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Department of Human Biology, Maastricht University, 6200 MD Maastricht, The Netherlands
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
FOOTNOTES
REFERENCES
ABSTRACT 
Jeukendrup, A. E., M. Mensink, W. H. M. Saris, and A. J. M. Wagenmakers. Exogenous glucose oxidation during exercise in endurance-trained and untrained subjects. J. Appl.
Physiol. 82(3): 835-840, 1997.
To investigate the
effect of training status on the fuel mixture used during exercise with
glucose ingestion, seven endurance-trained cyclists (Tr; maximum
O2 uptake 67 ± 2.3 ml · kg
1 · min1)
and eight untrained subjects (UTr; 48 ± 2 ml · kg1 · min1)
were studied during 120 min of exercise at ~60% maximum
O2 uptake. At the onset of exercise, 8 ml · kg1 · min1
of an 8% naturally enriched
[13C]glucose solution
was ingested and 2 ml/kg every 15 min thereafter. Energy expenditure
was higher in Tr subjects compared with UTr subjects (3,404 vs. 2,630 kJ; P < 0.01). During the second
hour, fat oxidation was higher in Tr subjects (37 ± 2 g) compared
with UTr subjects (23 ± 1 g), whereas carbohydrate
oxidation was similar (116 ± 8 g in Tr subjects vs. 114 ± 4 g in UTr subjects). No differences were observed in exogenous
glucose oxidation (50 ± 2 g in Tr subjects and 45 ± 3 g in UTr subjects, respectively). Peak exogenous glucose oxidation
rates were similar in the two groups (0.95 ± 0.07 g/min in Tr
subjects and 0.96 ± 0.03 g/min in UTr subjects). It is concluded that the higher energy expenditure in Tr subjects during exercise at
the same relative exercise intensity is entirely met by a higher rate
of fat oxidation without changes in the rates of exogenous and
endogenous carbohydrates.
training; carbon 13; breath test; stable isotopes; substrate
utilization
INTRODUCTION FOR MANY YEARS it has been known that substrate
utilization during exercise is dependent on the exercise intensity and
duration and that both training and diet may affect the relative
importance of carbohydrate (CHO) and fat as a fuel (3). As exercise
duration progresses, total CHO oxidation decreases while the
contribution of plasma glucose and fatty acids to total energy
metabolism increases (36). Prolonged exercise at moderate exercise
intensities [60-70% maximum
O2 uptake
( It has been shown that CHO ingestion may maintain blood glucose
availability and high rates of CHO oxidation late in exercise when
muscle glycogen levels are low (4, 7, 29). The increased rates of
glucose uptake (29) and oxidation (1) may be responsible for the
observed improvements in exercise time to exhaustion when CHOs are
ingested during exercise (7).
Training is another factor that provokes a large shift in substrate
utilization during submaximal exercise (6, 13, 14). After training, the
reliance on fat as an energy source is markedly increased, whereas the
contribution of CHO decreased, as indicated by a decreased respiratory
exchange ratio (RER) value (6, 13, 14, 22) and a slower rate of
muscle glycogen breakdown (21). In rats (2) and humans (6), training
also decreases blood glucose turnover during moderate-intensity
exercise. In addition, Jansson and Kaijser (16) reported lower leg
glucose uptake in trained compared with untrained men during exercise
at 65%
Together, these data indicate that the increase in fat oxidation in the
trained muscle during exercise reduces both the oxidation of muscle
glycogen and of blood glucose. We therefore hypothesized that untrained
subjects would also oxidize a larger amount of ingested CHO compared
with trained subjects because their rates of total CHO oxidation and
glucose turnover are higher.
To our knowledge, there is only one study that investigated the effect
of physical training on exogenous glucose oxidation. Krzentowski et al.
(23) measured the oxidation of orally ingested glucose during exercise
at the same absolute intensity (40% of the pretraining
Until now, no study has investigated the effect of training on the
composition of the fuel mixture oxidized during exercise at the same
relative exercise intensity when CHOs are ingested. Therefore, the
present study was undertaken to investigate the differences in total
fat and CHO oxidation and in the contribution of exogenous and
endogenous CHO oxidation between endurance-trained and untrained
subjects at the same relative, moderate intensity.
MATERIALS AND METHODS Table 1.
Subject characteristics
O2 max)] results
in muscle glycogen depletion and decreased blood glucose concentrations
as a result of decreased hepatic glucose production (1, 29).
O2 max as
determined by arteriovenous concentration differences of glucose and
estimated blood flow.
O2 max) before and
after a 6-wk training program. Although endurance training is known to
cause a large shift from predominantly CHO oxidation toward fat
oxidation (6, 13, 14), in their study Krzentowski et al. (23) observed
no changes in total CHO or fat oxidation. Yet, exogenous glucose
oxidation was increased by 17% by the training. These findings are in
contrast to a major body of literature and to the above-formulated
hypothesis.
Untrained (n = 7)
Trained
(n = 8)
Age, yr
20.9 ± 0.5
25.1 ± 1.4
Height, cm
183 ± 3
182 ± 2
Weight, kg
75.4 ± 3.8
72.3 ± 1.2
BMI, m/k2
22.6 ± 0.9
22.0 ± 0.5
Wmax, W
291 ± 12
414 ± 14*
O2 max, l/min
3.5 ± 0.1
5.2 ± 0.1*
Values are means ± SE; n = 15 subjects. BMI, body mass
index; Wmax, maximum workload;
O2 max, maximum
O2 uptake.
*
Significantly different between trained and
untrained subjects, P < 0.001.
O2 max was
measured on an electronically braked cycle ergometer (Lode Excalibur,
Groningen, The Netherlands) during an incremental exhaustive exercise
test (24) 1 wk before the first experimental trial. The results of this
test were used to determine the 50% maximum workload (Wmax; ~60%
O2 max) that was
later used in the experimental trials.
Experimental trials.
Each subject performed two exercise trials, each separated by at least
7 days. The order of the trials was counterbalanced. Each trial
consisted of 120-min cycling at 50% Wmax (~55-60%
O2 max). During one
test, subjects ingested a glucose solution with a high natural
abundance of 13C to study oral
glucose oxidation. The second test was employed with ingestion of a
glucose solution with a low natural abundance of
13C to allow correction for
changes in breath
13CO2
background enrichment during exercise. To avoid background shifts,
standard procedures were followed (18, 19). Subjects were instructed
not to consume any products with a high natural abundance of
13C during the entire experimental
period. This was done to minimize a shift in background enrichment due
to changes in endogenous substrate utilization. Furthermore, subjects
were instructed to keep their diet as constant as possible the days
before the trials.
Protocol.
Subjects reported to the laboratory at 8:00 AM after an overnight fast,
and before all trials a small standardized breakfast of two crackers
with cheese was provided [(in g) 14 CHO, 4 fat, 6 protein].
A Teflon catheter (Baxter Quick Cath DuPont) was inserted into an
antecubital vein, and at 8:30 AM a resting blood sample was drawn. Two
subjects were tested on the same day, starting the protocol 10 min
apart (i.e., the second subjects started the protocol 10 min later).
Resting breath gases were collected (Oxycon 
, Meinhardt, Mannheim,
Germany), and vacutainer tubes were filled directly from a mixing
chamber in duplicate to determine the
13C/12C
ratio in expired CO2. At 8:50 AM,
the first subject started a warm-up of 5 min at 100 W, followed by 5 min at 40% Wmax. At 9:00 AM, the workload was increased to 50% Wmax
for 120 min. During the first minute, subjects drank an initial bolus
(8 ml/kg) of an 8% glucose solution. Thereafter, every 15 min a
beverage volume of 2 ml/kg was provided. The average amount of glucose
provided during the 120 min of exercise was 127 ± 2 g in Tr
subjects and 132 ± 7 in UTr subjects. Blood samples were drawn at
30-min intervals until the end of exercise. Expiratory gases were
collected every 15 min.
Glucose solutions.
To quantify exogenous glucose oxidation, solutions were prepared from
corn-derived glucose (Amylum), which has a high natural abundance of
13C. The
13C enrichment of the glucose was
11.2 
/mil (
) vs. Pee Dee Bellemnitella (PDB;
0.01259 atom percent excess) and was determined by on-line combustion-isotope ratio mass spectrometer (Carlo Erba-Finnigan MAT
252, Bremen, Germany). During the control trial, subjects ingested an
8% solution prepared from potato-derived glucose (AVEBE). This glucose
had a 13C enrichment of
26.1 vs. PDB (0.02934 atom percent excess), which is similar to the 13C
enrichment of expired air of European subjects (39).
Analysis.
Blood (5 ml) was collected into EDTA-containing tubes and centrifuged
for 4 min at 4°C. Aliquots of plasma were frozen immediately in
liquid nitrogen and stored at 40°C until analysis of glucose (Uni Kit III, 0710970, La Roche, Basel, Switzerland), lactate (9), and
free fatty acid (FFA; Wako NEFA-C test kit, Wako Chemicals, Neuss,
Germany) concentrations that was performed with the COBAS FARA
semiautomatic analyzer (La Roche). Insulin was analyzed by radioimmunoassay (Linco Ultra-Sensitive Human Insulin radioimmunoassay kit). From indirect calorimetry [RER,
O2 uptake
(O2)], and
stable-isotope measurements (breath
13CO2/12CO2;
isotope ratio mass spectrometer, Finnigan MAT 252), total energy
expenditure and oxidation rates of total fat, total CHOs, and exogenous
glucose were calculated.
Calculations.
From CO2 uptake
(CO2) and
O2, total CHO and total fat
oxidation rates were calculated (32)
|
|
difference
between the
13C/12C
ratio of the sample and a known laboratory reference standard, according to the formula of Craig (8)
|
13C was then related to an
international standard, PDB.
The amount of ingested glucose oxidized was calculated according to the
formula
|
C is the 13C enrichment
of expired air in the control test (C; background),
exp is the
13C enrichment of expired air
during exercise at different time points,
ing is the
13C enrichment of the ingested
glucose, and k is the amount of
CO2 (in liters) produced by the
oxidation of 1 g glucose (k = 0.7467 l
CO2/g glucose).
In the present study and in previous studies (20, 34, 37,
39), it was shown that instructing the subjects not to eat any products of high natural 13C
abundance during the experimental period was effective in reducing the
background shift (change in
13CO2)
from endogenous substrate stores in European subjects (39). However,
although the background shift was small in the present study,
background correction was made by using the
13C enrichment of breath samples
in the CHO trial.
It should be noted that in the use of
13CO2
in expired air to calculate exogenous substrate oxidation is the
trapping of exogenous 13CO2
in the bicarbonate pool, a very large and slowly exchanging pool in
which an amount of CO2 arising
from decarboxylation of energy substrates is temporarily trapped each
minute (35). However, during exercise, the
CO2 production increases
severalfold so that a physiological steady-state situation will occur,
and
13CO2
in expired air will be equilibrated with the
13CO2/H13CO3
pool. The dilution of
13CO2
becomes negligible, and recovery of
13CO2
approaches 100% after 60 min of exercise (31). Therefore, in the
present study, data from the initial 60 min were not used for the
calculation of exogenous glucose oxidation.
Statistics.
An unpaired t-test was used to compare
the differences in substrate utilization and blood parameters between
Tr and UTr subjects. Analysis of variance for repeated measures was
performed to study differences over time within each group.
Scheffé's post hoc test was applied in case of a significant
(P < 0.05)
F-ratio to locate the differences.
RESULTS
O2 and heart rate.
The workload at 50% Wmax was 207 ± 7 W in the Tr subjects and 146 ± 6 W in the UTr subjects. Over the entire exercise period, O2 was significantly higher
in the Tr compared with UTr subjects (P < 0.01). On average,
O2 was 38 ml/kg in Tr
subjects and 29 ml/kg in UTr subjects, respectively, which corresponded
to 57 and 60% O2 max,
respectively. Despite the higher absolute work rate, the Tr subjects
exercised at a significantly lower heart rate. In Tr subjects, heart
rate increased from 127 ± 3 to 130 ± 3 beats/min (bpm) and in
UTr subjects from 129 ± 4 to 147 ± 4 bpm, respectively, toward
the end of exercise.
Total CHO and fat oxidation.
After 15 min of exercise, RER was 0.87 ± 0.01 in Tr subjects and
0.91 ± 0.01 in UTr subjects, respectively (P < 0.05),
and after 120 min of exercise the RER was 0.85 ± 0.01 and
0.89 ± 0.01 in Tr and UTr subjects, respectively
(P < 0.05). Total fat oxidation calculated over the second hour of exercise (60-120 min) was
significantly higher in Tr compared with UTr subjects (37.4 ± 2.3 g
in Tr subjects vs. 22.5 ± 1.4 g in UTr subjects; Fig.
1). No differences were observed in the
absolute amounts of CHO oxidized in this period (116.3 ± 7.5 vs.
113.7 ± 3.6 g in UTr subjects; Fig. 1).
O2,
O2 uptake. * Significant
difference between trained and untrained subjects, P < 0.05.
Exogenous glucose oxidation. Background 13C enrichments measured from the resting breath samples were comparable for the Tr and UTr subjects (
26.2 ± 0.2 vs. PDB in Tr subjects
and 25.6 ± 0.2 vs. PDB in UTr subjects, respectively). Changes in isotopic composition of expired
CO2 in response to exercise
are shown in Fig. 2. With
ingestion of the corn-derived glucose in CHO tests, the rise in
13C was significant, reaching an
enrichment difference of ~4 toward the end of 120-min
exercise (compared with resting breath sample). The changes in
background enrichment during exercise in the control trial were minimal
and not statistically significant. A background correction was made for
the calculation of exogenous glucose oxidation by using the data from
the control trial. In line with the breath isotopic enrichment,
exogenous glucose oxidation showed a gradual increase over time (Fig.
2). Peak oxidation rates were reached at the end of exercise (120 min)
and were 0.95 ± 0.07 and 0.96 ± 0.03 g/min in Tr and UTr
subjects, respectively. This difference was not statistically
significant. The amount of exogenous glucose oxidized over the 60- to
120-min period was slightly, but not significantly, higher in Tr
compared with UTr subjects (49.5 ± 1.5 vs. 44.8 ± 2.6 g; Fig.
1). Endogenous glucose oxidation, as calculated from total CHO
oxidation minus exogenous glucose oxidation, was also similar in Tr
and/or UTr subjects (68.9 ± 2.7 g in Tr and 66.8 ± 6.8 g in UTr subjects, respectively; Fig. 1).
vs. Pee Dee Bellemnitella (PDB)].
Values are means ± SE; n = 15 subjects. 
, PDB in untrained subjects; 
,
13C enrichment in untrained
subjects; 
, PDB in trained subjects; 
,
13C enrichment in trained
subjects. B: no difference was
observed in exogenous glucose oxidation in endurance-trained () and
untrained subjects () at same relative exercise intensity.
Blood parameters. Plasma glucose concentrations remained stable during exercise, between 4.5 and 4.9 mmol/l. No differences between the two groups were observed (Fig. 3A). Plasma FFA levels were also similar, although there was a tendency for the Tr subjects to have slightly higher plasma FFA concentrations (Fig. 3B). Plasma lactate concentrations were significantly higher in the UTr compared with the Tr subjects throughout the entire exercise period (Fig. 3C). In both trials, plasma insulin levels decreased during exercise from values of ~10-11 µU/ml to values of ~4-5 µU/ml. There were no differences between the Tr and UTr subjects (Fig. 3D).
) and untrained
subjects () during 120 min of exercise. * Significant
difference between 2 groups, P < 0.05.
DISCUSSION
We studied the composition of the fuel mixture and oxidation rates of
exogenous glucose oxidation in subjects with different training
backgrounds. A group of Tr and UTr subjects showed large differences in
Wmax and O2 max (Table
1). Therefore, endurance-trained subjects exercised at a 42% higher
absolute work rate, whereas relative exercise intensity was the same.
As a result, energy expenditure was also 29% higher in the Tr group.
One of the main adaptations to endurance training is a reduction in the
rate of CHO oxidation during exercise and a concomitant increased rate of fat oxidation. This effect has been observed at both the same absolute and relative exercise intensities (5, 6, 12, 14-16).
Also, in the present study a higher rate of fat oxidation and an
increased relative contribution of fat were observed in Tr compared
with UTr subjects when they exercised at the same relative exercise
intensity. However, despite markedly higher rates of fat oxidation, Tr
subjects displayed similar rates of exogenous, endogenous, and total
CHO oxidation. Although the absolute work rate in the Tr group was
higher, endogenous CHO utilization was similar in Tr and UTr groups.
A more appropriate way to look at the data during exercise at the same relative exercise intensity may be by expressing substrate utilization relative to energy expenditure (Fig. 1). The contribution of fat is higher in Tr subjects (42.3 vs. 30.2%). The reduction in the relative contribution is mostly explained by a lower contribution of endogenous glucose (33.7 vs. 42.3%), whereas exogenous glucose contribution is about equal in the Tr and UTr subjects (25.0 vs. 27.5%). Therefore, we could not confirm our hypothesis that UTr subjects have higher rates of exogenous CHO oxidation compared with Tr subjects.
To our knowledge, there is only one other study (23) that investigated
the effect of training on exogenous CHO oxidation rates. In a
comparison of our data with the findings of the study of Krzentowski et
al. (23), there seem to be some striking differences. In their study,
six subjects trained 60 min, 5 times/wk at a low intensity
(30-40% O2 max),
and oral CHO oxidation was investigated at the same absolute exercise
intensity before and after a 6-wk training program. A training-induced
increase in O2 max of
29% was reported, whereas CHO and fat oxidation changed little. Fat oxidation seemed to be slightly higher after training, but during the
later stages of exercise this difference was not statistically significant. Exogenous CHO oxidation, however, was increased by 17%
after training.
The difference in
O2 max between the Tr
and UTr subjects was much larger in the present study (46% in this
study vs. 29% reported by Krzentowski et al.) (23), and the exercise
intensity was higher (56-60%
O2 max in this study
vs. 40% O2 max
reported by Krzentowski et al.). Despite the larger difference in
training status, the Tr subjects did not have an increased exogenous
glucose oxidation, so we cannot confirm the suggestion brought about by Krzentowski et al. that training leads to an increased capacity to
oxidize ingested CHO. For both groups in our study, peak oxidation rates of the ingested glucose were 0.95-0.96 g/min. These values are close to the maximum oxidation rate of orally ingested CHO, which
is believed to be ~1.0 g/min (10, 38).
Of interest are also a paper by Massicotte et al. (26) and one by
Pirnay et al. (33). They looked at the effect of increasing exercise
intensity on exogenous glucose oxidation. With increasing exercise
intensity, the rate of oral CHO oxidation increases (26, 33), although,
at high work rates, oxidation rates may level off (33).
Apparently, the present study is not in line with these
findings: we found slightly but not significantly higher oxidation
rates for subjects exercising at
O2 of 38 and 29 ml · kg1 · min1.
The work rate in the UTr subjects in the present study was below the
value at which leveling off of the relationship between work rate and
oral glucose oxidation, as reported by Pirnay et al. (33), occurred.
Thus training seems to change the relationship between exercise
intensity and exogenous glucose oxidation.
The oxidation of orally ingested CHO has been extensively investigated
by using either stable or radioactive tracers. Both methods revealed
information regarding the factors that influence exogenous CHO
oxidation rates (see Ref. 10 for review). Among these factors are the
type (11, 25, 27, 30, 37) and the amount of CHO ingested (34, 38), the
feeding schedule (10), glycogen availability (17, 28), and the exercise
intensity (26, 33). Here we observed no differences in exogenous
glucose oxidation at ~60
O2 max in subjects with
a different training status. This may imply that UTr and Tr subjects
may equally benefit from CHO ingestion.
In conclusion, the present study demonstrates that exogenous and endogenous glucose oxidation rates during similar relative submaximal exercise intensities were not different in Tr and UTr subjects, even with large differences in the relative contribution of CHO and fat. One of the most profound observations in this study was the higher fat oxidation rates in the Tr subjects. The increase in energy expenditure in the Tr subjects was entirely met by this increase in fat oxidation without changes in the oxidation rates of total, endogenous, and ingested CHOs.
FOOTNOTES
Address for reprint requests: A. E. Jeukendrup, Dept. of Human Biology, Maastricht University, PO Box 616, NL-6200 MD Maastricht, The Netherlands (E-mail: A.Jeukendrup{at}HB.UNIMAAS.NL).
Received 15 July 1996; accepted in final form 1 November 1996.
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