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Department of Human Biology, Maastricht University, 6200 MD Maastricht, The Netherlands
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In this study, an oral glucose load was enriched with a [U-13C]glucose tracer to determine differences in substrate utilization between endurance-trained (T) and untrained (UT) subjects during submaximal exercise at the same relative and absolute workload when glucose is ingested. Six highly trained cyclists/triathletes [maximal workload (Wmax), 400 ± 9 W] and seven UT subjects (Wmax, 296 ± 8 W) were studied during 120 min of cycling exercise at 50% Wmax (~55% maximal O2 consumption). The T subjects performed a second trial at the mean workload of the UT group (148 ± 4 W). Before exercise, 8.0 ml/kg of a 13C-enriched glucose solution (80 g/l) was ingested. During exercise, boluses of 2.0 ml/kg of the same solution were administered every 15 min. Measurements were made in the 90- to 120-min period when a steady state was present in breath 13CO2 and plasma glucose 13C enrichment. Energy expenditure was higher in T than in UT subjects (58 vs. 47 kJ/min, respectively; P < 0.001) at the same relative intensity. This was completely accounted for by an increased fat oxidation (0.57 vs. 0.40 g/min; P < 0.01). At the same absolute intensity, fat oxidation contributed more to energy expenditure in the T compared with the UT group (44 vs. 33%, respectively; P < 0.01). The reduction in carbohydrate oxidation in the T group was explained by a diminished oxidation rate of muscle glycogen (indirectly assessed by using tracer methodology at 0.72 ± 0.1 and 1.03 ± 0.1 g/min, respectively; P < 0.01) and liver-derived glucose (0.15 ± 0.03 and 0.22 ± 0.02 g/min, respectively; P < 0.05). Exogenous glucose oxidation rates were similar during all trials (±0.70 g/min).
exogenous glucose; endurance training; carbohydrate metabolism; stable isotopes; substrate metabolism
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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CARBOHYDRATE (CHO) and fatty acids are the main fuels
oxidized by skeletal muscle to provide energy during prolonged exercise at intensities between 30 and 80% maximal
O2 uptake
(
O2 max) (29). The main
CHO sources are muscle and liver glycogen, liver gluconeogenesis, and
ingested CHOs (29). The relative contribution of these fuel sources
varies with exercise intensity (1, 3, 5, 37) and training status (2, 7,
9, 18-20, 22).
Whole body calorimetry measurements have clearly shown that endurance training leads to an increase in total fat oxidation and a decrease in total CHO oxidation during exercise in subjects investigated in the overnight-fasted state (4) and also in subjects investigated between 1 and 6 h after ingestion of a standardized CHO-rich meal (7, 15, 20). Stable isotope tracers have been used to show that endurance training decreases the flux and oxidation rate of blood glucose at the same absolute intensity, whereas no change in glucose flux was seen at the same relative intensity in subjects investigated 1-2 h after ingestion of a standardized breakfast (15).
CHO ingestion during prolonged exercise at moderate intensities can increase time to exhaustion (6, 10, 11) and, therefore, CHO ingestion has become widespread among athletes, both professional and amateur, in a wide variety of sports. CHO ingestion leads to a better maintenance of blood glucose concentration and increases the ability to maintain high CHO oxidation rates during more prolonged exercise periods (10, 11, 17). It has been shown previously that ingested CHOs are oxidized with a maximal rate of ~1 g/min (17, 22, 39) and may account for >50% of the total CHO oxidation rate (39). Fat oxidation is reduced by CHO ingestion (12).
However, little information is available on the effects of training
status on the relative use of CHO and fat as well as on the relative
use of the different CHO sources in subjects who ingest CHOs during
exercise. By using a
[13C]glucose tracer,
Krzentowski et al. (26) measured the oxidation rate of orally ingested
glucose in subjects before and after a training period during exercise
at 40% of pretraining
O2 max. They reported a
17% increase after training. They failed to find a decrease in total
CHO oxidation, nor did they observe an increase in total fat oxidation.
Jeukendrup et al. (22) compared a group of trained and untrained
subjects exercising at the same relative intensity. In contrast with
Krzentowski et al. (26), they found similar oxidation rates of the
ingested glucose, a decrease in total CHO oxidation, and an increase in
total fat oxidation. Blood glucose enrichment was not measured in any
of these studies, so it was not possible to quantitate the relative
contributions of muscle glycogen and of glucose released by the liver
to the total energy expenditure.
Therefore, the first aim of the present study was to investigate whether a group of trained subjects has a higher rate of fat oxidation than do untrained subjects during moderate-intensity exercise while ingesting CHO, as has been previously observed in subjects who were investigated after an overnight fast. The second aim was to investigate whether trained subjects, who are accustomed to ingest larger amounts of CHO in their regular diets and who ingest oral CHO solutions during training sessions, oxidize orally ingested CHO at a similar or possibly at a higher rate than do untrained subjects. The third aim was to quantitate the oxidation rate and relative contribution of the other main CHO sources (muscle glycogen and glucose released from the liver). Therefore, six healthy trained cyclists/triathletes and seven healthy untrained subjects were studied during 120 min of cycling exercise at 50% maximal workload (Wmax) while they ingested a glucose solution enriched with a [U-13C]glucose tracer. The trained subjects also performed a second exercise trial at the same absolute workload as the untrained group, so that comparisons can be made both at the same absolute and relative workload. Total fat oxidation and total CHO oxidation were measured by using indirect calorimetry and the oxidation rates of the CHOs that originated from the different sources were indirectly quantitated by using tracer methodology, as described in detail in the following section.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects.
Two groups of subjects participated in this study. One group consisted
of seven well-trained cyclists or triathletes. The other group included
eight healthy, fit, but untrained, subjects not active in any sport and
without any history of endurance training. Subjects' characteristics
are listed in Table 1. Subjects were informed about the nature and risks of the experimental procedures before their informed consent was obtained. This study was approved by
the local Ethical Committee.
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Pretesting.
O2 max and Wmax were
measured on an electronically braked cycle ergometer (Lode Excalibur,
Groningen, the Netherlands) during an incremental exhaustive exercise
test (27) 1 wk before the first experimental trial (Table 1) to
determine the 50% Wmax (~55%
O2 max) workload used
in the following experimental trials (148 ± 4 and 199 ± 5 W in
the untrained and trained groups, respectively).
Experimental trials. All subjects performed an exercise trial that consisted of 120-min of cycling at 50% Wmax. Subjects in the trained group performed a second identical trial, with the workload set at the mean absolute workload performed by the untrained subjects (148 W). This was done to study differences in fuel selection between the two groups when performing exercise at the same absolute workload. The order of the trials performed by the trained subjects was randomized, and trials were separated by at least 7 days. During the tests, subjects ingested a glucose solution that was enriched with a [U-13C]glucose tracer.
Protocol.
The subjects arrived at the laboratory at 8:00 AM after an overnight
fast. A Teflon catheter (Baxter, Utrecht, The Netherlands) was inserted
into an antecubital vein, and a resting blood sample was drawn at 8:30
AM. Resting breath gases were collected (Oxycon 
, Mijnhardt,
Mannheim, Germany), and Vacutainer tubes (Becton-Dickinson, Meylan,
France) were filled directly from a mixing chamber in duplicate to determine the
13C/12C
ratio in expired CO2. At 8:50 AM,
the subjects started a warm-up of 5 min at 100 W; this was followed by
5 min at 40% Wmax. At 9:00 AM, workload was set at 50% Wmax for 120 min. During the first minute, subjects drank an initial bolus (8 ml/kg)
of an 8% (80 g/l) glucose solution. Thereafter, a beverage volume of 2 ml/kg was provided every 15 min. This feeding schedule was chosen because it reflects fluid intake observed in cyclists during
competition and has proven in earlier studies (22, 23) to result in
tracer steady states after 60-90 min. On average, a total of 1.07 ± 0.03 and 1.07 ± 0.02 g/min glucose was ingested in the
untrained and trained groups, respectively. Blood samples were drawn at
15-min intervals, and expiratory gases were collected every 15 min
until the end of exercise.
Glucose.
The 8% (80 g/l) glucose solution provided was prepared from
corn-derived glucose (Amylum, Belgium), which has a high natural abundance of 13C
[
11.2 
vs. Pee Dee Bellemnitella (PDB)].
Glucose solutions were further enriched by adding 0.0526 g
[U-13C]glucose/l
(Cambridge Isotope Laboratories). The glucose solutions provided to the
subjects had a 13C-enrichment of
67.1 vs. PDB [determined by elemental
analyzer-isotope ratio mass spectrometry (IRMS; Carlo Erba-Finnigan MAT
252, Bremen, Germany)]. To minimize possible shifts in background
enrichment as a result of a change in endogenous substrate utilization
and differences in background enrichment of the different fuel stores, subjects were instructed not to consume any products with a high natural abundance of 13C during
the entire experimental period. The magnitude of shifts in background
13C enrichment reported in
subjects on a European diet (40) is <1%, compared with the
enrichment of the glucose solution used here, which obviates the need
for background correction. Subjects were further instructed to refrain
from any sort of heavy physical labor and to keep their diet as
constant as possible during the days before the trial(s).
Analysis.
Blood (7 ml) was collected in EDTA-containing tubes and was centrifuged
at 1,000 g and 4°C for 5 min.
Aliquots of plasma were frozen immediately in liquid nitrogen and were
stored at 40°C. Glucose (Uni Kit III, 07367204; La Roche,
Basel, Switzerland), lactate (16), free fatty acid (FFA; Wako NEFA-C
test kit, Wako Chemicals, Neuss, Germany), and glycerol concentrations
(GPO trinder method, 337, Sigma Diagnostics, St. Louis, MO) were
analyzed with a COBAS FARA semiautomatic analyzer (Roche, Basel,
Switzerland). Insulin concentrations were analyzed by RIA (Linco
ultrasensitive human insulin RIA kit). Breath samples were analyzed for
13C/12C
ratio by gas chromatography (GC)-IRMS (Finnigan MAT 252). To determine
the
13C/12C
ratio in plasma glucose, glucose was first extracted with
chloroform-methanol-water, and derivatization was performed with
butyl-boronic acid and acetic anhydride as described before (33). The
measured
13C/12C
ratios in the derivative (GC combustion-IRMS) were corrected for the
isotopic carbon dilution. This was done by measuring a series of
glucose standards both in the derivatized form (GC combustion-IRMS) and
by direct combustion of underivatized glucose (elemental
analyzer-IRMS). The standard curve thus constructed was linear over a
range from 0 to 500 vs. PDB. From
CO2 production
(CO2) and
O2 uptake
(O2) (Oxycon-,
Mijnhardt, Mannheim, Germany), total energy expenditure, CHO oxidation,
and fat oxidation values were computed by indirect calorimetry. From
CO2 and stable isotope
measurements
(13C/12C)
(GC combustion-IRMS, Finnigan MAT 252), the oxidation rates of
exogenous glucose, muscle glycogen, and glucose released from the liver
were calculated, as suggested by Derman et al. (14).
Calculations.
From the recorded O2 and
CO2, total CHO and fat
oxidation and energy expenditure were calculated (32)
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(1) |
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(2) |
difference between the
13C/12C
ratio of the sample and a known laboratory reference standard, according to the formula of Craig (13)
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(3) |
13C is then related to an international standard (PDB).
Exogenous glucose oxidation (EGO) was calculated by using the formula
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(4) |
Exp is the 13C enrichment
of expired breath during exercise at the relevant time point, Ing is
the 13C enrichment of the ingested
glucose, Expbkg is the
13C enrichment of expired breath
before exercise (background), and k
(0.7467) is the amount of CO2 (in
liters) produced by the oxidation of 1 g glucose.
Blood glucose enrichment was measured, and the following formula was
used to calculate plasma glucose oxidation (PGO)
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(5) |
PG is the plasma glucose
13C enrichment,
PGbkg is the plasma glucose
13C enrichment before exercise
(background), and constant k is the same as in Eq. 4.
Because PGO represents the oxidation of both glucose coming from the
gut (exogenous glucose) and the contribution of the liver (glycogenolysis/gluconeogenesis), the oxidation rate of glucose released from the liver could be calculated by the following formula
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(6) |
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(7) |
Statistics. All data are expressed as means ± SE. Unpaired t-tests were used to compare the differences in substrate utilization and blood parameters between the trained and the untrained group (at the same relative and absolute workloads). Analysis of variance for repeated measures was performed to study differences over time between groups. In case of a significant F-ratio, a Scheffé post hoc test was applied to locate the differences. Statistical significance was set at P < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Stable-isotope measurements.
Both breath
13CO2
enrichment and plasma glucose 13C
enrichment reached a steady state after 75 min of exercise (Figs.
1 and 2).
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Blood parameters.
No differences between the trained and untrained subjects were found in
plasma glucose, insulin, and glycerol levels (Fig. 3 A,
C, and
E, respectively). Plasma lactate
levels were significantly higher in the untrained subjects than in the
trained subjects both at the same relative and absolute workloads
(P < 0.05) almost during the entire
exercise period (Fig. 3D). A
slightly higher increase in FFA levels was found in the untrained
subjects. Differences were statistically different compared with the
trained group at 60 and 75 min (Fig.
3B).
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Energy expenditure.
Raw data for calorimetry are illustrated in Fig.
4. Fuel oxidation is summarized in Table
2 and illustrated in Fig.
5. At a workload of 50% Wmax,
O2 in the untrained and
trained group was 2.23 ± 0.08 and 2.76 ± 0.09 l/min,
respectively (56 ± 2 and 53 ± 2%
O2 max). Energy
expenditure was significantly higher in the trained than in the
untrained group (58 ± 1.8 vs. 47 ± 1.6 kJ/min, respectively)
when compared at the same relative workload. Mean heart rates were
different in the untrained and trained group (160 ± 4 and 144 ± 3 beats/min, respectively; P < 0.05). In the trained group at the same absolute workload (148 ± 0 W), O2 [2.19 ± 0.05 l/min (42 ± 1.2%
O2 max)] and
energy expenditure (46 ± 0.9 kJ/min) were similar to the untrained
group. At the same absolute workload, mean heart rates were
significantly higher in the untrained than in the trained group (160 ± 4 vs. 121 ± 4 beats/min, respectively;
P < 0.05).
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Fat and CHO oxidation. When compared at the same relative intensity, fat oxidation contributed significantly more to energy expenditure in the trained (23.2 ± 1.5 kJ/min or 0.57 ± 0.03 g/min; 40% of total energy expenditure) than in the untrained group (15.9 ± 1.2 kJ/min or 0.38 ± 0.03 g/min; 33% of total energy expenditure; P < 0.05). No differences were found in CHO oxidation (with percentages of total energy expenditure in parentheses) [trained, 35.1 ± 2.4 kJ/min or 2.17 ± 0.15 g/min (60%); and untrained, 31.5 ± 1.2 kJ/min or 1.95 ± 0.07 g/min (67%), respectively]. Consequently, the higher energy expenditure in the trained group was completely accounted for by an increased fat oxidation. When compared at the same absolute intensity, fat oxidation also contributed significantly more to total energy expenditure in the trained subjects [20.6 ± 1.6 kJ/min or 0.50 ± 0.03 g/min (44%); P < 0.05]. Concomitantly, TCO was lower in the trained compared with the untrained group [25.6 ± 0.9 kJ/min or 1.58 ± 0.05 g/min (56%) vs. 31.5 ± 1.2 kJ/min or 1.95 ± 0.07 g/min (67%), respectively; P < 0.05].
CHO sources.
No differences were found in TCO as well as in total endogenous CHO
oxidation between the trained and untrained groups at the same relative
intensity. PGO rates were similar in both groups [0.91 ± 0.04 g/min (69.3 ± 2.4 µmol · kg
1 · min1)
and 0.99 ± 0.07 g/min (76.1 ± 5.2 µmol · kg1 · min1)
in the untrained and trained groups, respectively].
Muscle glycogen oxidation was not different at the same relative
workload between the untrained and trained groups [1.03 ± 0.02 g/min (36%) vs. 1.20 ± 0.13 g/min (32%) respectively].
Oxidation rates of liver-derived glucose were also similar in the
untrained and trained subjects when compared during exercise at the
same relative workload [0.22 ± 0.02 g/min (7%) vs. 0.24 ± 0.05 g/min (7%), respectively]. PGO rates in the trained
group at the same absolute workload were similar (0.87 ± 0.04 g/min; 66.5 ± 4.0 µmol · kg1 · min1)
when compared with the untrained group. However, at the same absolute
workload, endogenous CHO oxidation was significantly lower in the
trained compared with the untrained subjects [0.87 ± 0.06 g/min (31%) vs. 1.25 ± 0.07 g/min (43%) respectively;
P < 0.005]. This could be
attributed to decreased oxidation rates of both muscle glycogen
[0.72 ± 0.08 g/min (26%) vs. 1.03 ± 0.06 g/min (36%)
respectively; P < 0.01] and
liver-derived glucose [0.15 ± 0.03 g/min (5%) vs.
0.22 ± 0.02 g/min (7%) respectively; P < 0.05].
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In this study, we investigated the effect of training status on fuel selection and oxidation in subjects exercising at the same absolute (148 W) and relative workload (50% Wmax) while ingesting glucose. By addition of a [U-13C]glucose tracer to the glucose solution taken repeatedly in boluses, a plateau was obtained in blood glucose 13C enrichment and breath 13CO2 enrichment after 75 min of exercise. This enabled us to quantitate the following components of CHO oxidation: TCO, oxidation of the ingested glucose, oxidation of glucose derived from the liver, and muscle glycogen oxidation.
We observed that endurance-trained subjects have a substantially increased fat oxidation during prolonged moderate-intensity exercise (37-50% Wmax) with glucose ingestion, as has been previously observed by others both in the presence (22) and absence (7, 8, 18, 20, 21) of glucose ingestion. When we made comparisons at the same relative workload (50% Wmax), we found a similar rate of TCO. The higher energy expenditure (as absolute workload is higher) recorded in the trained subjects was completely accounted for by the increased fat oxidation. When we compared both groups during exercise at the same absolute workload, fat contributed significantly more to total energy expenditure and, concomitantly, TCO was decreased in the trained group.
In this study, we found that training status had a significant effect
on total muscle glycogen utilization during prolonged exercise of
moderate intensity with glucose ingestion only when comparisons were
made at the same absolute workload. Previously, a glycogen-sparing
effect of endurance training has been reported in overnight-fasted
subjects at both the same relative (21) and the same absolute workload
(20). When compared at the same relative workload, oxidation of glucose
produced by the liver (coming from gluconeogenesis and glycogenolysis)
was not influenced by training status. However, oxidation rates of
liver-derived glucose were significantly lower in the trained compared
with the untrained subjects when both were exercising at the same
absolute workload. These findings have also been observed in a study by Friedlander et al. (15) 1-2 h after a standardized CHO-containing breakfast. Coggan et al. (7, 9) studied subjects before and after an
endurance training period at 60% of their pretraining peak
O2 max. Coggan et al.
observed that endurance training reduces both hepatic glycogenolysis
and gluconeogenesis during prolonged exercise at the same absolute
workload in subjects after an overnight fast (9) and 6 h after a
standardized light breakfast (7).
Combined data obtained from experiments in humans indicate that
splanchnic glucose output rises linearly with exercise intensity up to
50-60% O2 max
(25). This would explain the similar oxidation rates of glucose derived
from the liver in the trained and untrained subjects in our study
during exercise at the same relative intensity. One possible
explanation for the observed reduction in liver-derived glucose
oxidation in trained subjects at the same absolute intensity is that
the hormonal changes drive liver glucose output and are decreased after
endurance training. Both decreases in plasma insulin and increases in
epinephrine, norepinephrine, and glucagon have been implicated in the
control of glucose output during exercise (7, 9, 25). Coggan et al. (7,
9) observed smaller decreases in insulin levels and a diminished
increase in epinephrine, norepinephrine, and glucagon levels during
exercise after endurance training.
In this study, insulin concentrations did not decrease during exercise, most probably as a consequence of the glucose ingestion. This explains the similar insulin concentrations recorded during all three trials. Glucagon and catecholamines were not measured. Another factor that could contribute to a reduced hepatic glucose production is the reduced availability of gluconeogenic precursors during exercise (9). We observed lower plasma lactate concentrations (Fig. 3D) in the trained subjects at the same absolute intensity. However, when compared at the same relative intensity, oxidation rates of glucose released from the liver were similar, although blood lactate was lower in the trained subjects. The fact that gluconeogenesis is low in subjects ingesting glucose (25) also seems to argue against a major role for gluconeogenic precursor availability in the control of liver-derived glucose oxidation.
It is concluded that both oxidation of liver-derived glucose and muscle glycogen are affected by training status when compared at the same absolute exercise intensity. Glucose ingestion during exercise seems to have no effect on the decrease in reliance on endogenous CHO oxidation in trained subjects when compared at the same absolute intensity.
Training status had no effect on EGO rates during moderate-intensity
exercise at the same absolute and relative exercise intensity. Jeukendrup et al. (22) also did not find differences in oral glucose
oxidation rates during moderate-intensity exercise between trained and
untrained individuals at the same relative exercise intensity. EGO
previously has been suggested to be directly related to workload or
O2 (28, 31, 34, 35). However,
no significant differences were found between the trials, although EGO
rates tended to be higher in the trained subjects at the higher
workload (Table 2). Recently it was suggested that exogenous CHO
oxidation (up to a maximum of 1.0-1.1 g/min) is only limited by
the rate of absorption from the intestine (24, 39). The observed EGO rates were below maximal values because only low- to moderate-intensity exercise was performed. Furthermore, it has been suggested that endurance training, because of concomitant high dietary CHO intake and
regular CHO supplementation during and after exercise, could lead to an
adaptation in the gut that results in increased glucose absorption
rates during exercise (38). Nonetheless, training status did not seem
to affect EGO rates, at least not at this glucose-ingestion rate and workload.
In conclusion, this study shows that endurance training increases fat
oxidation during submaximal exercise when glucose is ingested. When
compared during exercise at the same relative intensity (55%
O2 max),
endurance-trained subjects oxidize more fat to meet the higher energy
demand, and they oxidize the same amount of CHOs. When they are
compared during exercise at the same (absolute) workload, trained
subjects have both an increased rate of fat oxidation and reduced
oxidation rates of muscle glycogen and liver-derived glucose. These
findings are similar to previous observations in studies of endurance
training performed in the absence of glucose ingestion. Exogenous
glucose oxidation rate is not affected by training status during
moderate-intensity exercise.
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ACKNOWLEDGEMENTS |
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We thank the Gatorade Sports Science Institute for partial funding of this study.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: L. J. C. van Loon, Dept. of Human Biology, Maastricht Univ., PO Box 616, 6200 MD Maastricht, The Netherlands (E-mail: L.vanLoon{at}HB.Unimaas.nl).
Received 22 September 1998; accepted in final form 18 June 1999.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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