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Comparison of the Type of Substrate Oxidation During Exercise Between Pre

and Post Pubertal Markedly Obese Boys

Article  in  International Journal of Sports Medicine · June 2006

DOI: 10.1055/s-2005-865751 · Source: PubMed

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Frederique Brandou Jean Frederic Brun

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F. Brandou1
A. M. Savy-Pacaux2
Comparison of the Type of Substrate Oxidation
J. Marie2
J. F. Brun1 During Exercise Between Pre and Post Pubertal
J. Mercier1 Markedly Obese Boys

Training & Testing

Abstract
The aim of this study was to investigate, in markedly obese chil-
dren, the effect of puberty on substrate oxidation during an acute
bout of exercise. Two groups of markedly obese boys (7 pre pu-
bertal, 8 post pubertal, matched for adiposity) performed an ex-
ercise-test designed for measuring carbohydrate and fat oxida-
tion with indirect calorimetry, and consisting of five six-minute
steady-state workloads at 20, 30, 40, 50, and 60% of the theoret-
ical maximal aerobic power. Fat oxidation (mg ´ min±1) is cor-
related to fat free mass (FFM) (r = 0.7, p = 0.02). When expressed
in crude flow rate units, fat oxidation is slightly higher in PostP
than PreP children (p < 0.05). However, when expressed per unit
of FFM or as a percentage of total fuel oxidation, fat oxidation is
lower in PostP than PreP children (p < 0.05). Multivariable anal-
ysis shows that the influence of age on the ability to oxidize fat
at exercise is explained by the pubertal increase in FFM. In mark-
edly obese children during puberty, the ability of each kg of FFM
to oxidize fat at exercise decreases (± 28% at 20%Wmax th), but
the pubertal increase in FFM overcomes this effect, resulting in
an increase in whole body ability to oxidize fat at exercise
(+ 17,3 % at 20%Wmax th).
Key words
Obesity ´ children ´ fat oxidation ´ indirect calorimetry

Abbreviations Introduction
1
BMI body mass index The lack of physical activity appears to be one of the most signif-
CHO carbohydrate icant factors which explains the increasing prevalence of obesity
FFA free fatty acids in children. Indeed, children today are far more sedentary than
FFM fat free mass ever before [20], as sedentary activities such as watching televi-
PreP pre pubertal sion and playing video games, both risk factors for obesity [40],
PostP post pubertal have greatly supplanted the active physical games of the past.
RER respiratory exchange ratio
WHR waist to hip ratio Skeletal muscle is largely involved in the development of obesity
Wmax th theoretical maximal aerobic power [31]. More precisely, muscular abnormalities could alter the bal-
ance of substrate utilization, thus facilitating fat accumulation in

Affiliation
1
Service Central de Physiologie Clinique, UnitØ CERAMM (Centre dExploration et de RØadaptation des
Anomalies MØtaboliques et Musculaires), CHU Lapeyronie, Montpellier Cedex 5, France and
DØpartement de Physiologie des Interactions, EA 701 «Muscles et pathologies chroniques»,
FacultØ de MØdecine, Montpellier Cedex 2, France
2
Perle Cerdane, Maison denfants à caract›re sanitaire spØcialisØ, Osseja Cedex, France

Correspondence
F. Brandou ´ DØpartement de Physiologie des Interactions, EA 701 «Muscles et pathologies chroniques»,
FacultØ de MØdecine ´ Bd Henri IV ´ 34060 Montpellier Cedex 2 ´ France ´ Phone: + 33 4 6760 0766 ´
Fax: + 33 4 6760 69 04 ´ E-mail: fredbrandou@yahoo.fr

Accepted after revision: April 15, 2005

Bibliography
Int J Sports Med 2005; 26: 1 ± 8  Georg Thieme Verlag KG ´ Stuttgart ´ New York ´
DOI 10.1055/s-2005-865751 ´
ISSN 0172-4622

adipose tissue. In contrast, regular exercise training, generally
recommended in obese people, induces muscular metabolic
changes, which can reverse these defects [11].
We have recently reported in obese children that two months of
exercise training increase fat oxidation during exercise [7].
Although the subjects served as their own controls in this study,
it was difficult to differentiate between the effects of training
and those of puberty, because the trained group consisted of
both pre pubertal (PreP) and post pubertal (PostP) children.
While some authors have investigated the changes in skeletal
muscle metabolism that occur during puberty [23, 33], there is a
paucity of data concerning this issue in obese children [6, 42].
Training & Testing
However several authors have used skeletal muscle biopsies to
investigate skeletal muscle composition and metabolism [13 ±
15]. These studies have shown a possible relationship between
anaerobic enzyme activity and maturation, initiating the concept
of limited anaerobic capacity in children. Taylor et al. [39] eval-
uated metabolic responses in the calf muscle of children, young-
er adults and older adults during exercise. They showed that, at
the same relative intensity of exercise, children relied less on gly-
colysis and more on oxidative metabolism to meet the energy
demand. However, others [18] showed no significant difference
in adults versus adolescents in citrate synthase activity.
Studies using calorimetry at rest generally indicate that the rate
of lipid oxidation is higher in obese children [24, 27], and that, in
normal weight children, it increases during puberty [3]. How-
ever, the influence of both puberty and childhood obesity on the
balance of substrates during exercise remains poorly known,
although exercise is more and more proposed as an important
2 component of the management of obesity. Recently, exercise cal-
orimetry has been developed by several teams in order to target
more closely training protocols in both adults [11, 31] and chil-
dren [7] suffering from obesity. Thus, it becomes important to
know to what extent puberty, on its own, modifies the balance
of substrates as assessed with this technique in obese children.
Therefore, this study was undertaken in order to investigate the
effect of puberty on the ability to oxidize lipids during exercise.
We hypothesize that puberty may alter the balance of CHO and
fat oxidation during exercise in obese children.
In an attempt to verify this hypothesis, we compared CHO and fat
oxidation during exercise between pre and post pubertal obese
children. CHO and fat oxidation rates were assessed using calori-
metric measurements.
Subjects and Methods
Subjects
Fifteen markedly obese adolescent boys (7 Pre pubertal, 8 Post
pubertal) participated in this study. A child was defined as obese
when his Body Mass Index (BMI) > 97th percentile defined by the
French curves [35]. None of these adolescents had chronic dis-
ease, endocrine disorders or diabetes mellitus.
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Initial instructions
All subjects were asked to fast for 12 h before the exercise test-
ing. The conditions and requirements of the exercise testing
(hospital routine measurements) were explained to each subject.
Evaluation of pubertal stage
Pubertal stage was evaluated according to the Tanner classifica-
tion [37, 38], regarding testicular volume and pubic hair, by a
trained physician. The subjects were distributed according to
stage of puberty: pre pubertal group (PreP group) who were in
Tanner stage 1 and post pubertal group (PostP group) who were
in Tanner stages 4 and 5.
Anthropometry
Weigh, height, waist and hip measurements were performed and
BMI was calculated as weight in kilograms divided by the square
of height in meter (kg/m2). Body composition, as fat mass and fat
free mass (FFM), was assessed with a multifrequency bioelectri-
cal impedance (Dietosystem Human IM Scan) using the follow-
ing frequencies: 1, 5, 10, 50, and 100 kHz. Analysis was performed
with the software Master 1.0. In this study, we used Houtkoop-
ers equation which has been cross-validated in a very rigorous
study [19] and which is accurate for subjects aged between 10
and 19 years, so that it was valid for all the subjects of the study.
Moreover, hydration conditions were standardized for measur-
ing body composition, and all children were examined in the
morning in a fasting state.
The Z-score for BMI was calculated according to Cole [9] and
Rolland-Cachera [35], with the following formula:
Z = [(Q/M)L ± 1]/LS
With: Q = BMI, M = median, L = power, S = coefficient of variation.
Individuals values of M, L and S were found in the tables of
Rolland-Cachera [35].
The BMI z-scores were 4.2  0.3 in the two groups showing that
we studied markedly obese children.
Exercise testing
The subjects performed an exercise test on an electromagneti-
cally braked cycle ergometer (Ergoline Bosh 500) connected to a
breath by breath device (ZAN 600) for gas exchange measure-
ments (VÇO2 and VÇCO2).
Before exercise, we calculated the theoretical maximal aerobic
power (Wmax th) using the Tanner (1991) equation: 3.5 Watts/
Fat Free Mass (FFM). As generally used to individualize the incre-
ment of exercise testing [36, 41], the workload of each step was
calculated from the theoretical maximal aerobic power (Wmax
th), i.e., power corresponding to the theoretical VÇO2max. In conse-
quence, the subjects underwent a test with the same relative in-
cremental workload and were compared at the same percentage
of their Wmax th.
The test consisted of five six-minute steady-state workloads cor-
responding to 20, 30, 40, 50, 60% of Wmax th. Heart rate was
monitored continuously throughout the test. Ventilatory param-
eters (VÇO2, VÇCO2) were recorded during the last three-minutes of
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each workload. Pedal frequency was maintained between 60 and

70 rpm throughout the test. Table 1 Anthropometric characteristics in Pre pubertal (PreP) and
Post pubertal (PostP) groups.
Fat and CHO oxidation
Whole body substrate oxidation was calculated from the meas- PreP PostP p
urement of the respiratory exchange ratio (RER = VÇCO2/VÇO2 in ex- n=7 n=8
pired gases) in order to determine whole body substrate oxida-
tion. RER is the simplest and most widely used method for deter- Tanners stage I IV ± V
mination of fuel utilization. VÇO2 and VÇCO2 were determined as Age, yr 10.6  0.5 13.5  1.1 0.001
the means of measurements during the last three-minutes of Body weight, kg 62.9  3.3 94.2  6.2 0.001
each workload, according to Mac Rae [7,11, 26, 31]. Height, m 1.5  0.02 1.7  0.02 0.001
BMI, kg ´ m±2 28.6  1.6 32.2  1.6 NS
The percentages of CHO and fat oxidation were calculated by us- Z-score 4.2  0.24 4.2  0.32 NS
ing the following equations [30]: Body fat, kg 29.3  5.2 33.2  2.6 NS

Training & Testing

Fat free mass, kg 36.5  2.7 60.9  4.02 0.001
% CHO = ([RER ± 0.71]/0.29) ´ 100
Waist, cm 85.7  3.3 95.7  3 0.01
Hip, cm 99.0  4.7 110.5  3.3 0.05
% Fat = ([1 ± RER]/0.29) ´ 100
WHR 0.86  0.01 0.86  0.02 NS

Fat and CHO oxidation rates were calculated from the gas ex- BMI = Body mass index; WHR = waist to hip ratio
change measurements according to the non-protein respiratory
quotient technique [32]:

CHO (mg ´ min±1) = 4.585 VÇCO2 ± 3.2255 VÇO2

Fat (mg ´ min±1) = ± 1.7012 VÇCO2 + 1.6946 VÇO2 with gas volume
expressed in milliters per minute. CHO and fat oxidation rate
were normalized by FFM.

We were thus able to determine the proportion of CHO and fat,

which is a function of the balance of substrates oxidized by the
body.
After smoothing the curves, we calculated a parameter represen-
tative of the balance between fat and CHO utilization induced by
increasing exercise intensity: the maximal fat oxidation point
[31]. This point (Lipox max) is the point where the increase in
fat oxidation induced by increasing workload reaches a maxi-
mum, which will then be followed by a decrease as CHO becomes
the predominant fuel. It is calculated from equations, deter-
mined in previous papers on children [7] and adults [31].
Data analysis
Unpaired Students t-tests were used to compare subject charac-
teristics. Significant differences between absolute oxidation
rates of fat and CHO were determined by using factorial ANOVA.
Significance of differences among groups and changes for RER
with the exercise intensity were determined by using repeated-
measures ANOVA. Post-hoc comparisons were made using
Sheffes test for significant difference. Finally, we used partial
correlations analysis to delineate the respective influence of age
and FFM on the ability to oxidize fat at exercise. For all statistical
analyses, values were expressed as mean ( SEM) and signifi-
cance was accepted at p < 0.05.
3
Fig. 1 Respiratory Exchange Ratio (RER) in PreP (closed circle) and
PostP (closed squares) groups, with the exercise intensity expressed
as relative power output (% Wmax th).
Results
Anthropometric characteristics
The PostP group (n = 8), although older and taller than the PreP
group (n = 7), had a similar amount of body fat and the same de-
gree of adiposity expressed as a Z-score on BMI charts. Moreover,
their BMI failed to be different and their WHR is quite the same.
The physical characteristics of the two groups are shown in Table
1. Fat free mass (FFM) showed a significant increase from pre
puberty to post puberty. No difference was noted among groups
in total body fat (kg).
Respiratory exchange ratio (RER)
RER increased proportionally to the intensity of exercise express-
ed as relative power output in both groups (p < 0.001). RER val-
ues tended to be higher in the PostP group than in the PreP
group, but the difference did not reach significance (Fig. 1).

Substrate oxidation
Fig. 2 a shows the changes in fat oxidation (expressed in
mg ´ min±1) during submaximal exercise between the two groups.

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Fig. 2 b Fat oxidation (mg/min/FFM) in PreP (closed circle) and Post

Fig. 2 a Fat oxidation (mg ´ min±1) in PreP (closed circle) and Post (closed squares) groups, with the exercise intensity expressed as rela-
Training & Testing

(closed squares) groups, with the exercise intensity expressed as rela- tive power output (% Wmax th). * p < 0.01 significantly different be-
tive power output (% Wmax th). * p < 0.05 significantly different be- tween the two groups.
tween the two groups.

The PostP group relied more on fat during exercise than the PreP
group (p < 0.05). Fat oxidation is higher in the PostP than in the
PreP group during exercise in obese children (for example,
+ 17.3 % at 20 % Wmax th). However, since FFM increases during
puberty, we normalized fat oxidation for FFM in order to neutral-
ize a possible effect. Accordingly, Fig. 2 b shows the same puber-
tal changes in fat oxidation during sub maximal exercise,
expressed as mg ´ min±1 ´ FFM±1. In this case, the PostP group re-
lied less on fat during exercise than the PreP group (p < 0.05).
Therefore, when fat oxidation is expressed per kg of FFM, puberty
seems to decrease the use of fat during exercise in obese children
(for example, ± 28% at 20 % Wmax th).

The power intensity at which the Lipox max occurs (expressed in

4 % Wmax th), is higher in PostP compared to PreP children (Fig. 3).
This result indicates that during puberty, the level of exercise in-
tensity at which fat oxidation is maximal is increased.
Figs. 4 a and b show the relationships among fat oxidation at Lip-
ox max, FFM and age. Expressed in mg ´ min±1, the rate of fat oxi-
dation at the level of the Lipox max increases proportionally with
both age (r = 0.66; p = 0.03) and FFM (r = 0.7; p = 0.002). When
this fat oxidation is expressed per kg of FFM, there is a non signi-
ficant tendency to decrease when age increases (data not
shown), but a significant decrease when FFM increases
(r = ± 0.66; p = 0.006) (Fig. 5). In order to delineate the respective
influence of age and FFM on the ability to oxidize fat at exercise,
we performed partial correlations analysis among age, fat oxida-
tion in mg ´ min±1 and FFM. If the variable ªFFMº is kept constant
by the statistical procedure, the correlation between age and fat
oxidation disappears (r = 0.417, ns), indicating that the variable
ªfat oxidationº is correlated to age only because age is correlated
to FFM. FFM is thus the explanatory variable of the increase in
whole body lipid oxidation associated with the increase in age
during the pubertal period. On the whole, this partial correlation
analysis indicated that in PostP children, there is an increase in
the ability to oxidize fat at exercise only because FFM increases
during puberty, while the ability to oxidize fat expressed per kg
of FFM rather decreases.
Fig. 6 shows the percentage of fat and CHO oxidation at each
workload of exercise in PreP and PostP groups. During rest and
Fig. 3 Fat oxidation at Lipox max expressed as % of Wmax th in PreP
and PostP groups. * p < 0.04 significantly different between the two
groups.
mild to moderate exercise, fat remains the predominant source
of energy for oxidation, while a shift towards CHO oxidation oc-
curs at exercise above 50% Wmax th (p < 0.01). This figure shows
that the PostP group has a greater dependence on CHO than the
PreP group. At 20% Wmax th, PostP children oxidize a signifi-
cantly lower percentage of fat and a higher percentage of CHO
compared to the PreP group (64.6 % 2.03 vs. 74.4 % 4.9 for fat
and 35.4% 2.03 vs. 25.6 % 4.9 for CHO, p < 0.05).
Fig. 7 shows substrate oxidation rates (expressed as
mg ´ min±1 ´ FFM±1) at each workload in PreP and PostP groups.
Fat oxidation rates were lower in the PostP group compared to
the PreP group (p < 0.01) at 20, 30, 40 % Wmax th (F = 7.92,
F = 7.14, F = 7.81, respectively). CHO oxidation (mg ´ min±1 ´ FFM±1)
increased with exercise intensity in both groups (p < 0.001) with-
out any significant difference between PreP and PostP groups.
The increase of exercise intensity, in Fig. 8, results in a significant
difference in the contribution of the relative rate of substrate ox-
idation between PreP and PostP groups. Actually, the rate of fat

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Training & Testing

Fig. 4 b Relationship between fat oxidation at Lipox max (mg ´ min±1)
Fig. 4 a Relationship between fat oxidation at Lipox max (mg ´ min±1)
and FFM r = 0.7, p = 0.002.
and age (years) r = 0.66, p = 0.03.

Fig. 6 Percentage of Fat and CHO oxidation rates, in relation to the

Fig. 5 Relationship between fat oxidation
(mg ´ min±1 ´ FFM±1) and FFM r = ± 0.66, p = 0.006.
exercise intensity expressed as relative power output (% Wmax th).
PreP: Closed circle = fat %, closed triangle = CHO %; PostP: Open circle
at Lipox max = fat %, open triangle = CHO %; * p < 0.01 significantly different be-
tween fat and CHO oxidation in both group; # p < 0.05 significantly dif-
ferent between PreP and Post in fat oxidation; ? p < 0.05 significantly
different between PreP and Post in CHO oxidation.

Fig. 7 Mean absolute substrate oxidation

rates (kcal ´ min±1 ´ FFM±1) in PreP and PostP
groups with the exercise intensity (% Wmax
th). § p < 0.01 significant difference in fat ox-
idation between the two groups.

oxidation was significantly lower in the PostP group than in the
PreP group but this difference was only significant at 20 and 30 %
Wmax th (p < 0.05, F = 5.56; p < 0.03, F = 5.22, respectively).
Discussion
Our results show that in markedly obese children, puberty is
associated with significant alterations in the balance of substrate
oxidation during exercise. The ability to oxidize fat, which is pro-

Brandou F et al. Substrate Oxidation in Markedly Obese Children¼ Int J Sports Med 2005; 26: 1 ± 8

Training & Testing
portional to fat free mass, actually decreases when it is expressed
per unit of fat free mass or as a percentage of total fuel oxidation.
However, when expressed in crude flow rate units, it increases
slightly, but this effect is only due to the gain in fat free mass dur-
ing this period which prides, to some extent, the diminishing ef-
fect of puberty.
Gender, age and adiposity may all be confounding factors, and
both the body mass index and the percentage of fat increase dur-
ing puberty. For this reason, we have tried to very carefully
match our subjects. Comparison of BMI measurements, express-
ed as Z-scores, shows that our subjects exhibit the same degree
of overweight. The Z-score indicates the degree to which an indi-
6 viduals measurement deviates from what is expected from the
height charts. Thus, a Z-score of 0 is equivalent to the 50th per-
centile and a Z-score of + 2.0 is equivalent to the 97th percentile.
In our study, a similar value of 4.2 was found for the Z-score of
the BMI in both groups. Such a Z-score confirms morbid obesity
and shows that PreP and PostP children were correctly matched
in terms of adiposity.
Indirect calorimetry is a usual method to quantify substrate oxi-
dation rates at rest and during exercise. Nevertheless, during ex-
ercise above the lactate threshold, the accuracy of the technique
has been discussed. The main concern is that lactate acidosis in-
creases CO2 production and is thus likely to increase the RER in-
dependent of the balance of substrates. However, the contribu-
tion of bicarbonate-derived CO2 to VÇCO2 has been studied and
seems to be rather negligible, so that the RER remains a fair mir-
ror of the balance of substrate oxidations during exercise [21].
These methodological aspects of the validity of the RER tech-
nique during six-minute workloads have been extensively dis-
cussed in some of our previous papers [31]. On the whole, exer-
cise calorimetry appears to be valid for measurements of sub-
strate oxidation during submaximal steady-state exercise bouts.
Such measurements have shown that obese people oxidize less
lipids at exercise than lean matched controls [31] and that low
intensity exercise training markedly reverses this defect in both
adult and adolescent obese subjects [7,11, 28].
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Fig. 8 Mean relative substrate oxidation
rates (%) in PreP and PostP groups with the
exercise intensity (% Wmax th). § p < 0.03
significant difference in fat oxidation be-
tween the two groups. * p < 0.03 significant
difference in CHO oxidation between the
two groups.
To individualize the increment of exercise testing [36, 41], the
workload of each step was calculated from the theoretical maxi-
mal aerobic power (Wmax th), i.e., power corresponding to the
theoretical VÇO2max. Moreover, to avoid overestimating Wmax th
in obese children in connection with an excess of fat mass, we
used the Tanner formulas, taking into account the fat free mass.
The exercise test was designed to make children exercise at the
same relative working intensities, expressed as percentage of
theoretical Wmax, and substrate oxidation rates were normal-
ized by fat free mass. Thus, our findings are not due to a differ-
ence in age resulting in a difference in exercise tolerance for sim-
ilar work loads. Actually, if it were the case, we would observe a
better tolerance of exercise in older children, and thus presum-
ably a higher lipid oxidation at similar work loads. Due to the
correct matching of children, we find the opposite and observe
that children exhibit a lower ability (per kg of FFM) to oxidize
fat at exercise after puberty.
Our finding of alterations in substrate oxidation during sub max-
imal exercise after puberty in markedly obese children should be
interpreted taking into account the fact that obese children ex-
hibit excess of both fat mass and fat free mass (FFM). In addition,
during puberty, boys gain lean tissue, especially skeletal muscle.
However, during this period of life, skeletal muscle becomes in-
sulin resistant [5,10]. This insulin resistance is likely to impair
metabolic flexibility [22], i.e., muscle ability to oxidize CHO at
rest and fat at exercise are both impaired. In other terms, the in-
sulin-resistant muscle is unable to adequately shift its balance of
substrate oxidations from the ªresting patternº to the ªexercise
patternº and thus burns too little CHO at rest and too little fat at
exercise [22]. This mechanism is consistent with our finding that
the whole capacity for fat oxidation at exercise (mg ´ min±1) in-
creases with puberty only because FFM increases, but if this in-
fluence of FFM is neutralized in order to analyze only the effect
of puberty, the ability to oxidize fat (mg ´ min±1 ´ FFM±1) during
exercise decreases in markedly obese children. Several authors
have previously reported an increase in fat oxidation with pub-
erty in normal weight children [3], but in those studies, fat oxi-
dation was not measured during exercise, but during a hyperin-
sulinemic euglycemic clamp. Therefore, this increase in fat oxi-

dation at rest does not rule out the possibility of an impairment
of the ability to oxidize fat at exercise due to the loss of metabolic
flexibility that characterizes muscular insulin resistance.
Whatever the exact mechanism of this defect of fat oxidation at
exercise, it is interesting to note that it occurs at a period where
insulin sensitivity is also known to markedly decrease [5,10].
Muscular insulin resistance, which is quite common in obese
adults, appears also to be associated with alterations of substrate
balance. There is also, in this case, a decrease in fat oxidation
ability and an early shift from lipid towards CHO-derived fuel,
compared to lean people [31], consistent with the above men-
tioned concept of impaired metabolic flexibility [22]. However,
the physiological mechanism linking low insulin sensitivity to
low fat oxidation in muscle is unclear.
Concerning puberty, however, this issue is even more compli-
cated, since the decrease in insulin sensitivity during this period
of life is a physiological event and not a disease, and its mecha-
nism is not well understood. This decrease in insulin sensitivity
is likely to be associated with other physical and hormonal
changes (including changes in growth hormone and testosterone
which are involved in the development of FFM). Recent studies
that investigated a lot of possible hormonal mechanisms sug-
gested that a possible candidate to explain pubertal insulin resis-
tance is the rise in plasma androstenedione that occurs during
this period [17].
Whatever the hormonal background, at the muscular level, some
previous studies show evidence of a possible conversion of fibre
phenotype towards fast twitch during puberty in lean children.
This mechanism is likely to result in a higher rate of glycolysis.
Actually, there is a relative paucity of muscle biopsy studies in
children compared to adults, because of an obvious ethical limi-
tation. Some authors have shown that children have a higher
proportion of slow twitch fibres in the vastus lateralis muscle as
compared with untrained adults [4,15]. The proportion of fast
twitch fibres increases significantly with age from the age of 5,
caused by a transformation of slow twitch to fast twitch [25].
This difference disappears during late adolescence [16].
Another finding of this study is that, as already known in adults,
substrate utilization shifts as a continuum from a greater de-
pendence on fats at low intensities of 20, 30 and 40 % Wmax th,
which is the zone of lipid oxidation, towards a preferential use of
CHO at exercise above 50 % Wmax th, when exercise intensity in-
creases. The physiological relevance and the mechanism of this
ªcrossoverº of substrates have been extensively investigated by
the team of G. Brooks [8]. The shift in substrate selection with ex-
ercise intensity is undoubtedly under multiple regulatory con-
trols. In this study, the PostP children exhibited an earlier shift
from fat to CHO-derived fuels during exercise than PreP children.
Fat oxidation, in percentage, was lower during exercise in PostP
group.
A recent study [34] demonstrated that in healthy weighting 11 ±
12 year-old boys, maximal fat oxidation occurs around 56%
VÇO2max (8.18 mg ´ min±1 ´ FFM±1) during an incremental type exer-
cise protocol derived from that of Achten [1]. In our study, we
show that the maximal fat oxidation (Lipox max) occurs around
Brandou F et al. Substrate Oxidation in Markedly Obese Children¼ Int J Sports Med 2005; 26: 1 ± 8
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50 % Wmax th (6.94 mg ´ min±1 ´ FFM±1) in PreP boys and around
47% Wmax th (5.43 mg ´ min±1 ´ FFM±1) in PostP boys. So, in com-
parison to the team of Riddell [34], maximal fat oxidation seems
to be lower in obese PreP boys than healthy PreP boys. Moreover,
we observed that PostP boys have a lower maximal fat oxidation,
because of the FFM parameter. We did not use the same protocol
as Riddell et al. for determining maximal fat oxidation. While
they used a protocol derived from that of the team of Achten
(12.5 Watts increments, 3 min intervals vs. 35 Watts, 5 min), in
our study, we used an individualized protocol with an increment
of 10% of Wmax th every 6 min. Despite this difference between
protocols, it appears that obese PreP children have a lower max-
imal fat oxidation (representing a lower capacity to oxidize fat
during exercise) than healthy PreP children, and higher maximal
Training & Testing
fat oxidation than PostP children.
It is, of course, interesting to try to further elucidate mechanisms
which lead to a lower fat oxidation in the PostP group than the
PreP group. However, this finding of an impairment of the ability
to oxidize fat at exercise during puberty in already markedly
obese children may be by itself an important issue for clinicians
involved in the management of pubertal morbid obesity. It may
help to explain the worsening of their overweight during this
period, if less fat is burned at exercise. Moreover, since endur-
ance training is known to markedly reverse this shift in the bal-
ance of substrates in both adults [12, 29] and children [7], such
findings emphasize the importance of regular exercise at this
particular period of life in the management of obesity. They also
demonstrate the importance of exercise training protocols at
lower intensities [2] in the late pubertal markedly obese adoles-
cents in order to utilize relatively more fat.
7
Conclusion
The current study shows that puberty alters the balance of sub-
strate oxidation during exercise in markedly obese children.
These modifications depend on fat free mass, which increases
during puberty. In order to elucidate the specific effect of pu-
berty, we corrected results for FFM, and so show that PostP obese
children rely less on fat oxidation (mg ´ min±1 ´ FFM±1) during ex-
ercise than PreP obese children. Exercise at the same relative
submaximal intensity elicits a higher CHO utilization in PostP
children. We suggest that this process may be involved in the dif-
ficulty to manage morbid obesity during puberty, and that such
findings strongly emphasize the importance of exercise at this
period of life in obese children or children prone to obesity. How-
ever, more studies will be required, although ethical and meth-
odological considerations obviously limit invasive research in
children.
Acknowledgements
The present study was supported by a grant from the Serono
Company.
The authors thank the staff of Perle Cerdane (Mr Barnole [direc-
tor], Mr Bauloz, Mme Maret-Fleuret, and Mme Borrocoso) and
EMO Company for their technical assistance.

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