Oxidative stress in response to aerobic and anaerobic power testing: influence of exercise training and carnitine supplementation


Bloomer, R.J.; Smith, W.A.

Research in Sports Medicine 17(1): 1-16

2009


The purpose of this study is to compare the oxidative stress response to aerobic and anaerobic power testing, and to determine the impact of exercise training with or without glycine propionyl-L-carnitine (GPLC) in attenuating the oxidative stress response. Thirty-two subjects were assigned (double blind) to placebo, GPLC-1 (1g PLC/d), GPLC-3 (3g PLC/d) for 8 weeks, plus aerobic exercise. Aerobic (graded exercise test: GXT) and anaerobic (Wingate cycle) power tests were performed before and following the intervention. Blood was taken before and immediately following exercise tests and analyzed for malondialdehyde (MDA), hydrogen peroxide (H2O2), and xanthine oxidase activity (XO). No interaction effects were noted. MDA was minimally effected by exercise but lower at rest for both GPLC groups following the intervention (p = 0.044). A time main effect was noted for H2O2 (p = 0.05) and XO (p = 0.003), with values increasing from pre- to postexercise. Both aerobic and anaerobic power testing increase oxidative stress to a similar extent. Exercise training plus GPLC can decrease resting MDA, but it has little impact on exercise-induced oxidative stress biomarkers.

Research
in
Sports
Medicine,
17:1-16,
2009
Copyright
©
Taylor
&
Francis
Group,
LLC
ISSN:
1543-8627
print/1543-8635
online
DOI:
10.1080/15438620802678289
Routledge
Taylor
&Francis
Group
ORIGINAL
RESEARCH
Oxidative
Stress
in
Response
to
Aerobic
and
Anaerobic
Power
Testing:
Influence
of
Exercise
Training
and
Carnitine
Supplementation
RICHARD
J.
BLOOMER
and
WEBB
A.
SMITH
Cardiorespiratory/Metabolic
Laboratory,
Department
of
Health
and
Sport
Sciences,
The
University
of
Memphis, Memphis,
Tennessee,
USA
The
purpose
of
this
study
is
to
compare
the
oxidative
stress
response
to
aerobic
and
anaerobic
power
testing,
and
to
determine
the
impact
of
exercise
training
with
or
without
glycine
propionyl-L-
carnitine
(GPLC)
in
attenuating
the
oxidative
stress
response.
Thirty-two
subjects
were
assigned
(double
blind)
to
placebo,
GPLC-1
(1g
PLC/d),
GPLC-3
(3g
PLC/d)
for
8
weeks,
plus
aerobic
exercise.
Aerobic
(graded
exercise
test:•
GX7)
and
anaerobic
(Wingate
cycle)
power
tests
were
performed
before
and
following
the
intervention.
Blood
was
taken
before
and
immediately
following
exercise
tests
and
analyzed
for
malondialdehyde
(MDA),
hydrogen
peroxide
(H
2
0
2
),
and
xanthine
oxidase
activity
(XO).
No
interaction
effects
were
noted.
MDA
was
minimally
effected
by
exercise
but
lower
at
rest
for
both
GPLC
groups
following
the
intervention
(p
=
0.044).
A
time
main
effect
was
noted
forH
2
O
2
(p
=
0.05)
and
X0
(p
=
0.003),
with
values
increasing
from
pre-
to
postexercise.
Both
aerobic
and
anaerobic
power
testing
increase
oxidative
stress
to
a
similar
extent.
Exercise
training
plus
GPLC
can
decrease
resting
MDA,
but
it
has
little
impact
on
exercise-induced
oxidative
stress
biomarkers.
KEYWORDS
malondialdehyde,
hydrogen
peroxide,
reactive
oxygen
species,
free
radicals,
exercise,
nutritional
supplements
Received
1
November
2007;
accepted
8
July
2008.
This
work
was
supported
by
Sigma-Tau
HealthScience
and
the
University
of
Memphis.
Address
correspondence
to
Richard
J.
Bloomer,
Cardiorespiratory/Metabolic
Laboratory,
161F
Elma
Neal
Roane
Field
House,
The
University
of
Memphis, Memphis,
TN
38152,
USA.
E-mail:
rbloomer@memphis.edu
1
2
R.J.
Bloomer
and
W.A.
Smith
INTRODUCTION
Exercise
of
sufficient
intensity
and
duration
increases
the
formation
of
reac-
tive
oxygen
and
nitrogen
species
(RONS),
creating
an
imbalance
between
oxidant
and
antioxidant
levels.
Such
a
condition,
referred
to
as
oxidative
stress,
can
lead
to
the
oxidation
of
lipids,
proteins,
and
other
molecules
(Halliwell
and
Gutteridge
1989).
This
has
been
demonstrated
in
multiple
studies
over
the
past
30
years
since
Dillard
and
colleagues
first
reported
in
1978
that
lipid
peroxidation
was
increased
following
cycling
exercise
(Dillard
et
al.
1978).
These
findings
are
evident
for
both
anaerobic
(Bloomer
and
Goldfarb
2004)
as
well
as
aerobic
exercise
(Finaud
et
al.
2006;
Vollaard
et
al.
2005).
Little
is
known
however,
regarding
the
extent
of
oxidative
stress
when
comparing
aerobic
and
anaerobic
exercise
modes
within
the
same
subject
population.
In
fact,
few
studies
have
investigated
oxidative
stress
in
response
to
both
aerobic
and
anaerobic
exercise
bouts
using
a
crossover
design
(Alessio
et
al.
2000;
Bloomer
et
al.
2005;
Magalhaes
et
al.
2007;
Vincent
et
al.
2004).
These
studies
have
used
either
isometric
handgrip
(Alessio
et
al.
2000;
Magalhaes
et
al.
2007)
or
resistance
exercise
(Bloomer
et
al.
2005;
Vincent
et
al.
2005),
and
no
study
has
included
an
anaerobic
power
test,
as
is
commonly
performed
in
several
lab
assessments,
for
com-
parison
with
the
aerobic
work.
Of
the
comparison studies
performed
to
date,
anaerobic
exercise
has
resulted
in
oxidative
stress
that
equals
or
exceeds
that
of
aerobic
exercise.
Hence,
the
initial
purpose
of
this
study
was
to
compare
the
oxidative
stress
response
with
aerobic
and
anaerobic
power
tests
within
the
same
subjects.
Excessive
oxidative
stress
has
been
implicated
in
a
wide
variety
of
disease
processes
(Dalle-Donne
et
al.
2006).
Based
on
these
observations,
some
concern
exists
related
to
increased
oxidative
stress
commonly
observed
in
response
to
acute
exercise.
As
such,
attempts
to
decrease
oxidative
stress
in
response
to
acute
exercise
are
common.
These
include
both
regular
exer-
cise
training
(Ji
et
al.
2006;
Powers
et
al.
1999)
and
antioxidant
supplemen-
tation
(Atalay
et
al.
2006;
Powers
et
al.
2004;
Urso
and
Clarkson
2003).
Related
to
the
former,
although
acute
exercise
increases
oxidative
stress
transiently,
this
same
exercise
stimulus
appears
necessary
to
allow
for
an
up-regulation
in
endogenous
antioxidant
defenses
(Ji
2002;
Ji
et
al.
2006).
As
for
antioxidant
supplementation,
several
isolated
nutrients
have
been
used
in
an
attempt
to
attenuate
the
increase
in
oxidative
stress
biomarkers
in
response
to
acute
exercise,
as
previously
discussed
in
detail
(Powers
et
al.
2004;
Urso
and
Clarkson
2003).
One
nutrient
that
has
shown
great
promise
as
an
antioxidant
in
both
animals
(Derin
et
al.
2004;
Di
Giacomo
et
al.
1993;
Loster
et
al.
2001;
Rauchova
et
al.
2002;
Vanella
et
al.
2000)
and
humans
(Corbucci
et
al.
1990;
Sachan
et
al.
2005;
Volek
et
al.
2002)
is
camitine.
The
effects
are
believed
to
be
mediated
by
a
reduction
in
xanthine
oxidase
activity
(Di
Giacomo
et
al.
Exercise
Induced
Oxidative
Stress
and
Carnitine
3
1993),
a
free-radical
scavenging
activity
(Vanella
et
al.
2000),
a
regulation
of
fatty
add
metabolism
(Rauchova
et
al.
2002)
or
all
of
these.
Propionyl-L-carnitine
appears
to
have
the
highest
affinity
for
carnitine
acetyltransferase
and
pos-
sesses
protective
effects
against
RONS-induced
oxidation
(Rauchova
et
al.
2002).
This
form
of
carnitine
recently
has
been
combined
with
the
amino
acid
glycine
in
a
unique
molecular
bonded
form
called
glycine
propionyl-L-
carnitine
(GPLC).
Previous
reports
indicate
that
glycine
independently
pro-
motes
positive
effects
on
lipid
peroxidation
(Senthilkumar
et
al.
2004a,
2004b).
To
our
knowledge,
only
one
study
to
date
has
used
carnitine
to
attenuate
exercise-induced
oxidative
stress
in
humans,
noting
favorable
results
(Volek
et
al.
2002).
Therefore,
an
additional
purpose
of
the
present
study
was
to
investigate
the
antioxidant
effects
of
carnitine
(in
the
form
of
GPLC),
in
conjunction
with
aerobic
exercise
training,
on
resting
and
exer-
cise-induced
oxidative
stress
in
human
subjects.
The
oxidative
stress
response
was
compared
using
two
common
forms
of
exercise
testing
in
a
research/clinical
lab:
A
Bruce
treadmill
protocol,
rep-
resenting
a
test
of
aerobic
power
(maximal
oxygen
consumption;
VO
2max
),
and
a
Wingate
cycle
test,
representing
a
test
of
anaerobic
power.
The
potential
attenuation
in
oxidative
stress
to
both
exercise
tests
was
assessed
by
measuring
oxidative
stress
biomarkers
before
and
following
an
8-week
intervention
of
supervised
aerobic
exercise
with
or
without
GPLC
supple-
mentation.
We
hypothesized
that
both
forms
of
exercise
would
induce
oxi-
dative
stress
and
that
oxidative
stress
would
be
lower
following
the
intervention
period
as
a
result
of
exercise
training,
and
to
a
greater
extent
with
GPLC
supplementation.
MATERIALS
AND
METHODS
Subjects
and
Screening
Thirty-two
sedentary
men
and
women
between
the
ages
of
20
and
40
years
completed
all
aspects
of
this
study
(from
an
initial
sample
of
42
enrolled
subjects).
Subjects
did
not
smoke,
use
nutritional
supplements,
or
have
any
cardiovascular,
metabolic,
or
orthopedic
problems.
Health
history,
drug
and
nutritional
supplement
usage,
and
physical
activity
questionnaires
were
completed
to
determine
eligibility.
Table
1
provides
baseline
descriptive
characteristics
of
subjects.
Subjects
were
informed
of
all
procedures,
poten-
tial
risks,
and
benefits
associated
with
the
study
and
signed
a
consent
form
approved
by
the
University
Institutional
Review
Board
for
Human
Subjects
Research.
During
the
initial
visit
to
the
laboratory,
stature,
body
mass,
and
body
fat
(seven
site
skinfolds)
were
measured
(Jackson
and
Pollock
1978)
in
order
to
characterize
subjects.
Resting
heart
rate
and
blood
pressure
were
measured,
and
subjects
were
familiarized
to
the
graded
exercise
test
(GXT;
4
R.J.
Bloomer
and
W.A.
Smith
TABLE
1
Subject
Baseline
Descriptive
Characteristics
Variable
Placebo
GPLC-1
GPLC-3
Age
(years)
27±2
26
±2
27
±2
Stature
(cm)
168
±
3
169
±
4
167
±
2
Body mass
(kg)
78
±
7
82
±
8
69
±6
Body
fat
(%)
25
±2
26
±3
27
±2
Resting
heart
rate
(bpm)
65
±
2
70
±
3
69
±
3
V0
2
.
(mL•kg•
-l
min
-1
)
32
±
2
30
±
3
28
±
2
Data
are
mean
±
SEM.
No
differences
were
noted
between
groups
for
any
measured
variable
(p
>
0.05).
by
performing
2
minutes
of
each
of
the
first
two
workloads)
and
the
anaerobic
power
test
(by
performing
a
practice
trial
of
this
cycle
test,
as
described
below).
Aerobic
and
Anaerobic
Exercise
Testing
A
maximal
GXT
using
the
Bruce
treadmill
protocol
was
conducted
while
expired
gases
were
collected
via
facemask
and
analyzed
(SensorMedics
Vmax
229
metabolic
system;
Viasys
Healthcare,
Yorba
Linda,
CA)
for
deter-
mination
of
VO
2
.
The
maximal
heart
rate
data
(via
electrocardiographic
tracings)
were
used
in
prescribing
the
exercise
intensity
during
the
intervention
period.
The
GXT
was
conducted
in
the
morning
following
an
overnight
fast
(minimum
of
8
hr—necessary
for
blood
collection
purposes
and
analysis
of
oxidative
stress
biomarkers),
and
subjects
were
asked
to
avoid
strenuous
activity
during
the
2
days
preceding
the
GXT.
The
test
continued
until
exhaustion,
and
the
highest
mean
1-minute
VO
2
value
was
used
to
represent
V0
2
..
Heart
rate
and
rating
of
perceived
exertion
(RPE)
were
recorded
at
the
end
of
each
3-minute
stage
of
the
test
and
at
the
conclusion
of
testing.
Two
days
following
the
GXT
(in
order
to
allow
for
adequate
recovery),
subjects
completed
a
Wingate
anaerobic
power
test
(30-second
cycle
sprint
test)
on
a
Lode
Excalibur
Sport
cycle
ergometer
(Lode
B.V.
Medical
Technology
Groningen-The
Netherlands)
interfaced
with
a
computer.
The
force
(N)
that
subjects
pedaled
against
was
determined
based
upon
their
lean
body
mass
and
equal
to
lean
body
mass
(kg)
x
0.7.
Prior
to
performing
the
test,
subjects
received
a
5-minute
warm-up
using
a
low
intensity
(75
watts),
in
which
they
performed
a
3-to-5-second
sprint
at
the
top
of
each
minute
in
order
to
famil-
iarize
subjects
to
the
protocol.
Heart
rate
and
RPE
were
recorded
at
the
end
of
the
test.
Total
work
performed
also
was
recorded.
These
exact
testing
proce-
dures
were
repeated
following
the
8-week
intervention.
Supplementation
Following
the
completion
of
the
above
tests,
subjects
were
randomized
in
a
double-blind
manner
to
one
of
following
three
groups,
with
the
addition
of
Exercise
Induced
Oxidative
Stress
and
Carnitine
5
aerobic
exercise:
1
g
PLC
+
348
mg
glycine
day
-I-
(GPLC-1;
n
=
11,
5
men,
6
women);
3
g
PLC
+
1044
mg
glycine
day
-I-
(GPLC-3;
n
=
12,
0
men,
12
women);
1
g
cellulose
placebo
(PL;
n
=
9,
4
men,
5
women).
Our
dosing
was
based
on
previous
studies
using
L-carnitine,
which
have
provided
dos-
ages
ranging
from
2-4
grams
per
day
(Heinonen
1996).
In
particular,
a
study
by
Volek
et
al.
(2002)
used
2
grams
per
day
of
L-carnitine,
and
mea-
sured
similar
dependent
variables
as
we
have
included
here.
Hence,
we
chose
to
use
dosing
slightly
less
than
and
greater
than
this
previous
work.
The
GPLC
consisted
of
a
molecularly
bonded
form
of
PLC
and
the
amino
acid
glycine
(GlycoCarnTM,
Sigma-tau
HealthScience
S.p.A.,
Rome,
Italy).
For
ease
of
reporting
throughout
this
article,
we
refer
to
the
two
dos-
ages
of
GPLC
as
simply
1
and
3
g•day
-I-
to
reference
the
actual
PLC
content.
Capsules
were
identical
in
appearance
and
were
provided
to
subjects
in
unlabeled
bottles
every
2
weeks.
Subjects
were
instructed
to
ingest
three
capsules
twice
daily
(morning
and
evening)
in
conjunction
with
a
carbohydrate-
rich
meal.
Supplementation
continued
until
all
postintervention
testing
was
completed.
The
8-week
treatment
period
was
chosen
based
on
previous
studies
using
L-carnitine
(Heinonen
1996),
in
addition
to
recommendations
for
improvements
in
functional
capacity
with
aerobic
training
(American
College
of
Sports
Medicine
[AGSM]
2005).
Aerobic
Exercise
Training
Following
randomization
all
subjects
began
an
8-week
supervised
program
of
aerobic
exercise
consisting
of
a
combination
of
walking,
jogging,
and
stationary
cycling,
performed
3
days
per
week.
The
combination
of
these
modes
allowed
for
specificity
to
both
of
our
chosen
exercise
tests
(treadmill
GXT
and
Wingate
cycle).
The
training
intensity
and
duration
followed
ACSM
guidelines
and
began
at
a
low
level
(55%-60%
HR
reserve
for
30
min)
and
progressed
to
higher
levels
over
the
8-week
period
(75%-85%
HR
reserve
for
45
min;
Week
1
=
55%-65%,
Week
2
=
65%-75%,
Week
3
=
70%-80%,
and
Week
4
8
=
75%-85%).
Intensity
was
verified
by
use
of
heart
rate
monitors
and
RPE.
Both
heart
rate
and
RPE
were
recorded
at
three
equally
spaced
times
during
each
exercise
session
by
research
assistants.
Blood
Collection
and
Biochemistry
Both
pre-and
postintervention,
venous
blood
samples
(-20mL)
were
taken
from
subjects'
forearm
via
needle
and
vacutainer
before
(following
a
10-minute
rest
period)
and
within
1
minute
following
both
exercise
tests.
We
chose
to
collect
samples
at
the
immediate
postexercise
time
point
because
in
most
(but
not
all)
studies,
this
time
has
been
associated
with
the
greatest
magnitude
of
postexercise
increase
in
our
chosen
markers.
Lactate
was
measured
in
whole
blood
(Accutrend;
Roche
Diagnostics,
Mannheim,
6
R.J.
Bloomer
and
W.A.
Smith
Germany).
The
remainder
of
blood
was
immediately
processed,
and
plasma
and
serum
was
stored
in
multiple
aliquots
at
—80°C
until
analyzed.
All
assays
were
performed
in
duplicate
on
first
thaw.
Antioxidant
capacity
was
measured
in
serum
using
the
Trolox-equivalent
antioxidant
capacity
(TEAC)
assay
using
procedures
outlined
by
the
reagent
provided
(Sigma
Chemical,
St.
Louis,
MO),
and
as
previously
described
(Rice-Evans
2000).
The
TEAC
was
measured
only
at
rest
(prior
to
the
GXT),
pre-
and
postintervention.
Malondialdehyde
(MDA)
was
analyzed
in
plasma
using
the
method
described
by
Jentzsch
et
al.
(1996).
Hydrogen
peroxide
and
xanthine
oxidase
activity
were
measured
in
plasma
using
the
Amplex
Red
reagent
method
as
described
by
the
manufacturer
(Molecular
Probes,
Invitrogen
Detection
Technologies,
Eugene,
OR).
Dietary
Records
All
subjects
were
instructed
to
maintain
their
normal
diet
during
the
inter-
vention
period.
Subjects
completed
7-day
food
records
during
weeks
1
and
8
of
the
intervention.
Records
were
analyzed
for
total
kilocalories,
protein,
carbohydrate,
fat,
vitamin
C,
vitamin
E,
and
vitamin
A
using
Diet
Analysis
Plus
(ESHA
Research,
Salem,
OR).
Statistical
Analysis
Malondialdehyde,
hydrogen
peroxide,
xanthine
oxidase
activity,
and
lactate
were
analyzed
using
a
3
(group)
x
2
(exercise
type)
x
2
(time:
pre/postexercise)
x
2
(pre/postintervention)
ANOVA.
Where
appropriate,
significant
interac-
tions
and
main
effects
were
further
analyzed
using
Tukey's
post
hoc
tests.
Dietary
and
descriptive
data
(e.g.,
weight,
body
fat
percentage),
as
well
as
TEAC
and
exercise
test
variables
(e.g.,
heart
rate)
were
analyzed
using
a
3
(group)
x
2
(pre/postintervention)
ANOVA.
Data
are
presented
as
mean
±
SEM.
The
level
of
significance
was
set
at
p
0.05.
All
analyses
were
per-
formed
using
JMP
statistical
software
version
4.0
(SAS
Institute,
Cary,
NC).
RESULTS
Compliance
to
supplementation
was
measured
every
2
weeks
via
capsule
counts
upon
bottle
return
and
was
greater
than
95%
in
all
three
groups,
with
no
statistical
difference
between
groups
(p
>
0.05).
Exercise
attendance
(85%-91%)
and
ability
to
maintain
the
appropriate
exercise
intensity
(90%-
94%)
was
not
different
between
groups
(p
>
0.05).
Although
only
32
sub-
jects
successfully
completed
all
aspects
of
this
study,
a
total
of
42
subjects
initially
were
enrolled
and
equally
randomized
to
the
three
groups
(n
=
14
per
group).
Ten
subjects
were
dropped,
either
due
to
their
request
or
their
Exercise
Induced
Oxidative
Stress
and
Carnitine
7
inability
to
maintain
compliance
above
80%
for
both
supplementation
and
exercise
training.
No
interactions
or
main
effects
were
noted
for
any
descriptive
characteristic
(e.g.,
age,
body
mass,
body
fat
percentage;
p
>
0.05).
In
addition,
no
interactions
or
main
effects
were
noted
for
dietary
variables
(p
>
0.05),
with
normal
intake
of
total
kilocalories,
macro-
and
micronutrient
intake
noted
(Table
2).
Maximal
heart
rate
or
RPE
were
not
different
between
groups
or
from
pre-
to
postintervention
for
either
the
GXT
or
Wingate
(p
>
0.05).
All
subjects
achieved
a
heart
rate
that
exceeded
93%
of
maximum
on
the
GXT
and
90%
for
the
Wingate,
and
reported
an
RPE
17
for
both
tests
(both
pre-
and
postintervention,
with
no
differences
noted
between
groups
or
from
pre-
to
postintervention;
p
>
0.05).
Total
work
performed
during
the
Wingate
test
did
not
differ
between
the
placebo
(202
±
21
kJ),
GPLC-1
(178
±
19
kJ),
and
GPLC-3
(168
±
18
kJ)
groups
(p
>
0.05),
and
increased
8%-12%
from
pre-
to
postintervention,
with
no
difference
detected
between
groups
or
across
time
(p
>
0.05).
Exercise
test
data
are
included
in
Table
3.
Antioxidant
capacity
as
measured
by
TEAC
was
not
different
between
placebo
(0.61
±
0.07
to
0.66
±
0.08
mmo11
-1
),
GPLC-1
(0.58
±
0.06
to
0.61
±
0.06
mmo11
-1
),
and
GPLC-3
(0.61
±
0.05
to
0.65
±
0.04
mmo11
-1
),
nor
was
1'FAC
different
from
pre-
to
postintervention
(p
>
0.05),
with
an
average
increase
of
5%-8%.
A
time
main
effect
was
noted
for
blood
lactate
(p
<
0.00001),
with
values
increasing
from
1.45
±
0.30
to
8.89
±
0.51
mmol•L
-1
from
pre-
to
pos-
texercise,
with
almost
identical
values
from
pre-
to
postexercise
for
the
GXT
(1.44
±
0.32
to
9.00
±
0.48
mmo11
-1
)
and
Wingate
test
(1.45
±
0.28
to
8.70
±
0.51
mmo11
-1
).
No
other
interactions
or
main
effects
were
noted
for
blood
lactate
(p
>
0.05;
Table
3).
Regarding
the
oxidative
stress
biomarkers,
a
group
by
pre/postintervention
interaction
was
noted
(p
=
0.044)
for
MDA,
as
well
as
a
group
main
effect
(p
=
0.040).
Values
were
lower
for
both
GPLC
groups
following
the
inter-
vention
compared
with
preintervention.
No
other
interaction
or
main
effects
were
noted
for
MDA
(p
>
0.05;
Figure
1).
A
time
main
effect
was
noted
for
TABLE
2
Subject
Dietary
Data
During
Weeks
1
and
8
of
an
8-Week
Intervention
of
Aerobic
Exercise
with
or
without
GPLC
Supplementation
Variable
Placebo
pre
Placebo
post
GPLC-1
pre
GPLC-1
post
GPLC-3
pre
GPLC-3
post
Kilocalorie
Protein
(g)
CHO
(g)
Fat
(g)
Vit
C
(mg)
Vit
E
(mg)
Vit
A(RE)
1800
74
223
67
85
4
866
±
120
±
8
±
20
±
7
±
27
±
2
±
111
2159
85
253
80
61
6
872
±
174
±
11
±
24
±
6
±
18
±
1
±
157
2059
83
241
75
56
6
864
±
168
±
10
±
21
±
5
±
12
±
2
±
138
1988
81
243
67
52
5
812
±
210
±
11
±
32
±
9
±
15
±
2
±
115
1800
76
233
75
68
6
921
±
174
±
9
±
22
±
8
±
15
±
2
±
101
1643
69
203
62
81
5
615
±
120
±
6
±
21
±
7
±
20
±
1
±
87
Data
are
mean
±
SEM.
No
interaction
effects,
time
main
effect,
or
treatment
main
effects
were
noted
for
any
dietary
variable
(p
>
0.05).
TABLE
3
Peak
Exercise
Test
Variables
Before
and
After
an
8-Week
Intervention
of
Aerobic
Exercise
with
or
without
GPLC
Supplementation
Variable
Placebo
pre
Placebo
post
GPLC-1
pre
GPLC-1
post
GPLC-3
pre
GPLC-3
post
'HR
(bpm)
189
±
4
186
±
4
187
±
3
185
±
5
188
±
4
187
±
5
'RPE
18
±
1
17
±
1
17
±
2
18
±
1
17
±
2
17
±
1
'Lactate
(mmol
L
-1
)
8.7
±
0.32
9.0
±
.48
8.9
±
0.42
8.7
±
0.49
9.1
±
0.38
8.9
±
0.41
'RER
1.22
±
0.08
1.19
±
0.10
1.20
±
0.10
1.15
±
0.11
1.22
±
0.13
1.18
±
0.11
'Exercise
time
(sec)
624
±
16
629
±
18
607
±
40
630
±
41
572
±
21
578
±
28
00
2
HR
(bpm)
181
±3
182
±4
182
±
3
180
±
5
184
±
4
182
±
3
2
RPE
18±2
18
±
1
17±2
18
±
1
19
±
2
18
±
1
2
Lactate
(mmol•L
-
')
8.2
±
0.30
8.6
±
.37
8.1
±
0.42
8.0
±
0.51
8.4
±
0.41
8.6
±
0.49
Data
are
mean±SEM.
No
interaction
effects,
exercise
type
effects,
pre/post-intervention
effects,
or
group
main
effects
were
noted
for
any
variable
(p
>
0.05).
'Represents
data
obtained
for
the
GXT.
2
Represents
data
obtained
for
the
Wingate
test.
Exercise
time
for
the
Wingate
test
was
equal
to
30
seconds
for
all
subjects
pre-
and
postintervention.
Respiratory
exchange
ratio
(RER)
data
were
not
collected
during
the
Wingate
test.
A10%
1.8
-
A
1.6
-
1.4
-
Exercise
A13%
T
Induced
A15%
Oxidative
Stress
and
Carnitine
9
IN
Pre
Ex
1
Post
Ex
1
OPre
Ex2
Al2%
111
Post
Ex
2
1.2
-
A17%
1
-
o
A13%
A16%
=
0.8
-
0.6
-
0.4
-
0.2
-
0
Placebo
GPLC-1
GPLC-3
MI
Pre
Ex
1
A5%
111
Post
Ex
1
A5%
Pre
Ex
2
1
1
Al2%
O
Post
Ex
2
0.4
-
0.2
-
A5%
0
Placebo
GPLC-1
GPLC-3
FIGURE
1
Plasma
malondialdehyde
(.tmoll
-1
)
before
and
following
a
GXT
(A)
and
Wingate
cycle
test
(B),
before
and
following
an
8-week
intervention
of
aerobic
exercise
with
or
with-
out
GPLC
supplementation.
Pre
Ex
1
=
Preexercise,
preintervention;
Post
Ex
1
=
Postexercise,
preintervention.
Pre
Ex
2
=
Preexercise,
postintervention;
Post
Ex
2
=
Postexercise,
postintervention.
*Group
by
pre/postintervention
interaction
(p
=
0.044);
group
main
effect
(p
=
0.040).
No
other
interaction
or
main
effects
were
noted
for
malondialdehyde
(p
>
0.05).
Percent
change
values
from
pre-
to
postexercise
are
included
above.
Data
are
mean
±
SEM.
hydrogen
peroxide
(p
=
0.05),
with
values
increasing
from
pre-
to
postexercise
(Figure
2).
No
other
interaction
or
main
effects
were
noted
for
hydrogen
peroxide
(p
>
0.05),
although
the
group
main
effect
approached
statistical
significance
(p
=
0.11).
Both
a
time
(p
=
0.003)
and
group
(p
<
0.0001)
main
10
R.J.
Bloomer
and
W.A.
Smith
16
-
A
A21%
A20%
14
-
12
-
1
0
-
8
6
-
4
-
2
-
0
Placebo
16-
B
A19%
A17%
14
-
12
-
1
0
-
6
-
4
-
2
-
0
Placebo
A20%
A18%
T
GPLC-1
IN
Pre
Ex
1
0
Post
Ex
1
OPre
Ex
2
0
Post
Ex
2
A16%
A20%
GPLC-3
A26%
A25%
IN
Pre
Ex
1
O
Post
Ex
1
Pre
Ex
2
O
Post
Ex
2
A18%
A22%
T
GPLC-1
GPLC-3
FIGURE
2
Plasma
hydrogen
peroxide
(Rmol•L
-1
)
before
and
following
a
GXT
(A)
and
Wingate
cycle
test
(B),
before
and
following
an
8-week
intervention
of
aerobic
exercise
with
or
without
GPLC
supplementation.
Pre
Ex
1
=
Preexercise,
preintervention;
Post
Ex
1
=
Postexercise,
preintervention.
Pre
Ex
2
=
Preexercise,
postintervention;
Post
Ex
2
=
Postexercise,
postintervention.
Time
main
effect
(p
=
0.05).
No
other
interaction
or
main
effects
were
noted
for
hydrogen
peroxide
(p
>
0.05).
Percent
change
values
from
pre-
to
postexercise
are
included
above.
Data
are
mean
±
SEM.
effect
were
noted
for
xanthine
oxidase
activity,
with
values
increasing
from
pre-
to
postexercise,
and
collectively
lower
for
GPLC-3
compared
with
GPLC-1
and
placebo.
No
other
interaction
or
main
effects
were
noted
for
xanthine
oxidase
activity
(p
>
0.05;
Figure
3).
Pre
Ex
1
Post
Ex
1
0
Pre
Ex
2
Post
Ex
2
A34%
*
A28%
M
7%
A24%
I
GPLC-1
GPLC-3
Exercise
Induced
Oxidative
Stress
and
Carnitine
11
Pre
Ex
1
Post
Ex
1
Pre
Ex
2
Post
Ex
2
A38%
A22%
I
*
A37%
A31%
A
16
-
14
-
12
-
1
0
-
E
A53%
A49%
6-
B
Placebo
16
A41%
A26%
14
12
10
-
3
8
E
4
2
0
Placebo
GPLC-1
GPLC-3
FIGURE
3
Plasma
xanthine
oxidase
activity
(.t.mL
-1
)
before
and
following
a
GXT
(A)
and
Wingate
cycle
test
(B),
before
and
following
an
8-week
intervention
of
aerobic
exercise
with
or
without
GPLC
supplementation.
Pre
Ex
1
=
Preexercise,
preintervention;
Post
Ex
1
=
Postexercise,
preintervention.
Pre
Ex
2
=
Preexercise,
postintervention;
Post
Ex
2
=
Postexercise,
postintervention.
*Group
main
effect
(p
<
0.0001);
time
main
effect
(p
=
0.003).
No
other
interaction
or
main
effects
were
noted
for
xanthine
oxidase
activity
(p
>
0.05).
Percent
change
values
from
pre-
to
postexercise
are
included
above.
Data
are
mean
±
SEM.
DISCUSSION
Findings
from
this
investigation
indicate
the
following:
(1)
markers
of
oxidative
stress
are
increased
in
response
to
both
aerobic
and
anaerobic
power
testing,
(2)
the
response
does
not
differ
between
exercise
modes,
(3)
an
8-week
12
R.J.
Bloomer
and
W.A.
Smith
intervention
of
aerobic
exercise
combined
with
GPLC
supplementation
decreases
resting
MDA,
and
(4)
exercise
training
alone
(at
the
intensity
and
duration
performed
here)
or
in
combination
with
GPLC
does
not
attenuate
the
increase
in
oxidative
stress
following
aerobic
or
anaerobic
power
testing.
Based
on
these
findings,
we
accept
our
hypotheses
that
both
forms
of
exer-
cise
would
induce
oxidative
stress
and
that
oxidative
stress
(with
regards
to
MDA)
would
be
lower
following
the
intervention
period
as
a
result
of
GPLC
supplementation.
We
must
reject,
however,
our
hypothesis
that
oxidative
stress
would
be
lower
following
the
intervention
of
exercise
training
(with
regards
to
all
oxidative
stress
variables).
Although
we
noted
small
increases
in
TEAC
(5%-8%)
for
all
groups,
these
failed
to
reach
statistical
significance.
It
is
possible
that
a
greater
increase
in
TEAC
would
have
been
related
to
more
robust
decreases
in
our
oxidative
stress
biomarkers.
These
insignificant
increases
in
TEAC
partly
could
be
due
to
our
relatively
short
exercise
intervention,
coupled
with
the
use
of
a
moderate
intensity
exercise
protocol.
In
relation
to
GPLC
supple-
mentation,
while
evidence
exists
for
an
antioxidant
effect
of
this
nutrient
(DiGiacomo
et
al.
1993;
Vanella
et
al.
2000),
it
may
not
be
related
specifically
to
1'FAC,
which
is
influenced
primarily
by
albumin
and
uric
acid
(Rice-Evans
2000).
The
GPLC
may
exhibit
antioxidant
properties
via
other
mechanisms,
such
as
a
free-radical
scavenging
activity
(Vanella
et
al.
2000)
and/or
a
reg-
ulation
of
fatty
acid
metabolism
(Rauchova
et
al.
2002),
which
were
not
measured
in
the
present
study.
With
the
exception
of
the
decrease
in
resting
MDA
in
both
GPLC
groups
and
the
insignificant
decrease
in
resting
MDA
in
the
placebo
group
(7%;
p
>
0.05),
minimal
changes
were
observed
in
all
groups
with
regards
to
resting
hydrogen
peroxide
or
xanthine
oxidase
activity.
Moreover,
the
percent
change
values
from
pre-
to
postexercise
were
not
different
between
exer-
cise
modes,
between
groups,
or
from
pre-
to
postintervention
(Figures
1-3).
These
findings
indicate
that
in
our
population
of
previously
untrained
subjects,
the
oxidative
stress
response
to
aerobic
and
anaerobic
power
testing
is
similar,
and
does
not
appear
affected
by
an
8-week
intervention
of
aerobic
exercise
alone
or
in
conjunction
with
GPLC
supplementation.
It
is
possible
that
the
rise
in
oxidative
stress
following
an
acute
exercise
stress
is
necessary
to
pro-
mote
adaptations
related
to
upregulation
of
endogenous
antioxidant
defenses
(Ji
2002;
Ji
et
al.
2006).
Additionally,
because
RONS
play
important
roles
in
cell
signaling
(Haddad
2002),
redox
regulation
of
gene
transcription
(Liu
et
al.
2005),
cellular
immunity (Fialkow
et
al.
2007),
and
apoptosis
(Lee
and
Wei
2007),
it
is
probable
that
transient
increases
in
oxidative
stress
following
exercise
serve
useful
purposes.
Thus,
RONS
appear
essential
for
normal
physiological
function,
and
minor
increases
in
response
to
strenu-
ous
exercise
in
otherwise
healthy
individuals
are
likely
not
problematic.
Only
a
few
studies
have
compared
aerobic
and
anaerobic
exercise
modes
in
regards
to
the
oxidative
stress
response
using
a
crossover
design.
Exercise
Induced
Oxidative
Stress
and
Carnitine
13
Bloomer
and
colleagues
(2005)
noted
a
similar
immediate
postexercise
increase
in
oxidative
stress
biomarkers
following
aerobic
(cycling)
com-
pared
with
anaerobic
(squatting)
exercise
when
matched
for
exercise
time.
A
recent
investigation
matched
aerobic
exercise
(treadmill
running)
with
climbing
(intermittent
isometric
exercise)
performed
at
the
same
percentage
of
VO
2
and
noted
greater
oxidative
stress
following
climbing
exercise
(Magalhaes
et
al.
2007).
Alessio
and
coworkers
(2000)
noted
higher
lipid
peroxidation
following
anaerobic
(isometric
handgrip)
exercise
and
higher
protein
oxidation
following
aerobic
exercise
to
exhaustion
(treadmill
test),
when
matched
for
total
time.
One
additional
investigation
matched
treadmill
walking
and
resistance
exercise
with
respect
to
heart
rate
and
noted
similar
increases
in
lipid
peroxidation
(Vincent
et
al.
2004).
Other
studies
have
compared
aerobic
and
anaerobic
exercise
in
subjects
performing
one
mode
or
the
other,
noting
similar
changes
in
oxidative
stress
biomarkers
(Inal
et
al.
2001;
Marzatico
et
al.
1997).
Although
the
protocols
have
differed
greatly
across
studies,
data
from
prior
studies
agree
with
the
findings
presented
here,
in
that
both
acute
aerobic
and
anaerobic
exercise
induce
oxidative
stress
to
a
similar
extent.
Although
our
percent
change
values
in
oxidative
stress
biomarkers
were
generally
higher
for
the
GXT
compared
with
the
Wingate
test
(Figures
1-3),
these
differences
were
not
of
statistical
significance.
The
generation
of
RONS
may
be
associated
with
a
variety
of
factors
including
increased
oxygen
flux
through
the
mitochondrial
electron transport
chain,
mechanical
stresses,
ischemia-reperfusion
conditions
(in
particular
in
inactive
skeletal
muscle
and
organ
tissue,
which
are
deprived
of
blood
flow
during
strenuous
exercise),
changes
in
blood
borne
variables,
in
addition
to
other
factors
as
previously
described
(Jackson
et
al.
2007).
Indeed,
aerobic
and
anaerobic
exercise
modes
rely
on
different
metabolic
pathways
for
ATP
production,
and
have
the
ability
to
induce
multiple
distinct
changes
within
biological
systems.
In
the
present
study,
as
well
as
in
most
other
human
studies
presented
in
the
literature,
only
blood
oxidative
stress
was
mea-
sured.
Therefore,
it
is
unknown
whether
or
not
differing
changes
in
skeletal
muscle
or
organ
tissue
oxidative
stress
may
have
occurred.
Moreover,
we
measured
oxidative
stress
only
before
and
within
the
1
minute
following
exercise.
It
is
possible
that
differences
between
exercise
modes
may
have
been
present
at
times
distant
to
our
postexercise
collection
period.
This
is
a
limitation
of
the
present
study.
Moreover,
because
we
did
not
include
non-
exercise
control
groups
(with
and
without
GPLC
supplementation)
in
our
design,
we
cannot
truly
assess
the
independent
contribution
of
GPLC
in
relation
to
the
decreases
observed
in
resting
MDA.
Previous
animal
(Derin
et
al.
2004;
DiGiacomo
et
al.
1993;
Loster
et
al.
2001;
Rauchova
et
al.
2002;
Vanella
et
al.
2000)
and
human
(Corbucci
et
al.
1990;
Sachan
et
al.
2005)
studies
have
reported
a
decrease
in
oxidative
stress
following
supplementation
with
camitine.
To
our
knowledge,
only
one
study
has
measured
oxidative
stress
following
carnitine
supplementation
in
14
R.J.
Bloomer
and
W.A.
Smith
response
to
acute
exercise
(Volek
et
al.
2002).
Findings
from
the
Volek
et
al.
(2002)
study
oppose
those
of
the
present
investigation,
in
that
subjects
con-
suming
L-carnitine
L-tartrate
(2
grams
per
day
for
3
weeks
before
performing
a
bout
of
resistance
exercise)
experienced
a
significant
attenuation
in
xan-
thine
oxidase
activity.
Despite
this
finding,
the
immediate
postexercise
response
for
MDA
was
similar
between
carnitine
and
placebo
groups.
It
is
possible
that
differences
in
the
protocols
used
between
the
Volek
et
al.
(2002)
study
and
the
present
study
could
be
responsible
for
the
mixed
results,
as
well
as
differences
in
the
type
of
carnitine
supplement
used.
In
summary,
oxidative
stress
is
increased
to
a
similar
extent
in
response
to
both
aerobic
and
anaerobic
power
testing.
Eight
weeks
of
aerobic
exercise
combined
with
GPLC
supplementation
decrease
resting
MDA,
but
have
little
impact
on
hydrogen
peroxide
or
xanthine
oxidase
activity
either
at
rest
or
in
response
to
acute
exercise.
It
is
probable
that
transient
changes
in
oxidative
stress
in
response
to
acute
exercise
are
necessary
for
normal
biological
functioning.
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