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Journal of Stress Physiology & Biochemistry, Vol. 4, No. 2, 2008, pp. 4! 2". #SSN ""$!08%8 riginal 'e(t )opyright * 2008 +y +-el!Sater

ORIGINAL ARTICLE

EFFECTS OF EXERCISE ON CARDIOVASCULAR DYSFUNCTIONS

INDUCED BY CIGARETTE SMOKING

Khaled A. Abdel-Sater

Department of Physiology, Faculty of Medicine, Al-Azhar University- Assiut Branch- Assiut, Egypt

e-mail: [email protected]

Received April 26, 2008

Abstract – Smoking is knon to adversel! a""ect man! organs and s!stems in h#man, herethe cardiovasc#lar s!stem is one o" the important targets. $oever, the e%act mechanisms b! hichcigarette smoke alters m!ocardial and endothelial cells "#nction and ind#ces cardiovasc#lar

patholog! are not clear. &here are no reports especiall! ith nitric o%ide '()*+, #ric acid andhemod!namics a"ter ac#te e%ercise in smokers #p to date. &his st#d! is designed to investigate therole o" o%idative stress, ()* and #ric acid in the pathoph!siologic mechanisms o" smoking- ind#cedcardiovasc#lar diseases.

0 apparentl! health! s#bects ere st#died. epending on their previo#s ph!sical

conditioning stat#s s#bects ere divided into e/#al "o#r gro#ps 'n10+, ph!sicall! activenonsmokers, ph!sicall! active smokers, sedentar! nonsmokers and sedentar! smokers. %ercisetolerance as eval#ated "or each s#bect b! #sing a r#nning race '3 kilometers+ a"ter a orming #p

period o" 4 min#tes.

&he obtained data revealed that reg#lar e%ercise signi"icantl! decreased the plasmamalonaldeh!de, total cholesterol, 55 and #ric acid levels belo sedentar! levels. re and post race

plasma level o" malonaldeh!de and #ric acid levels ere signi"icantl! increased, hile, plasmagl#tathione and ()* ere decreased in sedentar! smokers than the sedentar! non smokers,

ph!sicall! active smokers and ph!sicall! active non smokers.

&hese "indings point to the role o" ()*, #ric acid and lipid pero%ide in the pathoph!siologicmechanisms o" smoking ind#ced cardiovasc#lar diseases. Sedentar! smokers ma! be at an evengreater risk o" o%idative stress-related cardiovasc#lar diseases. 7inall!, ever! bod! sho#ld incl#de ina reg#lar e%ercise.

ey !ords" #$%A&E''E (M)$*% + EE$(E + #A&D$)A(#U.A& D/(FU*#'$)*(

JOURNAL OF STRESS PHYSIOLOGY BIOCHEMISTRY ol. (o. 2 2008

mailto:[email protected]:[email protected]:[email protected]

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ORIGINAL ARTICLE

EFFECTS OF EXERCISE ON CARDIOVASCULAR

DYSFUNCTIONS INDUCED BY CIGARETTE SMOKING

Khaled A. Abdel-Sater

Department of Physiology, Faculty of Medicine, Al-Azhar University- Assiut Branch- Assiut,

Egypt

e-mail: [email protected]

Received April 26, 2008

Abstract – Smoking is knon to adversel! a""ect man! organs and s!stems in h#man,here the cardiovasc#lar s!stem is one o" the important targets. $oever, the e%actmechanisms b! hich cigarette smoke alters m!ocardial and endothelial cells "#nction andind#ces cardiovasc#lar patholog! are not clear. &here are no reports especiall! ith nitric o%ide'()*+, #ric acid and hemod!namics a"ter ac#te e%ercise in smokers #p to date. &his st#d! isdesigned to investigate the role o" o%idative stress, ()* and #ric acid in the pathoph!siologicmechanisms o" smoking- ind#ced cardiovasc#lar diseases.

0 apparentl! health! s#bects ere st#died. epending on their previo#s ph!sical

conditioning stat#s s#bects ere divided into e/#al "o#r gro#ps 'n10+, ph!sicall! activenonsmokers, ph!sicall! active smokers, sedentar! nonsmokers and sedentar! smokers. %ercisetolerance as eval#ated "or each s#bect b! #sing a r#nning race '3 kilometers+ a"ter a orming#p period o" 4 min#tes.

&he obtained data revealed that reg#lar e%ercise signi"icantl! decreased the plasmamalonaldeh!de, total cholesterol, 55 and #ric acid levels belo sedentar! levels. re and postrace plasma level o" malonaldeh!de and #ric acid levels ere signi"icantl! increased, hile,

plasma gl#tathione and ()* ere decreased in sedentar! smokers than the sedentar! nonsmokers, ph!sicall! active smokers and ph!sicall! active non smokers.

&hese "indings point to the role o" ()*, #ric acid and lipid pero%ide in the pathoph!siologic mechanisms o" smoking ind#ced cardiovasc#lar diseases. Sedentar! smokersma! be at an even greater risk o" o%idative stress-related cardiovasc#lar diseases. 7inall!, ever!

bod! sho#ld incl#de in a reg#lar e%ercise.

ey !ords" #$%A&E''E (M)$*% + EE$(E + #A&D$)A(#U.A& D/(FU*#'$)*(

9igarette smoking is a ell knon risk "actor "or

cardiovasc#lar diseases. &his ma! be res#lt o"

str#ct#ral and "#nctional changes in cardiovasc#lar

and p#lmonar! s!stem '5ope< et al., 2008+. &here is

a mechanistic link beteen increased levels o"

o%idative stress associated ith smoking and the

onset and progression o" cardiovasc#lar diseases

'=loomer et al., 200>+. ?oreover, smokers ere

associated ith decreased o" antio%idant capacit!

'Kemal et al., 2004+. S#pplementation ith

antio%idants can red#ce s!mptoms and indicators o"

o%idative stress as a res#lt o" smoking '@ome

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o%!gen to prod#ce s#pero%ide anion, h!dro%!l

radical and h!drogen pero%ide 'anet et al., 2003+.

&he gas phase contains alk!l and pero%!l t!pe 'r!or

et al., 1BB8+. ;n one p#"" o" cigarette, the smoker is

e%posed to more than 1014 "ree radicals in gas phase

alone, ith addition e%pos#re in the tar phase e/#al to

more than 101> "ree radicals per gram 'r!or and

Stone, 1BB3+.

Smoking is associated ith increased o" lipid,

protein and (A o%idation 'Kirkham et al., 200+.

&he increased risk o" cardiop#lmonar! diseases and

atherosclerosis in cigarette smokers has been

attrib#ted in part to increased o%idation o" lipid and

protein 'Ambrose and =ar#a, 200+. )%idi+.

&he association beteen cigarette smoking andvasc#lar diseases is ell doc#mented, and there is a

general consens#s that it targets the vasc#lar

endothelial cells. $oever, the e%act mechanisms b!

hich cigarette smoke alters endothelial cells

"#nction and ind#ces cardiovasc#lar patholog! are

not clear.

&o m! knoledge, onl! to investigators has

been per"ormed to date to st#d! the combined e""ects

o" cigarette smoking and e%ercise on o%idative stress

'S#rmen-@#r et al., 1BBB and =loomer et al., 200>+.

&hese investigators ere #sed other mode o"

e%ercise, other personal selection and other

methodolog!. &here are no reports especiall! ith

nitric o%ide, #ric acid and hemod!namics a"ter ac#te

e%ercise in smokers #p to date. &here"ore, this st#d!

as designed toC 1+ investigated the e""ects o" single

ac#te e%ercise on hemod!namics and o%idative stress

in smokers, 2+ estimation o" ph!sical and

cardiop#lmonar! "itness 'b! d#ration o" e%ercise and

hemod!namic response+ a"ter ac#te e%ercise in

sedentar! and ph!sicall! active smokers and 3+

estimation o" vasc#lar "itness 'b! ()*, lipid pro"iles,

lipid pero%idation and #ric acid levels+ a"ter ac#te

e%ercise in sedentar! and ph!sicall! active smokers.

SUBJECTS AND METHODS

0 apparentl! health! s#bects ere st#died.

&he! ere selected "or age '20- 26 !ears+, se%

'males+, eight '60->0 kg+ and height '164-1>4 cm+.

All s#bects complete a detailed medical histor!

/#estionnaire and #nderent a ph!sical e%amination

Deight, height, heart rate '$R+, s!stolic blood

press#re 'S=+, diastolic blood press#re '=+ andrespirator! rate 'RR+E. %cl#sion criteria ere the

presence o" cardiac diseases, p#lmonar! diseases,

renal impairment, h!pertension or diabetes

doc#mented "rom medical histor! and F or

e%amination. Additionall!, medical histor! indicated

that participants did not #se medications 'e.g. anti-

in"lammator! or cardiovasc#lar dr#gs+ or n#tritional

s#pplements 'e.g. antio%idants+. &his as an

important consideration, as intake o" antio%idant

agents co#ld have impacted m! o#tcome meas#res.


16

http://ajpheart.physiology.org/cgi/content/full/291/5/H2354?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=1&andorexacttitle=and&titleabstract=smoking++&andorexacttitleabs=and&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&fdate=7/1/1995&tdate=1/31/2007&resourcetype=HWCIT#R27http://ajpheart.physiology.org/cgi/content/full/291/5/H2354?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=1&andorexacttitle=and&titleabstract=smoking++&andorexacttitleabs=and&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&fdate=7/1/1995&tdate=1/31/2007&resourcetype=HWCIT#R27

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?en ere labeled as ph!sicall! active i" the!

e%ercised "or at least 30 min#tes tice eekl! #p to

the level o" d!spnea and seating. &he! ere

sedentar! i" the! not per"orming reg#lar e%ercise

d#ring the prior !ear 'illa- 9aballero et al., 200>+.

;n addition, to /#ali"! "or smoker stat#s, participants

needed to reg#larl! smoke at least "ive cigarettesFda!

"or minim#m o" si% months immediatel! be"ore

e%periment itho#t interr#ption. articipants ere

eligible to be enrolled as nonsmokers onl! i" the! had

not smoked ithin the past !ear '=loomer et al.,

200>+. All s#bect provided both verbal and riting

in"ormed consent prior to participating. epending

on their previo#s ph!sical conditioning stat#s

s#bects ere divided into e/#al "o#r gro#ps 'n10+

as "olloings:

1-@ro#p ;: h!sicall! active nonsmokers.

2-@ro#p ;;: h!sicall! active smokers.

3-@ro#p ;;;: Sedentar! nonsmokers.

-@ro#p ;: Sedentar! smokers.

E!"rc#s" Pr$t$c$% a&' H"($')&a(#c

M"as*r"("&ts+ articipants ere instr#cted not to

per"orm an! activit! d#ring the 8 ho#rs period

preceding the e%periment. (onsmokers ere

instr#cted to avoid smoking locations and direct

contact ith smokers d#ring last 8 ho#rs be"ore the

e%periment '=loomer et al., 200>+. Active smokers

had re"rained "rom smoking "or more than 12 ho#rs

be"ore this st#d! in order to minimi

cholesterol, $5 and 55 cholesterol ere

per"ormed #sing plasma "olloing standard

en

man#"act#rer '=io ?erie#%, 7rance+ '5a#ra et al.,

200>+.

&he meas#rement o" plasma ()* is di""ic#lt

beca#se this radical is poorl! sol#ble in ater and has

a short hal"-li"e '10G60 s+, b#t its hal"-li"e ma! be as

long as min. in the presence o" o%!gen '=akan et

al., 2002+. 7or these reasons, the ()* itsel" can be

determined onl! ith di""ic#lt! and re/#ires the

handling o" radioisotopes. ;n spite o" this, the end

prod#cts o" the phenomena, nitrate and nitrite, are

pre"erentiall! #sed in clinical biochemistr!. lasma

nitrite pl#s nitrate levels ere meas#red ith #se o"

the @riess reagent as described previo#sl! '@reen et

al., 1B82+.

Stat#st#ca% A&a%)s#s $. E!,"r#("&ta% Data

'Iister, 2000++ Statistical anal!sis as done #sing

the comp#ter program 'prism+. &he /#antitative data

ere presented in the "orm o" mean J standard error

'mean J S+. &he signi"icance o" di""erences beteen

mean val#es as determined #sing St#dents L t L test.


1>

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Also correlation coe""icients 'r-val#e+ ere done. A

M0.04 as considered signi"icant "or all anal!ses.

RESULTS

9haracteristics o" s#bects are presented in table

1. &he s#bects o" the "o#r gro#ps ere similar in age,

eight and height. (o other statistical demographic

di""erences ere detected beteen gro#ps. #ration

o" smoking per !ear and n#mber o" cigarettes per da!

ere similar in ph!sicall! active and sedentar!

smokers.

&here ere di""erences in the hemod!namic

response be"ore and a"ter e%ercise among the

s#bects. #ring the e%ercise, s#bects o" gro#p ;, ;;

and ;;; had a longer time on the race, in comparison

to gro#p ; s#bects '16 J 4.4, 21 J 2.3 and 14 J 1.B

min. vers#s B J 1.3 min. respectivel!+. ?ost o"

persons o" gro#p ; are not completed the race. ;n

addition, gro#p ; s#bects had a higher heart rate,

respirator! rate and arterial blood press#re than other

gro#p s#bects. ?ean heart rate as 18.2 J 10 beatF

min. in sedentar! smokers a"ter e%ercise, hereas it

as BB.4 J 8, 114.1 J 6 and 136. J 2.3 in gro#ps ;,

;; and ;;; respectivel! 'table 2+. $eart rate and

s!stolic blood press#re levels ere signi"icantl!

increased a"ter ac#te e%ercise in sedentar!

nonsmokers and sedentar! smokers gro#ps above pre

ac#te e%ercise levels in the same gro#p. &here as a

signi"icant di""erence beteen pre and post

respirator! rates in ph!sicall! active smokers and

sedentar! gro#ps.

Tab%" /+ D"($-ra,0#c c0aract"r#st#cs $. s*b1"cts #& t0" '#.."r"&t -r$*,s+

Gr$*,s

Para("t"rs

Gr$*, I Gr$*, II Gr$*, III Gr$*, IV

(#mber 10 10 10 10

Age '!ear+ 23.6J 1 22.2J 0.1 21.2 J 0.8 23J1

Ieight 'kg+ 62.> J 0.8 68.2J 2 60.3J 4 63.2J 0.4

$eight 'cm+ 16BJ 0.8 16>.J 0.4 162.2J 2 161.1J

#ration o" smoking '!ear+ >. J1.1 (A 6.6 J1 (A

(#mber o" cigarettes 'da!+ 12J 4 (A 8J2 (A

ach val#e represents the mean J S. (A, not applicable.

(o statistical di""erences ere noted beteen gro#ps "or an! o" the above variables 'pM 04+.

Tab%" 2+ H"($')&a(#c r"s,$&s" t$ ac*t" "!"rc#s" #& ,0)s#ca%%) act#3" a&' s"'"&tar) s($4"rs a&'

&$&s($4"rs+

Gr$*,s

Para("t"rs

Gr$*, I Gr$*, II Gr$*, III Gr$*, IV

Pr"

rac"

P$st

rac"

Pr"

rac"

P$st

rac"

Pr" rac" P$st rac" Pr" rac" P$st rac"

D*rat#$& $.

"!"rc#s" 5(#&616 J 4.4 21 J 2.3 14 J 1.B B J 1.3

H"art rat"

5b"ats7 (#&*t" >2.3 J>.1

BB.4 J

8.0≠N 80.6 J4.4

114.1 J6.0O 84 J8.0P

136. J2.3O 102JB.>OP

18.2 J

10.0O≠

S)st$%#c b%$$'

,r"ss*r"

5((H-6

110.3 J

B.0

13.4 J

10.2≠N122.2 J

11.B

143.4 J

14.4O110.B

J18.0P160.8 J

14.>O13.1 J

1>.OP180 J

13.O≠

D#ast$%#c b%$$'

,r"ss*r"

5((H-6

>.2 J8.1

>8.B J

10.0≠N>0.6 J10.6

84.1J18.BO 80.6 J 12

B0 J18.6O

84. J1.O

100.1 J

12.2O≠

R"s,#rat$r) rat"

5b"ats7 (#&*t"612.0J2.0

24.6 J

2.0≠N1.0J3.0P

28.B J2.0O

14.0 J4.0P

30.2 J2.0O

18.0 J3.0OP

38.> J

2.0O≠

ach val#e represents the mean J S.

8 Signi"icantl! di""erent "rom gro#p ;.

≠

Signi"icantl! di""erent "rom gro#p ;;.9 Signi"icantl! di""erent "rom gro#p ;;;.

: Signi"icantl! di""erent "rom post race in the same gro#p.


18

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Fig. (5): Plasma triglyceridelevels (mg %) (mean ± SE) in the

four different groups.

0

100

200

300Pre race group I

Post race group I

Pre race group II

Post race group II

Pre race group III

Post race group III

Pre race group IV

Post race group IV

#•*#•*

#•#•

*†*

* *

roups

P l a s m a t r i g l y c e r i d e

l e v e l s ( m g % )

Fig. (!): Plasma totalcholesterol levels (mg %)

(mean ± SE) in the four differentgroups.

0

100

200

300

400

#• #•

** *

*

#• #•

†

roups

P l a s m a t o t a l c h o l e s t e r o l

l e v e l s ( m g % )

**

Fig. ("): Plasma #$ levels(mg%) (mean ± SE) in the four

different groups.

0

25

50

75

100Pre race group I

Post race group I

Pre race group II

Post race group II

Pre race group III

Post race group III

Pre race group IV

Post race group IV

# #

*•*•

##

*•

*•

roups

P l a s m a # $ l e v e l s

( m g % )

†

Fig. (&): Plasma $ levels (mg%) (mean ± SE) in the four

different groups.

0

100

200

••

• •

*#

*#*#

*#

roups

P l a s m a $ l e v e l s

( m g % )

†

†

Fig. ('): $iastolic lood

pressure (mm#g.)(mean SE)

in the four different groups.

0

50

100

150Pre race I

Post race I

Pre race II

Post race II

Pre race III

Post race III

Pre race IV

Post race IV

roups

$ i a s t o l i c l o o d

p r e s s u r e ( m m # g . )

#•

* * *

* #

Fig. (*): +espiratory rate(eat,min.)(mean SE) in the


0

10

20

30

40

50

#•

†

*

† †

*#

roups

+ e s p i r a t o r y r a t e

( e a t , m i n . ) *

*

Fig. (-): #eart rate

(eat,min.)(mean SE) in the


0

100

200Pre race I

Post race I

Pre race IIPost race II

Pre race III

Post race III

Pre race IV

Post race IV

*#

*

**

# •†

†

roups

# e a r t r a t e ( e a t , m i n . )

Fig. (): Systolic lood

pressure (mm#g.)(mean SE)in the four different groups.

0

100

200

#

* **

*

#

††•

roups

S y s t o l i c l o o d

p r e s s u r e ( m m

# g . )

1B

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Fig. (/): Plasma malonaldehydelevels (0mol,ml)(mean

SE) inthe four different groups.

0.00

0.25

0.50

0.75

1.00Pre race group I

Post race group I

Pre race group IIPost race group II

Pre race group III

Post race group III

Pre race group IV

Post race group IV

#• † #•

*•

*• *• #

*#*#

†#

roups

P l a s m a m a l o n a l d e

h y d e

l e v e l s ( 0 m o l , m

l )

*•

Fig. (-1): Plasma glutathione

levels (n mol,ml) (mean SE) inthe four different groups.

0.0

2.5

5.0

7.5

10.0

#•#•

**

*• #*• #

**

roups

P l a s m a g l u t a t h i o n e

l e v e l s ( n m o l , m l )

Tab%" ;+ P%as(a %#,#' ,r$.#%" %"3"%s 5(- #N2.83 J0.2ON

3 J

0.1>ON.33 J

0.46O#P4.16 J

0.2O#>.40 J

0.84O#NP8.36 J

0.3O#N

NO@ 5?($%7(%6 183.3 J

3.68#N1>8.3 J

4.14#N160 J

8.4ONP143.3 J

8.81ON12B. J

11.4O#P122.8 J

8.30O#>> J 8.B4O

#N

>6 J

>.31O#N

ach val#e represents the mean ± S.8 Signi"icantl! di""erent "rom gro#p ;.# Signi"icantl! di""erent "rom gro#p ;;.9 Signi"icantl! di""erent "rom gro#p ;;;.

P Signi"icantl! di""erent "rom post race in the same gro#p.

&he obtained data revealed that reg#lar e%ercise

signi"icantl! decreased the plasma malonaldeh!de,

total cholesterol, 55 and #ric acid levels belo

sedentar! levels. re and post race plasma levels o"

malonaldeh!de and #ric acid ere signi"icantl!

increased, hile, plasma gl#tathione and ()* ere

signi"icantl! decreased in sedentar! smokers than the


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779&S )7 R9;S ...

sedentar! non smokers, ph!sicall! active smokers and

ph!sicall! active non smokers 'tables 3 and +.

lasma malonaldeh!de, #ric acid and total

cholesterol levels o" sedentar! smokers pre and post

race ere signi"icantl! increased above ph!sicall!

active nonsmokers, ph!sicall! active smokers and

sedentar! non smokers levels. Signi"icant increase o"

plasma 55 level as observed beteen sedentar!

smokers pre and post race and ph!sicall! active non

smokers and ph!sicall! active smokers levels.

Sedentar! smokers pre and post race prod#ce

signi"icant decrease o" plasma gl#tathione, ()* and

trigl!ceride levels belo ph!sicall! active

nonsmokers, ph!sicall! active smokers and sedentar!non smokers levels. Signi"icant decrease o" plasma

$5 level as observed beteen sedentar! smokers

pre and post race levels and ph!sicall! active

nonsmokers and sedentar! non smokers levels.

&he obtained data in the present ork clearl!

demonstrated that the post race plasma malonaldeh!de

and #ric acid levels in sedentar! smokers ere

signi"icantl! increase above levels o" pre race in the

same gro#ps. &here as a signi"icant di""erence

beteen pre and post malonaldeh!de levels in

ph!sicall! active nonsmokers. h!sicall! active

smokers a"ter ac#te e%ercise prod#ce signi"icant

increase o" plasma trigl!ceride and total cholesterol

levels above pre race levels in the same gro#p. Ihile, it

prod#ces signi"icant decrease o" plasma ()* and 55

levels belo pre race in the same gro#p also. A"ter

ac#te e%ercise, sedentar! nonsmokers prod#cesigni"icant increase o" plasma 55 and #ric acid above

be"ore e%ercise levels in the same gro#ps. Ihile, it

prod#ces signi"icant decrease o" plasma ()* levels

belo pre race levels in the same gro#p also.

&here as a positive correlation beteen plasma

cholesterol level and each o" #ric acid level and

malonaldeh!de level in sedentar! smokers 'r0.8BC

pM0.02 and r0.B2C pM0.022 respectivel!+. ?oreover,

a signi"icant positive correlation as observed

beteen ser#m ()Q and trigl!ceride in sedentar!

smokers 'r 0.B2C pM0.02>+.

DISCUSSION

&he present st#d! con"irms n#mero#s positive

e""ects o" reg#lar e%ercise over cardiovasc#lar

conditioning in smokers 'Iilliam et al., 2002C

onathan, 2003C iitala et al., 200C Kerr! et al.,

2004C ?agkos et al., 2006C Ra#l, 2006C illa-

9aballero et al., 200>C @ome

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A0del-(ater

Tab%" + C$rr"%at#$& b"t""& t"st"' ,ara("t"rs %"3"%s #& s"'"&tar) s($4"rs -r$*,+

T"st"'

,ara("t"r

Tr#-%)c"r#'"s T$ta% c0$%"st"r$% Ma%$&a%'"0)'" Ur#c ac#' NO@

Tr#-%)c"r#'"s R 0.B2 pM0.02>T$ta% c0$%"st"r$% R0.B2 pM0.022 R0.8B pM0.02

Ma%$&a%'"0)'" r0.B2 pM0.022

Ur#c ac#' R0.8B pM0.02

NO@ R 0.B2 pM0.02>


22

Fig. (-'): 2orrelation et3eenplasma total cholesterol level

and malonaldehyde level insedentary smo4ers

0 100 200 300 4000.00

0.25

0.50

0.75

1.00

Plasma total cholesterol level(mg%)

p l a s m a l e v e l a n

d

m a l o n a l d e h y d e l e v e l

( 0 m o l , m l )

Fig. (-*): 2orrelation et3eenplasma total cholesterol level

and uric acid level insedentary smo4ers

225 250 275 300 325 3506

7

8

9

10

11

plasma total cholesterol level(mg%)

p l a s m a

u r i c

a c i d

l e v e l ( m g %

)

Fig. (-5): 2orrelation et3eenplasma triglyceride level and

6 level in sedentary smo4ers

0 25 50 75 100 1250

50

100

150Legend

Plasma triglyceride level (mg%)

p l a s m a

5 6

l e v e l

( 0 m o l , m l )

Fig. (--): Plasma uric acid

levels (mg %) (mean

SE) in

the four different groups.

0.0

2.5

5.0

7.5

10.0Pre race I

Post race I

Pre race II

Post race II

Pre race III

Post race III

Pre race IV

Post race IV

*•*•

#• #•

*• #*• #

*#*#

†

roups

P l a s m a u r i c a c i d

l e v e l s ( m g

% )

†

Fig. (-): Plasma nitrite plusnitrate levels (0mol,ml) (mean

SE) in the four different groups.

0

100

200#•

#•

*•

*

*

*#

*• #

*• #

†

†#

roups

P l a s m a n i t r i t

e p l u s

n i t r a t e l e v

e l s

( 0 m o l , m

l ) •

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779&S )7 R9;S ...

increase o" the arterial blood press#re and increase o"

the cardiac o#tp#t 'Antonio et al., 2008+. &he smaller

stroke vol#me at all levels o" e%ercise despite o" the

s!mpathetic stim#lation ca#sed b! smoking, co#ld

represent an added negative inotropic e""ect on

m!ocardi#m or be d#e to decrease in veno#s ret#rn,

ca#sing a compensator! increase in heart rate

'Iilliam et al., 2002+.

Regardless the mechanism, the net e""ect o"

smoking is to decrease the e""icienc! o" the heart

d#ring e%ercise in the #pright position b! ca#sing a

smaller stroke vol#me and higher rate at an! given

level o" e%ercise. Since the maor hemod!namic

e""ects o" ph!sical training are to increase the stroke

vol#me over pre training levels, cigarettes can th#s to

said to prod#ce change in opposite direction o" those

o" ph!sical conditioning. So, the stopping "rom ac#te

e%ercise in smokers is d#e to inabilit! o" the heart to

increase its stroke vol#me and cardiac o#t p#t vol#me

#p to need in normal "ashion. A"ter smoking, the

heart becomes less e""icient as a p#mp and re/#ires

more energ! to do the same amo#nt o" ork in non

smokers 'Kerr! et al., 2004+.

ecreased o" e%ercise per"ormance in smokers

ma! be also d#e to rapid d!spnea that ma! be d#e to

1+ constriction o" the terminal bronchioles o" the

l#ngs, hich increases the resistance o" air"lo into

and o#t o" the l#ngs. 2+ &he irritating e""ects o" the

smoke itsel" ca#se increased "l#id secretion into the

bronchial tree, as ell as some selling o" the

epithelial linings and 3+ nicotine paral!

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"#nctions o" endothelial cells. ;n the vitro model,

cigarette smoking as associated ith red#ced ()*

s!nthases activit! as ell as decreased ()*

prod#ction 'Iang et al., 2000+. 9omponents o"

cigarette smoke can react ith 5-arginine to "orm an

5-arginine add#ct. &his reaction ma! have to

possible e""ects. 7irst, it ma! decrease the amo#nt o"

5-arginine in the bod! and th#s, less ()* is prod#ced

since there is less o" its prec#rsor. Secondl!,

the add#ct "ormed ma! bind to the ()S itsel" and

inhibit its "#nction 'Iong, 1BBB+. Another possible

mechanism is reactive o%!gen species depress ()*

s!nthesis thro#gh their inhibitor! e""ect on

endothelial receptors "or acet!lcholine and other

vasodilators, hile the! directl! react ith ()* to

"orm pero%!nitrite, decreasing in this a! ()*

bioavailabilit! '5a#rsen et al., 2001+.

Raveendran et al., '2004+ reported that cigarette

smoke can ind#ce e%cessive apoptosis in endothelial

cells and other cell t!pes. &his apoptosis ma! be

mediated b! the activation o" p38 ?AK 'mitogen

activated protein kinase+, (KFSAK '#n kinase

kinaseF stress activated protein kinase+ and caspases.

ndogeno#s ()* prod#ction ma! be an important

protective mechanism against smoking-ind#ced

endothelial damage. &he decrease in ()*

bioavailabilit! in vessel all sti""ness ma! e%plain

h! smoking is an important risk "actor "or coronar!

arter! disease '@#o et al., 2006+.

(#mero#s a#thors have reported increased resting

o%idative stress in cigarette smokers '5ee#enb#rgh

and $einecken, 2001C ietrich et al., '2003+C olidori

et al., 2003C Kirkham et al., 200C ?#scat et al.,

200C A!cicek et al., 2004 and =loomer et al., 200>+.

5ikeise, an e/#al or greater n#mber o"

investigations have reported elevations in protein,

lipid and (A o%idation "olloing ac#te e%ercise

'Shlomit et al., 2003C )rhan et al., 200C 7ato#ros et

al., 200C Kemal et al., 200C iitala et al., 200C

(ishino et al., 2004C R#ssell et al., 2004C @ome illa-

9aballero et al., 200> and acker et al., 2008+. Some

st#dies 'S#rmen-@#r et al., 1BBB and Alessio et al.,

2000+ have "o#nd little, or no, change in detectable

malon!ldialdeh!de val#es in smoking and ac#te

e%ercise. &he e%act reason "or this is #nknon b#t its

ma! be d#e to methodical variation beteen st#dies

or even the ver! nat#re o" malon!ldialdeh!de

detection. ;t ma! also be d#e to the rapid clearance o"

malon!ldialdeh!de "rom plasma 'i%on et al., 2006+

and hich can make it di""ic#lt to obtain acc#rate in

vivo meas#rements o" malon!ldialdeh!de 'Sachdev

and Kelvin, 2008+.

7ree radicals ere generated in smokers "rom

several so#rceC 1+ the mitochondria, "rom hich

o%!gen radicals that have escaped scavenging

en

sarcoplasm, 2+ the capillar! endotheli#m b! %anthin

o%idase, here a h!po%ia or reo%!genation process is

created d#ring e%ercise 'Kemal et al., 200+ and 3+ an

o%idative b#rst "rom in"lammator! cells mobili

red#cing (A+ can be converted to %anthine

o%idase, hich "#nctions b! red#cing molec#lar

o%!gen. A& catabolism res#lts in prod#ction o"

h!po%anthine, thereb! prod#cing s#bstrate "or

%anthine o%idase. Ihen o%!gen is reintrod#ced

'reper"#sion+ %anthine o%idase prod#ces s#pero%ide

and h!drogen pero%ide as b!-prod#cts, contrib#ting

to overall o%idant and "ree radical "ormation '(ishino


2

http://ajpheart.physiology.org/cgi/content/full/291/5/H2354?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=1&andorexacttitle=and&titleabstract=smoking++&andorexacttitleabs=and&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&fdate=7/1/1995&tdate=1/31/2007&resourcetype=HWCIT#R27http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=http://luce.sunymaritime.edu:2078/science?_ob=ArticleURL&_udi=B6X1H-4PB6VRD-2&_user=696742&_coverDate=01%2F31%2F2008&_alid=688073504&_rdoc=1&_fmt=full&_orig=search&_cdi=7243&_sort=d&_docanchor=&view=c&_ct=2&_acct=C000038902&_version=1&_urlVersion=0&_userid=696742&md5=ce3c106124b7c8a8ed1e7543a6d66b82#bib89%23bib89http://luce.sunymaritime.edu:2078/science?_ob=ArticleURL&_udi=B6X1H-4PB6VRD-2&_user=696742&_coverDate=01%2F31%2F2008&_alid=688073504&_rdoc=1&_fmt=full&_orig=search&_cdi=7243&_sort=d&_docanchor=&view=c&_ct=2&_acct=C000038902&_version=1&_urlVersion=0&_userid=696742&md5=ce3c106124b7c8a8ed1e7543a6d66b82#bib31http://luce.sunymaritime.edu:2078/science?_ob=ArticleURL&_udi=B6X1H-4PB6VRD-2&_user=696742&_coverDate=01%2F31%2F2008&_alid=688073504&_rdoc=1&_fmt=full&_orig=search&_cdi=7243&_sort=d&_docanchor=&view=c&_ct=2&_acct=C000038902&_version=1&_urlVersion=0&_userid=696742&md5=ce3c106124b7c8a8ed1e7543a6d66b82#bib31http://ajpheart.physiology.org/cgi/content/full/291/5/H2354?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=1&andorexacttitle=and&titleabstract=smoking++&andorexacttitleabs=and&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&fdate=7/1/1995&tdate=1/31/2007&resourcetype=HWCIT#R27http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=http://luce.sunymaritime.edu:2078/science?_ob=ArticleURL&_udi=B6X1H-4PB6VRD-2&_user=696742&_coverDate=01%2F31%2F2008&_alid=688073504&_rdoc=1&_fmt=full&_orig=search&_cdi=7243&_sort=d&_docanchor=&view=c&_ct=2&_acct=C000038902&_version=1&_urlVersion=0&_userid=696742&md5=ce3c106124b7c8a8ed1e7543a6d66b82#bib89%23bib89http://luce.sunymaritime.edu:2078/science?_ob=ArticleURL&_udi=B6X1H-4PB6VRD-2&_user=696742&_coverDate=01%2F31%2F2008&_alid=688073504&_rdoc=1&_fmt=full&_orig=search&_cdi=7243&_sort=d&_docanchor=&view=c&_ct=2&_acct=C000038902&_version=1&_urlVersion=0&_userid=696742&md5=ce3c106124b7c8a8ed1e7543a6d66b82#bib31http://luce.sunymaritime.edu:2078/science?_ob=ArticleURL&_udi=B6X1H-4PB6VRD-2&_user=696742&_coverDate=01%2F31%2F2008&_alid=688073504&_rdoc=1&_fmt=full&_orig=search&_cdi=7243&_sort=d&_docanchor=&view=c&_ct=2&_acct=C000038902&_version=1&_urlVersion=0&_userid=696742&md5=ce3c106124b7c8a8ed1e7543a6d66b82#bib31

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779&S )7 R9;S ...

et al., 2004+. 3- =! ne#trophils and other phagoc!tes

as part o" a heightened and e%tensive imm#ne

response to tiss#e in#r! ith the s#bse/#ent

prod#ction o" "ree radicals b! (A$ o%idase

'?oro+ =! depletion o" thiols and an

increase o" intracell#lar 9a ma! potentate "ree

radical generation in ac#te e%ercise 'Iilli#m and

onald, 2000+. 8+ =! a#to-o%idation o"

o%!hemoglobin to methemoglobin res#lts in the

prod#ction o" s#pero%ide 'Iilli#m and onald,

2000+.

i et al. '1BB3+ e%amined the mechanism o" the

change in gl#tathione in the blood in response to

e%ercise. &he! "o#nd that hen s#bects per"ormed

the same e%ercise b#t ingested carboh!drate,

s#""icient to increase blood gl#cose and ins#lin over

the control condition, there as no increase in

gl#tathione. &he increased o" gl#tathione b! reg#lar

e%ercise ma! be d#e to hepatic gl#tathione e""l#% b!

gl#cagon.

;t is ver! clear that reg#lar e%ercise training

ind#ces adaptive responses that permit improved

e%ercise per"ormance 'Sachdev and Kelvin,

2008+.&hese adaptive responses incl#de red#ced

basal prod#ction o" o%idants, red#ction o" radical leak

d#ring o%idative phosphor!lation, increased the

activit! o" antio%idant en

o%idative damage repair s!stems to improved

ph!siological "#nction and enhanced resistance to

o%idative stress 'Radak et al., 2008+. %ercise also

has a large impact on the availabilit! and bioactivit!

o" endothelial-derived nitric o%ide. &he stim#l#s "or

endothelial ()* prod#ction is the increased "lo

thro#gh the vessels, hich res#lts in shear stress and

increased activation o" endothelial nitric o%ide

s!nthase 'Koda and $ambrecht, 2004+.

CONCLUSION AND RECOMMENDATIONS+

&hese "indings point to the role o" ()Q, #ric acid

and lipid pero%ide in the pathoph!siologic

mechanisms o" smoking ind#ced cardiovasc#lar

diseases. &he "ree radicals are "ormed in e%cess in

smokers especiall! a"ter ac#te e%ercise. Sedentar!

smokers ma! be at an even greater risk o" o%idative

stress-related cardiovasc#lar diseases. &he

signi"icance o" in"ormation obtained tho#gh this

st#d! is not onl! el#cidation o" the mechanism o"

smoking ind#ced cardiovasc#lar disease, b#t also

provide a possible better method o" treatment and

diagnosis "or smokers ho have developed

cardiovasc#lar disease s!mptoms thro#gh the

possibilit! o" 5-arginine, antio%idants, %anthine

o%idase inhibitor replacement therapies. &here is a

need o" more prospective st#dies regarding o%idative

stress and diverse e%ercise t!pes and regimens insmokers. =eca#se the risk o" cardiovasc#lar

morbidit! and mortalit! appears greater ithin an

aging pop#lation, "#t#re investigations sho#ld "oc#s

on older, more established smokers, hile giving

speci"ic attention to the n#mber and method o"

cigarettes smoked per da!, to determine i" more

rob#st "indings are noted. 7inall!, ever! bod! sho#ld

incl#de in a reg#lar e%ercise.

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