Fat balance in obese subjects: role of glycogen
stores
Patrick
Schrauwen,
Wouter D. Van Marken
Lichtenbelt,
Wim H. M.
Saris, and
Klaas R.
Westerterp
Department of Human Biology, Maastricht University, 6200 MD
Maastricht, The Netherlands
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ABSTRACT |
In a previous
study, we showed that lean subjects are capable of rapidly adjusting
fat oxidation to fat intake on a high-fat (HF) diet when glycogen
stores are lowered by exhaustive exercise. However, it has been
proposed that obese subjects have impaired fat oxidation. We therefore
studied the effect of low glycogen stores on fat oxidation after a
switch from a reduced-fat (RF) diet to an HF diet in obese subjects.
Ten healthy, obese male and female subjects (26 ± 2 yr, body mass
index 31.8 ± 1.4, maximal power output 228 ± 14 W) consumed an
RF diet (30, 55, and 15% of energy from fat, carbohydrate, and
protein, respectively) at home for 3 days on four occasions
(days 1-3). On two occasions, subjects came to the laboratory on day
3 at 1500 to perform an exhaustive glycogen-lowering
exercise test (Ex), after which they went into a respiration chamber
for a 36-h stay. On the other two occasions, subjects directly entered
the respiration chamber at 1800 for a 36-h stay. In the respiration
chamber, they were fed, in energy balance, either an HF diet (60, 25, and 15% of energy from fat, carbohydrate, and protein, respectively)
or an RF diet. All diets were consumed as breakfast, lunch, dinner, and
two or more snacks per day. Twenty-four-hour respiratory quotient was
0.91 ± 0.01, 0.89 ± 0.01, 0.84 ± 0.01, and 0.81 ± 0.01 with RF diet, RF + Ex, HF, and HF + Ex treatments, respectively. With the HF treatment, fat oxidation was below fat intake, indicating the
slow change of oxidation to intake on an HF diet. After the HF + Ex
treatment, however, fat oxidation matched fat intake. In conclusion,
obese subjects are capable of rapidly adjusting fat oxidation to
fat intake when glycogen stores are lowered by exhaustive exercise.
respiration chamber; obesity; fat oxidation
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INTRODUCTION |
THE HIGH and still increasing prevalence of obesity in
affluent societies is known to produce major health hazards. Apart from
environmental factors, it is now commonly accepted that obesity is also
under the influence of genetic factors. However, the impact of
environmental factors in the prevalence of obesity has been illustrated
by Ravussin and Tataranni (17). They studied two populations with
similar genetic background (Pima Indians) living in different
environments (Mexico and Arizona). The Mexican Pima Indians have a body
mass index that is 7-10 units lower than the Arizona Pima Indians,
a difference that might be explained by the higher fat intake and lower
spontaneous physical activity observed in the Arizona Pima Indians.
Other studies (11, 15) also suggest an association between obesity and
a high-fat (HF) intake. In humans, it has been shown that fat intake
does not promote its own oxidation (21). Furthermore, in preobese or obese subjects, an impaired ability to oxidize fat has been shown (3,
6, 24, 27). Flatt (7) postulated a two-compartment model, in which it
is stated that fat oxidation can be increased to match fat intake
1) by maintaining glycogen stores in
a lower range or 2) by expansion of
the adipose tissue mass. In a previous study (20), we showed that lean
subjects were capable of rapidly (within 24 h) adjusting fat oxidation
to fat intake when glycogen stores were lowered by exhaustive exercise,
whereas no complete adjustment of fat oxidation to fat intake occurred
without glycogen-lowering exercise. However, obesity has been described
as a misadaptation to an HF diet (1). This might suggest that preobese
or obese subjects are not capable of rapidly adjusting fat oxidation to an HF intake by maintaining glycogen stores in a lower range. Another
possibility is, however, that they have fewer fluctuations in the
amount of glycogen stored, possibly due to low levels of physical
activity. We therefore investigated whether obese subjects are capable
of rapidly increasing fat oxidation on an HF diet when glycogen stores
are lowered by exhaustive exercise. We hypothesized that, compared with
the lean subject in our previous study, the obese subjects are less
capable of rapidly adjusting fat oxidation to fat intake on an HF
diet when glycogen stores are lowered by exhaustive exercise.
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MATERIALS AND METHODS |
Subjects
The characteristics of the 10 volunteers (4 men, 6 women) participating
in this study are shown in Table 1. All subjects were
healthy, untrained (not active in any sport, no training history), and
obese. No gender differences in the measured parameters of interest
were observed, and therefore data of males and females are pooled.
Subjects' habitual energy intake was 9.5 ± 0.6 MJ/day, with 30.3 ± 1.9, 51.4 ± 2.2, 15.2 ± 0.8, and 3.1 ± 1.1% of energy from fat, carbohydrate, protein, and alcohol,
respectively. The study was approved by the Ethical Committee of the
Maastricht University, and subjects gave their written informed
consent.
Experimental Design
Each subject followed four different treatments. Treatments were
separated by at least 1 wk and conducted in random order. Each
treatment consisted of a 36-h stay in a respiration chamber. To ensure
a similar dietary macronutrient composition before all four treatments,
food intake was controlled for 3 days before the treatments. Subjects
were given a reduced-fat (RF) diet for consumption at home for
days 1-3. On two occasions,
subjects came to the laboratory on day
3 at 1500 to perform an exhaustive glycogen-lowering exercise test (Ex) and then entered the respiration chamber at 1800 for
a 36-h stay. In the respiration chamber, they were given either an HF
diet (HF + Ex, 60 energy% fat) or an RF diet (RF + Ex). The RF diet
contained 30 energy% fat, as is often recommended in the prevention of
obesity (4). On the other two occasions, no glycogen-lowering exercise
was performed, but subjects directly entered the respiration chamber at
1800 for a 36-h stay, where they were given either an HF or RF diet. On
the morning of day 5, subjects left
the respiration chamber at 0800.
Maximal power output.
One week before the experiments, each subject performed an incremental
exhaustive exercise test on an electronically braked cycle ergometer
(Lode Excalibur, Groningen, The Netherlands) to determine maximal heart
rate and maximal power output
(Wmax). Exercise was performed until voluntary exhaustion or until the subject
could no longer maintain a pedal rate of >60 rpm. Subjects started
cycling at 75 W for 5 min. Thereafter, workload was increased by 50 W
every 2.5 min. When subjects were approaching exhaustion, as indicated
by heart rate and subjective scoring, the increment was reduced to 25 W. In practice, this meant that the last one to three load increments
were 25 W. Heart rate was registered continuously using a Polar Sport
Tester (Kempele, Finland). In each individual,
Wmax was
calculated from
where
Wout is the
highest workload completed by the subject,
t is the time (in s) performed on the
last workload, and
W is the final
uncompleted load increment (12).
Glycogen-lowering exercise.
During the Ex experiments, the subjects came to the laboratory at 1500, after fasting for 2 h, to perform a glycogen-lowering exercise test. It
has been shown repeatedly in our laboratory by Kuipers et al. (13) and
Wagenmakers et al. (25) that glycogen stores in muscle are
significantly decreased in both male and female subjects after this
exercise test. After a warm-up at 50% of
Wmax for 5 min,
subjects cycled for 2 min at 80% of
Wmax, followed by
2 min at 50% of
Wmax. This was
repeated until subjects were no longer able to perform the
high-intensity exercise. The maximal intensity was then lowered to 70%
of Wmax. The test
was ended after exhaustion, i.e., when subjects could no longer
maintain a pedal rate of >60 rpm. Subjects were allowed to consume
water during exercise. During the exercise, heart rate was measured continuously with a Polar Sport Tester. Energy expended during exercise
was calculated assuming a mechanical efficiency of 20% (9).
Diets
Before the experiment, subjects completed a 3-day food intake record to
estimate habitual diet composition. Metabolizable energy intake and
macronutrient composition of the diet were calculated using the Dutch
food composition table (23). In this table, metabolizable energy is
calculated by multiplying the amount of protein, fat, and carbohydrate
by the Atwater factors (16.74, 37.66, and 16.74 kJ/g for carbohydrate,
fat, and protein, respectively) (14). The amount of protein, fat, and
carbohydrate was multiplied by 0.909, 0.948, and 0.953, respectively,
to correct for digestibility of macronutrients. All experimental diets
were consumed as breakfast, lunch, dinner, and two or more snacks per
day. The composition of experimental diets is given in Table
2. All snacks had the same macronutrient
composition as the experimental diet. Food quotient (FQ) was defined as
the ratio of CO2 produced
(
CO2) to
O2 consumed
(
O2) during oxidation of a
representative sample of the diet consumed (8).
On days 1 and
2 and the first part of
day 3, an RF diet was provided for
consumption at home. Subjects were given a fixed amount of food (based
on their food intake record) and ad libitum access to snacks. On the
evening of day 3, subjects consumed
their dinner and evening snack (either RF or HF) in the respiration chamber. In the RF and HF treatments, energy intake for dinner and
evening snack was fixed at 35 and 10% of estimated daily energy expenditure, respectively [1.7 · BMR based on
Harris and Benedict equations; for women, BMR = 2.74 + 0.774 · H + 0.040 · BM
0.020 · A, and
for men, BMR = 0.28 + 2.093 · H + 0.058 · BM
0.028 · A, where
BMR is basal metabolic rate (in MJ/day),
H is height (in m), BM is body mass
(in kg), and A is age (in yr)] (10). In the RF + Ex and HF + Ex treatments, the evening snack had an energy content equal to
energy expended during the exercise test. On day
4, subjects were given an amount of energy equal to
1.55 times sleeping metabolic rate (SMR), as measured during the
preceding night. In a previous study (16), it was shown that, with a
comparable activity protocol used in the chamber, a physical activity
index of 1.58 was reached.
Procedures
Body composition.
Subjects weighed themselves in the respiration chamber on the morning
of days 4 and
5 without clothing, after voiding, and before eating and drinking. Measurements were done on a digital balance
(Seca Delta model 707) with an accuracy of 0.1 kg.
Whole body density was determined by underwater weighing in the morning
with the subjects in a fasted state. Body weight was measured on a
digital balance with an accuracy of 0.01 kg (Sauter type E1200). Lung
volume was measured simultaneously by use of the helium-dilution
technique using a spirometer (Volugraph 2000, Mijnhardt, The
Netherlands). Percent body fat was calculated using the equations of
Siri (22). Fat-free mass (FFM, in kg) was calculated by subtracting fat
mass from total body mass.
Indirect calorimetry and physical activity.
O2 and
CO2 were measured in a
whole-room indirect calorimeter (19). The respiration chamber is a
14-m3 room furnished with a bed,
chair, television, radio, telephone, intercom, wash bowl, and toilet.
The room is ventilated with fresh air at a rate of 70-80 l/min.
The ventilation rate is measured with a dry gasmeter (Schlumberger type
G6). The concentrations of O2 and
CO2 are measured using a paramagnetic
O2 analyzer (Hartmann & Braun type Magnos
G6) and an infrared CO2 analyzer (Hartmann & Braun type Uras 3G). Ingoing air is analyzed every 15 min and outgoing air once every 5 min. The gas sample to be measured is selected by a computer that also stores and processes the data. Energy expenditure is calculated from
O2 and
CO2 according to the method
of Weir (26).
In the respiration chamber, subjects followed an activity protocol
consisting of fixed times for breakfast, lunch, and dinner, sedentary
activities, and bench-stepping exercise. The bench-stepping exercise
was performed for 30 min at intervals of 5 min of exercise alternated
with 5 min of rest, at a rate of 60 steps/min and a bench height of 33 cm, and was repeated three times a day. Thus subjects exercised for 45 min/day at a relative low-to-medium intensity. In the daytime, no
sleeping or additional exercise was allowed during the stay in the
respiration chamber. All physical activity of the subjects was
monitored by means of a radar system based on the Doppler principle.
Urinary nitrogen excretion.
During the stay in the respiration chamber, urine was collected in two
batches, the first from 2000 to 0800 and the second over the subsequent
24-h interval. Subjects were requested to empty their bladders at 0800. The urine produced was included in the urine sample of the previous
batch. Samples were collected in containers with 10 ml
H2SO4
to prevent nitrogen loss through evaporation; volume and nitrogen
concentration were measured, the latter with a nitrogen analyzer
(Carlo-Erba type CN-O-Rapid).
Twenty-four-hour energy expenditure and substrate oxidation.
Subjects stayed in the respiration chamber for 36 h. Data from 2000 on
day 3 to 0800 on day
4 are presented for a study of the short-term effects
of treatments. For calculation of balances, 24-h energy expenditure
(24-h EE) and 24-h respiratory quotient (24-h RQ) were measured from
0800, on day 4 to 0800 on day
5. SMR was defined as the lowest mean energy expenditure
measured during 3 subsequent hours between 2400 and 0800, with a
minimal activity level indicated by the radar system.
Carbohydrate, fat, and protein oxidation were calculated by using
O2,
CO2, and urinary nitrogen
losses with the equations of Brouwer (5)
where
N is the total nitrogen excreted in urine (g/day),
O2 and
CO2 are measured in liters
per day, and P is protein oxidation (g/day).
Blood analysis.
On all four occasions, blood samples were taken on the morning of
days 4 and
5 after an overnight fast. For the
collection of blood on day 4, without
disruption of the respiration chamber measurement, subjects put an arm
through an air lock with a rubber sleeve to fit around the upper arm,
positioned under a window for eye contact. On one occasion, blood was
sampled on the morning of day 3.
Venous blood (10 ml) was sampled in tubes containing EDTA to prevent
clotting and immediately centrifuged at 3,000 rpm (100 g) for 10 min. Plasma was frozen in
liquid nitrogen and stored at
80°C until further analysis.
Plasma substrates were determined using the hexokinase method (LaRoche,
Basel, Switzerland) for glucose, the Wako NEFA C test kit (Wako
Chemicals, Neuss, Germany) for free fatty acids (FFA), the glycerol
kinase-lipase method (Boehringer Mannheim) for glycerol and
triacylglycerols, and the ultrasensitive human insulin RIA kit (Linco
Research, St. Charles, MO).
Statistical Analysis
All data are presented as means ± SE. Equality of RQ, FQ, energy
intake, energy expenditure, substrate intake, and substrate oxidation
was determined by calculating the 95% confidence intervals for
differences. Repeated-measures one-way ANOVA was used to detect differences in any variables between treatments. When significant differences were found, a Scheffé post hoc test was used to
determine the exact location of the difference. Differences in any
variables between days 4 and
5 were tested by using a paired
t-test.
 |
RESULTS |
Time until exhaustion during the exercise test was not significantly
different between the RF + Ex and HF + Ex treatments: 61 ± 3 and 67 ± 6 min, respectively. Also, no differences in
energy expended during the exercise tests were found: 2.5 ± 0.2 and
2.8 ± 0.3 MJ for RF + Ex and HF + Ex treatments, respectively.
Body weight, as measured in the respiration chamber, was not
significantly different between any of the treatments (Table 3).
SMR measured during the first night was significantly increased in the
HF + Ex treatment compared with the RF treatment
(P < 0.05), most likely because of
the effect of exercise on postexercise energy expenditure. However, SMR
measured during the second night was not significantly different
between any of the treatments (Table 3). Twenty-four-hour energy
expenditure (Table 4) and physical activity
index (24-h EE/SMR; Table 3) were not significant different between
treatments.
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Table 4.
Energy intake, energy expenditure, and energy balance as measured in
respiration chamber on four different treatments
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First 12-h Measurements
On the evening after the exercise test, subjects were given an amount
of energy, as HF or RF diet, to compensate for the energy expended
during the exercise bout. Of course, a positive energy balance was
therefore measured during the first 12 h in the chamber. However, this
positive energy balance was not significantly different between the RF + Ex and HF + Ex treatments (2.10 ± 0.26 vs. 2.46 ± 0.35 MJ).
RQ during the first 12 h in the respiration chamber was 0.890 ± 0.009, 0.862 ± 0.014, 0.848 ± 0.006, and 0.807 ± 0.01 for the RF, RF + Ex, HF, and HF + Ex treatments, respectively, and
was significantly different between treatments
(P < 0.01). The RQ in the HF + Ex
was significantly lower compared with the RF, RF + Ex, and HF
treatments (P < 0.01). RQ values in
the RF and HF treatments were also significantly different
(P < 0.01). In the RF + Ex
treatment, a positive carbohydrate balance of 94.5 ± 16.5 g and a
positive fat balance of 4.5 ± 6.4 g were reached, whereas in the
HF + Ex treatment, those values were +27.1 ± 11.7 and
+38.8 ± 5.7 g for carbohydrate and fat, respectively.
Thus glycogen was more replete in the RF + Ex treatment compared with the HF + Ex treatment, and, as a result, differences in glycogen store
were obtained.
Twenty-Four-Hour Measurements
In all four tests, 24-h energy balance (day
4) was not significantly different from zero (Table
4). Twenty-four-hour RQ was significantly different among all
treatments (P < 0.05). RQ in the RF
and RF + Ex treatments was significantly higher compared with the HF
and HF + Ex treatments (Fig. 1). RQ was
significantly different from FQ in the RF, HF, and HF + Ex treatments
(P < 0.05). In the RF + Ex
treatment, RQ and FQ were not significantly different (Fig. 1).

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Fig. 1.
Twenty-four-hour respiratory (RQ) and food quotients (FQ) as measured
in respiration chamber for day 4 (means ± SE). HF, high-fat diet; RF, reduced-fat diet; Ex,
glycogen-lowering exercise.
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Twenty-four-hour protein oxidation was not significantly different
between treatments (Table 5). In all
treatments, 24-h protein balance was significantly different from zero
(Fig. 2, P < 0.05).
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Table 5.
Carbohydrate, fat, and protein intake and oxidation as measured in
respiration chamber on four different treatments
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Fig. 2.
Twenty-four-hour energy and substrate balances for day
4 as measured in respiration chamber (means ± SE).
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Twenty-four-hour carbohydrate oxidation was significantly different
between the RF and HF or HF + Ex treatments as well as between the RF + Ex and HF or HF + Ex treatments (P < 0.01, Table 5). Carbohydrate balance was significantly different from
zero in the RF, HF, and HF + Ex treatments (Fig. 2).
Twenty-four-hour fat oxidation was significantly different between the
RF and HF or HF + Ex treatments and between the RF + Ex and HF + Ex
treatments (P < 0.05, Table 5). Fat balance was significantly different from zero in the RF
and HF treatments (Fig. 2). Fat oxidation can be adjusted for
energy balance by assuming that, in the case of a positive energy
balance, this surplus in energy will be stored as fat, and in case of a
negative energy balance, the deficit in energy is accomplished by
increasing fat oxidation. When adjusted for energy balance, 24-h fat
oxidation was 90 ± 13, 106 ± 15, 161 ± 16, and 178 ± 14 g/day in the RF, RF + Ex, HF, and HF + Ex treatments, respectively.
Blood Variables
Plasma triacylglycerol concentration increased significantly between
days 4 and
5 in the RF + Ex treatment and
decreased significantly in the HF treatment. On day
4, plasma triacylglycerol concentration was
significantly different between the RF and HF + Ex treatments. On
day 5, plasma triacylglycerol
concentration was significantly higher in the RF treatment compared
with the HF and HF + Ex treatment. In the RF + Ex treatment, plasma
triacylglycerol concentration was significantly higher compared with
the HF + Ex treatment (P < 0.05, Table 6). Plasma glucose concentration
significantly decreased in the RF treatment between
days 4 and
5 and increased in the RF + Ex and HF + Ex treatments. On day 4, plasma
glucose concentration was significantly higher in the RF treatment
compared with the HF and HF + Ex treatments. In the RF + Ex treatment, plasma glucose concentration was significantly higher compared with the
HF + Ex treatment. On day 5, no
differences in glucose concentrations between treatments were found
(P < 0.05). There were no
significant differences between any days and treatments in plasma FFA
and glycerol concentrations.
 |
DISCUSSION |
The results of the present study demonstrate that obese subjects are
capable of rapidly adjusting fat oxidation to fat intake when glycogen
stores are lowered. Therefore, these results are in concordance with
the results obtained in lean subjects and do not provide evidence
for an impaired capacity to rapidly change fat oxidation in obese
subjects. After glycogen-lowering exercise, fat balance was reached
when subjects consumed either an RF or HF diet. These results indicate
that obese subjects are capable of maintaining fat balance on an HF
diet when glycogen stores are sufficiently lowered.
One model that can explain the high prevalence of obesity in Western
societies is the two-compartment model of Flatt (7). According to this
model, fat oxidation can be raised by two mechanisms. First, fat
oxidation can be increased when glycogen stores are maintained in a low
range. However, in Western societies, with the abundance of food
available, people will eat to maintain glycogen stores filled. On an HF
diet, this means that people overeat and therefore gain weight (7).
Second, the associated expansion of the fat mass will lead to an
increase in fat oxidation until a new equilibrium is reached in which
average fat intake equals fat oxidation. Therefore, obesity can be seen
as a mechanism to adapt to an HF intake (1). The need for the human
body to expand its body fat mass in response to an HF intake can be
prevented by regular physical activity (18). It is evident that
individuals who are regularly physically active are much less prone to
become obese compared with sedentary individuals. Exercise reduces
glycogen levels, thereby allowing fat oxidation to increase between
meals. In this way, fat oxidation can become commensurate with fat
intake without expansion of the body fat mass (8). In the present study, we found that fat oxidation was increased sufficiently to match
fat intake when glycogen stores were lowered by exhaustive exercise.
During the first 12 h in the respiration chamber, carbohydrate balance
was more positive in the RF + Ex compared with HF + Ex treatment (94 ± 16 vs. 27 ± 12 g, respectively). It can therefore be assumed
that glycogen was more replete in the RF + Ex treatment. The difference
in 24-h fat oxidation between the RF + Ex and HF + Ex treatments can
thus be explained by differences in both glycogen stores and exogenous
carbohydrate availability. The higher fat oxidation in the HF + Ex
treatment compared with the HF treatment (same exogenous carbohydrate
availability) indicates the role of the glycogen in the regulation of
fat oxidation. Therefore, these results are in agreement with the model
of Flatt and show the impact of physical activity on fat oxidation and
indirectly on the prevention of obesity.
It is known that exercise can result in other (hormonal) adaptations
that might influence fat oxidation. However, in a study of energy
metabolism in the postexercise period, it was found that, 2.5 h after
cessation of exercise, FFA, glycerol, and glucagon concentrations
returned to their control values (2). The (hormonal) disturbances
induced by exercise therefore are not long lasting. In contrast, the
elevation of fat oxidation on the HF + Ex treatment was long lasting,
indicated, for example, by RQ during sleep, which was not significantly
different between the first and second nights in the respiration
chamber (data not shown). We therefore conclude that the increase in
fat oxidation cannot be explained by the exercise itself.
The present study was performed as a follow-up to our previous study in
which we showed that lean subjects were capable of rapidly adjusting
fat oxidation to fat intake on an HF diet when glycogen stores were
lowered by exhaustive exercise. Here we show the same capacity for
obese subjects. However, there are some differences between the two
studies. We therefore used the data as described previously (20) to
detect any difference between obese and lean subjects by use of
unpaired t-tests. RQ during the first
12 h was not significantly different between obese and lean subjects.
Twenty-four-hour RQ was significantly lower in the RF + Ex
and HF + Ex treatments in lean subjects. However, the results might be
influenced by differences in energy balance between the two studies.
Energy balance was significantly correlated with fat balance in both
obese and lean subjects (Fig. 3;
r2 = 0.51, P < 0.001). When fat
balance was corrected for energy balance, no differences in fat balance
between treatments was found in obese and lean subjects. We therefore
conclude that obese subjects are as capable as lean subjects of
increasing fat oxidation to match fat intake on an HF diet when
glycogen stores are lowered. Although the type of exercise used in this
study is not likely to be performed by obese people in daily life, the
results still indicate the importance of regular exercise in the
prevention and/or management of obesity.

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Fig. 3.
Relation between 24-h energy balance and 24-h fat balance in obese
(present study) and lean subjects (from Ref. 20).
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Our results seems to be in contrast with studies showing an impaired
uptake or oxidation of FFA by the muscle in obese subjects (3, 6).
However, it is difficult to compare those studies with the present
study, because we used a 24-h approach. Although we did not find, with
prior glycogen-lowering exercise, an impaired capacity to increase fat
oxidation on an HF diet when comparing obese with lean subjects, this
does not rule out the possibility that there might be an impaired
uptake and/or oxidation of FFA on the level of the muscle under
certain (stimulated) circumstances. However, further studies must
reveal the impact of impaired muscle FFA uptake rates on 24-h fat
oxidation.
When we pool the data obtained in obese and lean subjects, we find a
negative correlation between carbohydrate balance found during the
first 12 h in the respiration chamber and next 24-h fat oxidation
during RF + Ex and HF + Ex treatments (Fig.
4;
r2 = 0.29, P = 0.005). Carbohydrate
balance was calculated as measured carbohydrate balance
(2000-0800) minus estimated carbohydrate oxidation during
exercise. To estimate the latter, it was assumed that 80% of energy
expended during exercise was provided by carbohydrate (RQ ~0.94),
which is a reasonable value for this kind of extremely intensive
exercise. When carbohydrate oxidation was assumed to provide 90% of
energy expended during exercise, the correlation did not change.
These data therefore show the important role of glycogen stores in
determining the rate of fat oxidation.

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Fig. 4.
Relation between carbohydrate balance measured in respiration chamber
from 2000 to 0800 and 24-h fat oxidation for obese (present study) and
lean subjects (from Ref. 20) in RF + Ex and HF + Ex treatments.
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In conclusion, this study shows that obese subjects are capable of
rapidly adjusting fat oxidation to fat intake on an HF diet when
glycogen stores are lowered by exhaustive exercise. These results may
indicate that a lower level of regular physical activity is a
predisposing factor for obesity.
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FOOTNOTES |
Address for reprint requests: P. Schrauwen, Dept. of Human Biology,
Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.
Received 5 December 1997; accepted in final form 19 February 1998.
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