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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.
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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.
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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$r) rat"
5b"ats7 (#&*t"612.0J2.0
24.6 J
2.0≠N1.0J3.0P
28.B J2.0O
14.0 J4.0P
30.2 J2.0O
18.0 J3.0OP
38.> J
2.0O≠
ach val#e represents the mean J S.
8 Signi"icantl! di""erent "rom gro#p ;.
≠
Signi"icantl! di""erent "rom gro#p ;;.9 Signi"icantl! di""erent "rom gro#p ;;;.
: Signi"icantl! di""erent "rom post race in the same gro#p.
JOURNAL OF STRESS PHYSIOLOGY BIOCHEMISTRY ol. (o. 2 2008
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JOURNAL OF STRESS PHYSIOLOGY BIOCHEMISTRY ol. (o. 2 2008
Fig. (5): Plasma triglyceridelevels (mg %) (mean ± SE) in the
four different groups.
0
100
200
300Pre race group I
Post race group I
Pre race group II
Post race group II
Pre race group III
Post race group III
Pre race group IV
Post race group IV
#•*#•*
#•#•
*†*
* *
roups
P l a s m a t r i g l y c e r i d e
l e v e l s ( m g % )
Fig. (!): Plasma totalcholesterol levels (mg %)
(mean ± SE) in the four differentgroups.
0
100
200
300
400
#• #•
** *
*
#• #•
†
roups
P l a s m a t o t a l c h o l e s t e r o l
l e v e l s ( m g % )
**
Fig. ("): Plasma #$ 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
four different groups.
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
four different groups.
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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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>
JOURNAL OF STRESS PHYSIOLOGY BIOCHEMISTRY ol. (o. 2 2008
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
JOURNAL OF STRESS PHYSIOLOGY BIOCHEMISTRY ol. (o. 2 2008
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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