic pressure
to flow. The rela tion ship of the arte ries dur ing ven
tricu lar
out put is give n belo w: the bloo d is ejec ted into is obta ined whe n
). The dias tolic pres sure
con trac tion s (sys tole rela xatio n
arte ries duri ng ven tricu lar
Me an Blo od Pre ssu re (P) the bloo d drai ns from the
Car diac out put (Q) = Res ista nce (R) (dia stole ).
mm
sure rang!:!s from 110 -125
In an adu lt, the syst olic pres Hg. A bloo d
or P= Ox R rang es from 65-S 0mm
Hg and the dias tolic pres sure , seve ral
is con side red norm al. How ever
or R = P/Q pres sure of 120 /80 mm Hg
rcis e, and dise ase atte ct
tion s, exe
fact ors like age , sex , emo
blood pressure.
Res ista nce to Blo od Flo w
rence between the systo\ic
also referred as total peripheral The pulse pressure is the diffe
Res ista nce to Blo od Flo w is mean arteria\ pressure is the
the friction between the blood
and and the diastolic pressure. The
resistan_ce. This is cau sed by of the pu\se pressure.
With increas ing frict ion, there is an diastolic pressure plus one third
I wal ls of the blo od ves sels . dep end s
cula r frict ion, 1/3 Pu\se Pressure
inc rea se in resistance to flow
. The vas PMean = Diastolic Pressure +
cited below:
upo n few fac tors which are ECTING BLOQOJPRESSURE
' nt. CIRCULATORY FACTORS AFF
~-
is related to the red cell cou
(a) Blo od Viscosity - It gre ater sure occurs due to the change
s
eases, it causes a The changes in the blood pres
t3 When the viscosity ofb too d incr
the blood vessels and as a in the following circulatory para
meters:
fric tion with in the waits of
of blood also increases. An increased cardiac output wm
t:, res ult the res ista nce to flow • Incr eas ed cardiac output:
arteries which wi\\ increase the
- With incr eas e in the length
of incr eas e the blood flow in the

,
r, (b) Blo od Vessel'~ len gth
the blo od ves sel , the sur fac
inc rea ses the reb y inc rea sin
e in con tac t with the blo od
g the res ista nce .
pre ssu re with in the walls of
the arteries.
\
 I

138
Exe rcis e Phy sio log Car d/o vas cut sr Res 139
• Siz e of the blo od ves y pon se to Exe rcis e
& Tra inin g
sel s: Th e res ista nce posture and the activit
will inc rea se wit h a to the blo od flow
dec rea se in the siz y is sto pp ed imm ed iat
(va soc ons tric tion ). e of the blo od ves sel
s of blood in the dilated ely . Pooling r
Th e hea rt has to for blood ve ssl es of the
thr oug h tne se sm aU cef ully pum p the blo
od occur (Venous Pooling). leg mu scl es 1
ves sel s, the reb y inc Following exercise, as
pre ssu re.. However rea sin g the blo od return towards the he the venous
, wit h an increase in the art de cre as es , the re
ves sel s (va sod ilat ion size of the blood in the cardiac output as is a de cre as e
the reb y ,reducing the ) the resistance to flow well. As a result, the blo
blood pressure. will decrease falls to a great extent. od pre ssu re
Such a dra stic pre ssu
the blo od flo w to re ma y red uc e
• Blood Volume: Wit h the bra in res ult ing
larger volumes of blood, consciousness. In ord in \co sin g
will increase an d with the blood pressure er to av oid su ch a
smaller volumes it wil intensity of exe rci se sit ua tio n, the
l decrease. sh ou ld be de cre as ed
aft er the exe rci se is for so me tim e
. However, oth er fac over. Th is he lps in the
tor s discussed earlie of the blo od flo w fro red ist rib uti on
mf lue nce the blo od r (age, sex etc.) als o m the ac tiv e are as
pre ssu re. While ob ser tow ard s ce ntr al
response, the sys tol vin g the exercise circulation.
ic an d the diastolic
tre ate d se pa rat ely be pre ssu re should be
ca us e the y reveal dif Blo od Pre ss ure Re
ferent changes. sp on se to Tra ini ng
BL OO D PR ES SU RE En du ran ce tra ini ng ha
RE SP ON SE TO EX ER s pro ve d a fav ou rab
CIS E pressure esp eci ally in le eff ec t on b\o od

~;
• With lon g du rat ion ae the eld erl y as rep ort
rob ic exercise, the sys (1986). The following ed by Ha gb erg Se als
tolic pre ssu re are the eff ec ts of tra ini ,
inc rea se s pa ral lel ly ng on b\o od pre ss ure
wit h an inc rea se in • A low er sys tol ic an :
exe rci se. Th e dia sto the int en sity of d dia sto lic pre ss ure
lic pre ssu re do es no is ob se rve d in the
t cha ng e much. ph ysi ca lly ac tiv e me
• Du rin g sta tic typ e n tha n in the ina cti
of ex erc ise (isometric ve me n.
is an inc rea se in the contraction) there '· 4 • Fo llo win g an en du
sys tol ic as well as dia ran ce tra ini ng pro gra
sto lic pre ssu re. su bje cts , the blo od m for the e\d er\ y
Su ch an inc rea se pe pre ss ure at the sa
rha ps oc cu rs .to inc rea loa d wa s low er wh en me ab so \ut e wo rk
flo w to be co ntr ac tin se the blo od co mp are d to be for e
g mu scl es , tha t ,is ca tra ini ng (K i\b oro ,
ref lec ts ari sin g in ac us ed by ne ura l 1971 ). Co nti nu ou s
tiv e mu scl es t(1Lim;t, tra ini ng pro gra m red
reL al., 19 66 ). an d ex erc ise blo od uc es the res t,n g
• Dy na mi c mu sc ula pre ss ure in su ch me
r wo rk es pe cia lly wit 19 71 ) an d wo me n (K n (P o\\ oc k, et. a\. ,
wa ist lev el ca us es a h arm s ab ov e the ilb orn an d As t ran d,
gre ate r inc rea se in the 19 71 ).
ab ov e the no rm al blo od pre ssu re • Po st co ron ary
va lue s. Su ch typ e pa tie nts wi th hig h
of wo rk sh ou ld be blo od pr es su re ca
av oid ed by a he art im pro ve the ir blo od n
pa tie nt. Th e sm all er pre ss ure wi th 3 to
va sc ula r be d in 8 mo nth s of ae ro bic
the sm all er mu sc les tra ini ng .
(ar ms ) tha t are ex erc
an inc rea se d res ist isin g, cre ate s
an ce to the blo od flow • Pa ffe n Ba rge r et. a\.
the blo od pre ss ure , tha t inc rea se s ,.(1 98 3) rep ort s a
(St ein be rg, As tra nd 1.3 fo\ d gr ea ter ris
et. al. , 19 67 ). of de ve lop ing hig h k
blo od pre ss ure (h
• So on aft er the yp er ten sio n) in me
co mp let ion of an ex wh o ex pe nd s les s n
ha us tiv e ex erc ise , tha n 20 00 KC al. pe
the re is a sig nif ica r we ek tha n th os
nt fal l in the sy sto lic wh o ex pe nd 20 00 e
pre ss ure . Th is is K. Ca l. or mo re pe
r we ek .
cle arl y ob se rve d wh
en a su bje ct ex erc ise • Su bje _c ts wi th
s in a sta nd ing hig h blo od pr es
su re ar e sig niH
be ne f ,tte d by a sc ca n\ \v
ien tifi ca \\y p\a nn
ed an d co ns ,s\ en
t
4
 13 9

Po ol in g
us e/ es
14 0 Ph ys iol og y & Training 14 1
ve no us .. e
Ex er cis to Exercise
lar Re sp on se
et. al 1 Ca rdi ov as cu rate and the
•c re as e • g pr og ra m (M an n d1t1on, following . creased heart
tra •in in
., 9~9). In ad e •
results in a de Ho\\y, 19 87 ).
es su re n in is om et ri a period of 5
to C1rcu1t training ll (Harris and
a pa rti ci pa tio c1 se ~v er pressure as we
/ed uc e we re d th e bl oo ~ e~er e hy pe rtensive resting diastolic
, 8 we ek s lo p es su re ,n th
lic
bs in g ct of t • . e sy st ol ic an d the diasto TH E BL OO D
m en . Th e ef fe rarn,ng onpethrte su bj ec ts than
who lty in
• ns iv e action and is sa ich
'1,. th e ea te r in th e hy flu id of ~lkaline re wh
pr es su re ,s grrange d is a red litres o1 blood
ar e in no rm al The bl oo ains about 5 ...

t of an adult cont ight. The blood and the Iymp,,

tim e
sy st ol ic and tas~e. The body l body we
tio n tra in in g, th e of the to ta
ent of the orga
nis m.
en du ra nc e t 11 mm.Hg weighs 11 3rd
tra / • Fo llo w in g an av er ag e ab ou t ·t t h •internal environm
pr es su re re du ce on an fo r di as to lic cons I u e t e
di as to hc d 8 m m . Hg
st ol ic pr es su re an , so m e studies th e Bl oo d
fo r th e sy n th e co nt ra ry Fu nc tio ns of
to n, 19 91 ). O oo d pr es su re
in
ludes :
pr es su re (T ip re du ct io n in bl of the blood inc
gn ifi ca nt , 19 80 ). The functions
re po rt no si la eu an d De try to the \ungs an
d
su bj ec ts (D ep m the tissues
hy pe rte ns iv e in in g pr og ra m an sp or ta tion of Co 2 fro ;su es
po d ne fit s of th e tra (a) Tr
the lungs to th
e ti;:
se d on th e be iv e subjects ox yg en from to
~Is, Ho we ve r, ba th e hy pe rte ns herals tissues
th e bl oo d pr es su re in pe rts to de sig n et ab ol ic wa st es from perip
re : in re du ci ng ex m
g in he lp in g th e fit ne ss fo r th e (b) Carrying cretion (Kidne
ys etc.).
ur ag in
ng pr og ra m th e sites of ex
le se em s en co
is te r su
an d ad m ine su bj ec ts .
ita bl e tr ai ni
ut io n of nu tri en ts absorb
ed in the diges
or
ti'Je tract
\h e \i'Jer.
hy pe rte ns iv (c) Di st rib adipose tissue
th e m st or ag e in
in lo we rin g or released fro body.
l fa ct or s th at he lp ts balance in the
Th e ph ys io
lo gi ca
pe rte ns iv e
su bj ec
la tin g th e ac id ba se (pH)
su re in th e hy (d) Re gu sse\s at iniul)'
re st in g bl oo d pr es : h damaged 'Je
tio ne d be lo w id lo ss es th ro ug in the 'Jesse\
in in g ar e m en (e) Re st ric ts flu br ea ks
fo llo w in g tra . tti ng ab ilit y se al s the d 'J0lume
rin g Exercise sit e. Th e clo
ge s in the bl oo
n O cc ur in g du ev en tin g ch an cu \a to ry
(a) Vasodilatio n eb y pr
dy Compositio wa lls , th er d cir
d pr es su re an
ie ta ry Pa tte rn and·the Bo m ay af fe ct th e bl oo
the D th at
(b) C ha ng es in fu nc tio ns .
la r Fitness th e bo dy
C ar di ov as cu ni sm : Th e bl
oo d de ie nd s
(c) Im pr ov ed De fe ns iv e M ec ha ns pp rts th e
n (f) Th e bl oo d tra
R en al Fu nc tio ns an d pa th og en s. to co m ba t
(d) Im pr ov ed ag ai ns t to xi su es
odium Excret
ion pe rip he rg \s tis
d Fl ui d an d S ite bl oo d ce lls to th e tib od ies which
t In cr ea se wh
is an d deliver
s an
(e) C on se qu en in fe ct io ns or
re m ov e de br
di ng or ga ni sm s or
fluence at at ta ck in va
ympathetic In pr ot ei ns th od uc ed
(f) R ed uc ed S g ar e sp ec ia l s th e to xi ns pr
od Vo_lume th
rough Sweatin fo re ig n co m po un ds . \t al so re ce ive
ers th em
e B lo tivity an d de\\v

~·1~
e in th m et ab ol ic ac
(g) D ec re as la m in es /R en
in
by in fe ct io n, in iu ry or et e th em .
tr es s/ C at ec ho tiv at e or ex cr
e d ia te d S an d ki dn ey , w hi ch in ac
M er
(h) E xe rc is e to th e liv
~:.~ Reduc tio n do not
· re si st an ce type exercise
• C hr on ic
ex po su re to ne, Fleck, Trip
lett
st in g bl oo d pressure (Sto
re
in cr ea se th e
er 1991 ).
an d K ra em
 I

'\43
Exercise & Training '\44
Exercise Physiology Cardiovascular Response to lasma water out of t_he ·~
142 shitting of the p . the liquid portion P..n i.ncrec
Rcgutntion of Body Temperature: The blood absorbs the volume is caused by. haemoconcentrat1on, . components phenomena~
(g) hear nnd redistributes ,t. It carries away the heat blood. In other words, ,n d the cellular and protein d the blood
(.a~ P.. grel
produced U}' the active skeletal muscles and other of the blood is reduced a~·on of the blood volume a: shifting of
a rnaior cm
tissues. The excess body heat is lost through the surface represents a greater frac it d In haemodilution , _t e the blood
oncemra e • .. ces into ·~ tne p\asm
of the skin. When the body temperature is low, warm becomes more c the interst1t1al spa d protein
d out increases)
blood is redirected towards the important temperature tHe plasma water from the various cellular an
sensitive organs. occurs. In such ~aseds, These components are sprea b\ood.
et dilute • • f \asma water.
From exercise point of view, the transportation, component s g lb)OU
temperature regulation and the acid base balance is through a greater volume o. P h blood volume decreases normonE
of prime importance. . . the bicycle, t e w·,th
During exercise in . an untrained subject. to ret~\~
· occurs) m .
(haemoconcen trat1on . dur·,ng cycling, there will be a Hae
EFFECT OF EXERCISE AND TRAINING ON BLOOD
•t· of exercise lasma volume reduces
increasing intens1 ,es . Th
durat\<!
greater haemoconcen trat1on. e pl so'10 decrease in the
The blood of all the subjects exposed to exercise and training o,0 which revea s a \10\U"j
maximally by about 5 t ga0). The
Rogers Joos e, 1
1 ,

does not respond exactly in a similar manner. As the metabolic total blood volume (s enay, ' f n ettect during and~
rate incrP.ases during exercise, the functions of the blood significance behind such haemoconc_e ntra ,o
-~
becomes more important for the enhancement of performance. bicycle exercise is probably as follows. .
. pression at vems the
We shall be discussing the various changes that take place
• Due to muscular contraction, the com . the ca i\\aries the
within the blood in order to meet these increased demands. the c;i\\aries
occur. This leads to a less amount of blood lea~in~
The Effect of Exercise and Training on Blood Volume than that enters throught the arteries. Finally, w,
. . t
'° th
ome p\asma au o,
t , the
the pressure 1s increased that orces s
.
The effect of exercise on the blood volume depends on the capillaries to the tissue spaces.
type and intensity of exercise, trained state of an athlete and
• With increasing intenstrties -0i exercise, a great~r
'
acclimatisatio n to heat. Fol/owing an endurance training, the
accumulation of lactic acid and the production of other metabo\tc
resting blood volume increases approximatel y by 8%. Such an
end products (potassium, phosphate) occur. These take out
increase is greater with greater intensity of training. Such an
plasma water from the capillaries.
increase in the blood volume is caused by a 12% increase in ,.._,,
~ .
,~
the plasma volume and a slight increase in the red blood cells On the contrary, the blood vohame and the plasma volume
volume (Convertino et. al., 1980). varies to a great extent whHe running. At times, a
haemoconce ntration may occur or haemodi\utio n may resu\t and
' ''-
During strenuous exercise in a hot climate, the sweating rate
at times there may be no changes at a\\. ,he probab\e reason
is from 1 to > 2 litres per hour. This increased sweating may
behind ~uch difference in running and cyc\ing is the sma\\er
reduce the total blood volume by 3% or more (Harrison, 1985).
muscle mass used during cyc\ing. This as mentioned before
An increase in the blood volume is referred as causes a greater compression of veins than in running. As a
Haemodilution; whereas a reduction in the blood volume is result, the plasma water is forced out of the capi\\aries. Another
referred as Haemoconcentration.• A decrease in the blood reason is the accumulatio n of the \acttc acid which is ear\ier in
cycling than in running (Senay, et. a\., 980).
~i

(&,
.<
 43

e
_}~
14 4
n Ph ys ic ,~'.Y
. &e rc is &
Is • cr ea se - in th :e Pl as m a v
ol um e is ca
us ed by two '
C rdIO VtJscutar Re
sp on se to
i
&;;Jl9,c se & Training 14 5
A n tn a
ntrar
f Ph en om en on
:
.
. oun-ng exercise, when haemocon. ce. IOf\ occurs, theun RB Cs
te nt io no fp la sm a 1s re as e W ith h
n, the RB Cs co t
w,11
(a ) A gr ea te
r re m ;,; ~ten
•: count wi ll inc d a~mod1 lut1o sed
ic co nc ~~ ~: ::~ ~~ ~~ ::~ a. ea se . Ac tu ~II
ex ec ,s e wi th increaer
mb ol
or to os m ot t· de cr . Y, ur in g in the total nu
rib ut s: flL ';
e is no change
a m aj or co nt pr ot e· in iinere.a:se
-
re ' aJ•so . er ter the
th e pl as m a•
11
'd IC
'>rnO . pr es.su . haemoco~c~ ntrat1 on th leak ou t or en
•· wnt
ou '"'-fl
i=a~
1n the e cells cannot
as a re su lt
rn or e am
' u, 1s re ta in ed
~s . ~h is is because, thes em oc on ce ntr ation occurs in
• cr ea se s, RB The ha
in a great extent. od, which shall
increase
bl oo d. cap1llan~s to Cs per unit of blo to be a
of anti-diuretic re as e the RB . "T his pr ov es
er a is an in cr ea se rel ease the kidneys order to inc
rry in g ca pa cit y of the blood rform an ce .
er ci se lft s ca us es t~e ~~ygen ca s endurance pe
(b) D urin g ex st er on e. llh es e ho rm oi ,epl as m a. t co nt ribution toward
d al do bl oo d ni fic an re ase in
rm on e an ea se s th e . sig e may be an inc
ho er Which in cr '
e training, ther e is
to re ta in w at su bj ec ts durin
Qi long Followi ng en du ra nc the pla sm a vo lum
d in t.a in ed · we ve r, an increase in the blo od
n is ot >s er ve
ct io n of th is blO.Od the RBCs coun
t. Ho
ter fluid traction
of
H ae m od ilu tio t hu m id cl im at es . A fra m cl es ,
us hi gh er th at causes a grea pla sm a vo lum e reduces
ci se in ho m th e activ.e much ase in the
du ra tio n ex er in , aw ay Im 1991 ). An incre sistance to flow
of

:::;:
to th e sk e. (Green et. al., lting in less re
vo ·tu m e is sh
ift ed as m a vo lu m e bl oo d; re su an ce .,h e
i1t:ui:ss-t#:Je pl th e viscosity
of th durance perfo
rm
sw ea tir rg · re eet sm may aid en of the
an d he av y d is ab le to.,m blood. Such a m ec ha ni r m ov em en t
lu m e of bl oo lps in the easie
hl et e w ith gr re at er vo
es an d th e sk
in th an d viscosity he e capillaries.
Thus, it
A tr ai ne d at ac tiv e m us cl reduced bloo ta nce within th
ds . ot th e ou t m uc h re sis
sit y en ha nc es the
or y de m an bl oo d wi th ced blood visco
th e- ci rc ul at d su bj ec ts . tione d th at re du
nce ercise.
ex
th e un tr ai ne t sh ift s less could be men during endura
in ed su bj ec pp ly to th e active tissues
ci se : th e tra a un tra in ed ox yg en su concentration
an da rd ex er an Ih ease the RBCs
D ur in g a· st to th e sk in ve ss el s th of lo si ni oc on ce nt ra tio n may incr rit by 40 to 50% also
th ei r bl oo d tte r ca pa bl e Ha em in the haemat
oc
vo lu m e o f ai ne d ar e be . An in cr ea se ay not change
.
re as on be in g th e tr
·' by 20 to 25 % Cs content m
su bj ec t. T he ea t,r :rg t th e to ta l nu m be r ot RB l vo lum e ot b\oo d
ug hi sw • _. oc cu rs . Bu en tage of the tota
at th ro ro bi c th e pe rc d by
he flu en ce th e ae Th e ha em at
oc rit is ocrit is measu
re
vo lu m e m ay in . Th e haemat
n in th e bl oo d
th e st ro ke v0 lu m e ai ns th e to ta l RBCs e RBCs sett\e
down
A n y al te ra tio e to a al te ra tio n in th at co nt
m pl e in a tube un
til th
b\ood
rs du e ox yg en a bl oo d sa oi th e
ca pa ci ty . Th
is oc cu
th at fin al ly
af fe ct s th ce nt rif ug in g eans th at 40%
ia c ou tp ut m . A ha em at oc rit of 40 m
al ca rd at th e bo tto
a n d m ax im 0 max. e RB Cs .
sp or t ca pa ci ty o r \l 2 co ns tit ut es th e plasma vo\u
me
tr an at oc rit , wh en th
in th e ha em tion or
n RB-C's An y de cr ea se RBCs produc
d Tr :a in in go ld re ve al a de cr ea se d yg en .
rc is e aR re d, w ou
reduce the ox
E ff ec t o f E xe ood cell is also
is no t m ea su ru ct io n. Th is may
nstituent of bl d RBC s de st
a c0 an in cr ea se
'

c e ll (R B C s) , ve nuclei. Its oo d.
R e d b lo o d cell do not ha ci ty of the bl
I
ti>lood yi ng ca pa ect
e· r:e d
oglobin (Hb)
. ca rr a tra in ed ~ub\
ro cy te s. Th t called haem m ea su re d in
ca lle d E ry th n pi gm en W he n th e pl
as m a vo lu m e is
a\ter exerc\s~\
· n~ \
nt ai ns a pr ot ei
d. The Hb co
ntains rin g re st or
cy to pl as m co ce to th e bloo to he at du oc n
\n th e haema:
\
an ygen. irn at is ed
co lo ur ap pe ar
tation of ox w ho is ac c\ ,h e de cr ea se
H b gi ve s re d
t.
is ttre:transpor ev id en
RBCs is
t· fu nc tio n de fic ie nc y of
im po rt an
ir o n (F e) ; its
 14 6
ma~• oc cu r
th ro h an Exercise Ph
benetic1a l factorug. in cr ea se in
the plasma
ys io lo gy
s on se to . & Tr ai ni ng "\ 47
volume whi ca rd io va sc £J<erc1 58
ch is a ul ar Ae P
VJhe
bl oo d vonlu ~n un tr ai ne d sub1 ouring exer ise, the de gr ee of h a e rn o c~ ce n tr a ti o n o r
c n
t1on. T h e H b w i\\
m e de cr ea ec . es the Hb
se s. t pe rf or m s bi
cycle ex er haemod1l. u~. determ1n con centra·t . .
ci se his 1onhaemocon . h
In flu en ce increase with centrat1on an d f al\s w1 haemod1\ut1o n.
o f P la sm a d ance trai . f R B C S s\
V ol um e on Following en ning, the pr ig ht \y
, . A s m en V02 Max. increases. In ur . also a sl ig o_ duct1~:: in th
tio ne d be fo turn, there ,s ht ,ncre e to ta \ H b .
,o llo w ,n g en re . an in cr
du ra nc e tra ea se in th · 1asma vo th e H b a\ so
a re su lt, th in in g in cr ea ~ pl as m a With an incr
er e is an in se s the bloo vo lu m e ease inm \ume, g e ts d i\u te
am ou nt of
bl oo d en te
cr ea se in the
st ro ke volu
d vo lu m e to
o. A s oue to t h.,s reason, so Pe athletes in sp ite o f · a n o rm a \ Hd .
b
rir ·J ~he he m e, du e to gr r to b e an em h a vi n g
at m ax im al
le ve l of ex er ar t. M or eo ve
r, as th e he
ea te r ~ yv :l :~ ~ :x ic . su e a ca se ca n b e tr e a te d
h
tr ai ni ng , th ci se do es no ar t ra te ;~ ~ = :f o r fe . d th e \e
er ef or e, an t ch an ge fo w da ve \ o1
in du ce d th in cr ea se in
th e m ax im
llowing en du
ra nc e aldosterone t ns to n o y1s ;~ ~ :~ ;;~ ~ :: s e :~
ro ug h an in al ca rd ia c ou re ur rm a \~ a d th e e
cr ea se d st sodium io . . th xt ra
A n in cr ea
ro ke vo lu m
e.
tp ut is ns a nd w at er in e fo rm of u ri n e .
se d ca rd ia
A low leve
av ai fa bi /it y
of ox yg en
c ou tp ut w
ou ld re fle ct ls of H b.. .d e n o te s a n a e m ia . E n d u ra
n ce a th \e te
th e V 0 m to th e ac tiv an in cr ea se are greater t anaem . th e . s
2 ax . e tis su es ,
th er eb y in d p~one od.b ia a s y lo se ir o n th ro
cr ea si ng faeces, inte ladaer b le e u g h sw e a
O n th e co stinal an d in g , a n d th t,
nt ra ry ; w he of iron (Hay e p o o r a b so t·
(d et ra in in g
oc cu rs ), th
n a tr ai ne
d su bj ec t mes an d L a m a n e a , 1 9 8 9 ) In th e fe m a le r~ ,o n
er e is a re st op s tr ai a n a·d~itiotn f . •
o c c u rs d s, e sp e c, a
w hi ch w ou du ct io n in ni ng u ri n g m e \\ y,
H em m er t
ld de cr ea se
th e V 0 m ax to
th e pl as m a
vo lu m e Approx1ma ealyl olno::go o~ri~:n is n s tr u a t,•o
an d C og ge a gr ea t ex lo st in th e sw e n•
n, 19 86 ). • 2 te nt (C oy le both th e se • a t a n d fa e
, xe s ev er yd c e s in
Effects o f ay .
Exercise T he re fo re ,
an d Training se ve re a n a
on Haemo endurance e m ia m a y
H ae m o g lo globin performance af1ect th e
b in (H b ) is
may d e cr e . A n in te n si V 0 2 _~ax a th
bl oo d cell. a pr ot ei n co a se th e H b ve e n d u ra n nd e
A si ng le re m pl ex foun ce tra1n1ng
ha em og lo bi d bl oo d ce d in the red (F re d ri ck so p ro g ra m
n m ol ec ul es ll contains T h e re fo re , n e t •.a\., 1
. H b about 25 0 a s th e e n d 9 8 3 ).
o f Hb ca n binds with ox million u ra n ce e ve
bi nd with 4 ygen. Every o xy g e n su
can bind with m ol ec ul es molecule p p ly , n e c e n ts re lie s
o f ox ygen. Thus, ea a d m in is te re s s a ry d ie h e a vH y o
up to billion
s of oxygen ch RBCs d to im p ro ta ry m a n n th e
males, th e m ol ec ul es . ve ip u \a ti o n
Hb ranges fro In no rm al he re co m m e n H b concen s h o u \d b
and from 12 m 14.0 to 18 althy d e d d a ily in tr a ti o n in e
to 16.0 gm .0 gms. 100 an d fe m a le ta ke o f ir o a th \e te s .
s.
100 mt.- 1 in ml.- 1
blood of s re sp e ct iv n is 1 0 mg. and 1 'T h e
Hb plays a healthy fem th e d e fi ci e e ly . T h e a 4 m g . fo r m
significant ro ales. n ci e s m a y d e q u a te d ie ta ry a \e s
oxygen carryi le in endura b e co rr e ct ir o n in ta k
ng compoun nce events liquid su p p e d a ft e r a n a ly e a n d
d that is deliv , as it is le m e n ts (C s is b y io n
During exer ered a re d u ct io le m e n t a n d ta b \e t o r
cise there is to the active n in H b o f Sawchuk,
1 9 8 4 ). A p p
being, the R no change tissues. 0 .3 g m s. 1
BCs that co in the total H VO 2 of 1% . 0 0 m L -1 c o ro x im a te \y
during exerci ntains Hb do b. The reas T h u s, if th rr e s p o n d
es not leave on e H b s to a ia \\ in
se, the capillari 1 5 .5 g m . 1 o1 a n e n d u ra
es 0 0 ml.- 1 to n c e a th le
1 4 gm. 10 te fa\\s f ra m
5% d e cr e a se 0 mL-' ,t w
in V 0 m a o u \d c o rr
p e rf o rm a n 2 x w h ic h w o e s p o n d to a
ce . - u \d ti n a \\ y
a tt e c t th e
e n d u ra n c
e