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High exogenous carbohydrate oxidation rates from a mixture of glucose and fructose ingested during prolonged cycling exercise

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A recent study from our laboratory has shown that a mixture of glucose and fructose ingested at a rate of 1.8 g/min leads to peak oxidation rates of approximately 1.3 g/min and results in approximately 55% higher exogenous carbohydrate (CHO) oxidation rates compared with the ingestion of an isocaloric amount of glucose. The aim of the present study was to investigate whether a mixture of glucose and fructose when ingested at a high rate (2.4 g/min) would lead to even higher exogenous CHO oxidation rates (>1.3 g/min). Eight trained male cyclists (VO2max: 68+/-1 ml/kg per min) cycled on three different occasions for 150 min at 50% of maximal power output (60+/-1% VO2max) and consumed either water (WAT) or a CHO solution providing 1.2 g/min glucose (GLU) or 1.2 g/min glucose+1.2 g/min fructose (GLU+FRUC). Peak exogenous CHO oxidation rates were higher (P<0.01) in the GLU+FRUC trial compared with the GLU trial (1.75 (SE 0.11) and 1.06 (SE 0.05) g/min, respectively). Furthermore, exogenous CHO oxidation rates during the last 90 min of exercise were approximately 50% higher (P<0.05) in GLU+FRUC compared with GLU (1.49 (SE 0.08) and 0.99 (SE 0.06) g/min, respectively). The results demonstrate that when a mixture of glucose and fructose is ingested at high rates (2.4 g/min) during 150 min of cycling exercise, exogenous CHO oxidation rates reach peak values of approximately 1.75 g/min.
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High rates of exogenous carbohydrate oxidation from a mixture of glucose
and fructose ingested during prolonged cycling exercise
Roy L. P. G. Jentjens and Asker E. Jeukendrup*
Human Performance Laboratory, School of Sport and Exercise Sciences, University of Birmingham, Edgbaston B15 2TT, UK
(Received 12 August 2004 Revised 26 October 2004 Accepted 4 November 2004)
A recent study from our laboratory has shown that a mixture of glucose and fructose ingested at a rate of 1·8 g/min leads to peak oxidation rates of approxi-
mately 1·3 g/min and results in approximately 55 % higher exogenous carbohydrate (CHO) oxidation rates compared with the ingestion of an isocaloric
amount of glucose. The aim of the present study was to investigate whether a mixture of glucose and fructose when ingested at a high rate (2·4 g/min)
would lead to even higher exogenous CHO oxidation rates (. 1·3 g/min). Eight trained male cyclists (VO
2max
:68^ 1 ml/kg per min) cycled on three differ-
ent occasions for 150 min at 50 % of maximal power output (60^ 1% VO
2max
) and consumed either water (WAT) or a CHO solution providing 1·2 g/min
glucose (GLU) or 1·2 g/min glucoseþ 1·2 g/min fructose (GLUþ FRUC). Peak exogenous CHO oxidation rates were higher (P, 0·01) in the GLUþ FRUC
trial compared with the GLU trial (1·75 (
SE 0·11) and 1·06 (SE 0·05) g/min, respectively). Furthermore, exogenous CHO oxidation rates during the last
90 min of exercise were approximately 50 % higher (P, 0·05) in GLUþFRUC compared with GLU (1·49 (
SE 0·08) and 0·99 (SE 0·06) g/min, respectively).
The results demonstrate that when a mixture of glucose and fructose is ingested at high rates (2·4 g/min) during 150 min of cycling exercise, exogenous CHO
oxidation rates reach peak values of approximately 1·75 g/min.
Substrate utilization: Stable isotopes: Intestinal carbohydrate transport
Numerous studies have shown that carbohydrate (CHO) sup-
plementation during prolonged exercise at moderate to high inten-
sities can increase exercise performance (Coyle et al. 1986;
Coggan & Coyle, 1987). This effect is thought to be due to the
prevention of hypoglycaemia and the maintenance of high rates
of CHO oxidation late in exercise when endogenous CHO
stores become depleted (Coyle et al. 1986; Bosch et al. 1994).
Therefore, high exogenous CHO oxidation rates have the poten-
tial to improve prolonged exercise performance.
In a recent review we suggested that the maximal oxidation rate
of (most) ingested carbohydrates is 1·01·1 g/min (Jeukendrup &
Jentjens, 2000). When large amounts of glucose or glucose poly-
mers are ingested (. 1·2 g/min; Jentjens et al. 2004b), intestinal
glucose transporters (SGLT1) may become saturated and there-
fore intestinal CHO absorption may be a limiting factor for
exogenous CHO oxidation (Hawley et al. 1992; Jeukendrup
et al. 1999; Jeukendrup & Jentjens, 2000; Jentjens et al.
2004b). Of note, free fructose and most probably fructose released
during sucrose hydrolysis use a different intestinal transporter
(GLUT-5) from glucose (SGLT1; Davidson & Leese, 1977;
Sandle et al. 1983; Burant et al. 1992; Ferraris & Diamond,
1997). Interestingly, Shi et al. (1995) demonstrated with an intes-
tinal perfusion study that a beverage containing glucose and fruc-
tose resulted in approximately 65 % higher CHO absorption rates
compared with an isoenergetic glucose solution. This effect was
attributed to the separate intestinal transport mechanisms for glu-
cose and fructose.
We have recently shown that a mixture of glucoseþ fructose
(Jentjens et al. 2004b), glucoseþsucrose (Jentjens et al. 2004c)
or glucoseþfructoseþ sucrose (Jentjens et al. 2004a) results in
approximately 2055 % higher exogenous CHO oxidation rates
compared with the ingestion of an isocaloric amount of glucose
and can lead to peak oxidation rates of approximately 1·7 g/min
(Jentjens et al. 2004a). Although speculative, a faster intestinal
CHO absorption might have increased the availability of
exogenous CHO for oxidation and hence this could explain
the high exogenous CHO oxidation rates (. 1·1 g/min)
observed when a mixture of glucoseþfructose or glucoseþsucrose
(þsucrose) was ingested (Jentjens et al. 2004a,b,c). Interestingly,
ingestion of equal amounts of glucose and sucrose at a rate of
2·4 g/min resulted in relatively low oxidation rates (approximately
1·2 g/min; Jentjens et al. 2005). It has been suggested that when
SGLT1 transporters become saturated (either from free glucose
and/or glucose released from sucrose hydrolysis), hydrolysis of
sucrose is inhibited (Gray & Ingelfinger, 1966; Sandle et al. 1983)
and this might limit the amount of sucrose available for absorption
and subsequent oxidation. This could explain why exogenous CHO
oxidation rates were relatively low (1·2 g/min), despite a fairly high
CHO intake rate (2·4 g/min; Jentjens et al. 2005).
The results of the studies described above suggest that the
‘maximum’ rate of exogenous CHO oxidation may depend on
the amount of glucose and fructose available for absorption and
the ‘maximum’ intestinal transport capacity for glucose and
fructose. However, in our previous study (Jentjens et al. 2004b)
* Corresponding author: Dr Asker E. Jeukendrup, fax þ44 (0)121 414 4121, email A.E.Jeukendrup@bham.ac.uk
Abbreviations: CHO, carbohydrate; FRUC, fructose; GI, gastrointestinal; GLU, glucose; HR, heart rate; PDB, Pee Dee Bellemnitella (international standard); RPE, rate of
perceived exertion; WAT, water; W
max
, maximum power output.
British Journal of Nutrition (2005), 93, 485–492 DOI: 10.1079/BJN20041368
q The Authors 2005
the fructose ingestion rate (0·6 g/min) was relatively low and
hence it is possible that not all fructose transporters were satu-
rated. In an attempt to saturate the SGLT1 and GLUT-5 transpor-
ters, in the present study, fructose was ingested at a higher intake
rate (1·2 g/min) and glucose was ingested at a rate of 1·2 g/min.
Saturation of both CHO transport systems might further increase
the rate of intestinal CHO absorption and this could potentially
lead to even higher (and maximal) exogenous CHO oxidation
rates. Therefore, we hypothesized that a mixture of glucose and
fructose when ingested at a high rate (2·4 g/min) would further
increase the rate of exogenous CHO oxidation (. 1·3 g/min).
Methods
Subjects
Eight trained male cyclists or triathletes took part in the present
study. Their characteristics are presented in Table 1. Prior to par-
ticipation, each of the subjects was fully informed of the purpose
and the risks associated with the procedures, and a written
informed consent was obtained. All subjects were healthy as
assessed by a general health questionnaire. The study was
approved by the Ethics Committee of the School of Sport and
Exercise Sciences of the University of Birmingham, UK.
Preliminary testing
At least 1 week before the start of the experimental trials an incre-
mental cycle exercise test to volitional exhaustion was performed
in order to determine the individual maximum power output
(W
max
) and maximal oxygen consumption (VO
2max
). This test
was performed on an electromagnetically braked cycle ergometer
(Lode Excalibur Sport, Groningen, The Netherlands), modified to
the configuration of a racing bicycle with adjustable saddle height
and handlebar position. After reporting to the laboratory, body
mass and height were recorded. Subjects then started cycling at
95 W for 3 min, followed by incremental steps of 35 W every
3 min until exhaustion. Heart rate (HR) was recorded continuously
by a radiotelemetry heart rate monitor (Polar Vantage NV, Kem-
pele, Finland). W
max
was calculated from the last completed
work rate, plus the fraction of time spent in the final non-com-
pleted work rate multiplied by the work rate increment (Kuipers
et al. 1985). The results were used to determine the work rate cor-
responding to 50 % W
max
, which was later employed in the exper-
imental exercise trials. Breath-by-breath measurements were
performed throughout exercise using an online automated gas
analysis system (Oxycon Pro, Jaeger, Hoechberg, Germany).
The volume sensor was calibrated using a 3 litre calibration syr-
inge and the gas analysers were calibrated using a CO
2
–N
2
gas
mixture (5·03 %:94·97 %). Oxygen uptake (VO
2
) was considered
to be maximal (VO
2max
) when at least two of the three following
criteria were met: (1) a levelling off of VO
2
with increasing work-
load (increase of no more than 2 ml/kg per min); (2) HR within 10
beats/min of predicted maximum (HR 220 minus age); (3) RER
. 1·05. VO
2max
was calculated as the average oxygen uptake
over the last 60 s of the test. The VO
2max
and W
max
achieved
during the incremental exercise test were 68 (
SE 1) ml/kg per
min and 376 (
SE 12) W, respectively (Table 1).
Experimental design
Each subject performed three exercise trials which consisted of
150 min of cycling at 50 % W
max
while ingesting a glucose
drink (GLU), a glucoseþfructose drink (GLUþ FRUC; ingested
glucosefructose ratio of 1:1) or plain water (WAT). In order
to quantify exogenous glucose oxidation, corn-derived glucose
monohydrate (Cerestar, Manchester, UK) and crystalline fructose
(Krystar 300; A.E. Staley Manufacturing Company, Decatur, IL,
USA) were used which have a high natural abundance of
13
C
(2 10·70 and 2 10·69 d v. Pee Dee Bellemnitella (PDB),
respectively). The
13
C-enrichment of the ingested glucose and
fructose was determined by elemental analyser-isotope ratio
mass spectrometry (IRMS; Europa Scientific GEO 20-20,
Crewe, UK). To all CHO drinks 20 mmol/l NaCl (Sigma-Aldrich,
Poole, UK) was added. The order of the experimental drinks was
randomly assigned in a crossover design. Experimental trials were
separated by at least 5 d. The composition of the experimental
drinks is shown in Table 2.
Diet and activity prior to testing
Subjects were asked to record their food intake and activity pat-
tern 2 d prior to the first exercise trial and were then instructed
to follow the same diet and exercise activities before the other
three trials. In addition, 57 d prior to each experimental testing
day, they were asked to perform an intense training session
(‘Glycogen depleting’ exercise bout) in an attempt to empty
any
13
C-enriched glycogen stores. Subjects were further
instructed not to consume any food products with a high natural
abundance of
13
C (CHO derived from C
4
plants: corn, sugar
cane) at least 1 week before and during the entire experimental
period in order to reduce the background shift (change in
13
CO
2
) from endogenous substrate stores.
Protocol
Subjects reported to the Human Performance Laboratory in the
morning (between 07.00 and 09.00 hours) after an overnight
fast (1012 h) and having refrained from any strenuous activity
or drinking any alcohol in the previous 24 h. For a given subject,
all trials were conducted at the same time of the day to avoid any
Table 2. Composition of the three experimental
beverages
WAT GLU GLUþFRUC
Glucose (g/l) 92·3 92·3
Fructose (g/l) 92·3
NaCl (mmol/l) 20 20
GLU, ingestion of glucose; GLU þ FRUC, ingestion of glu-
cose and fructose; WAT, ingestion of water only.
Table 1. Subject characteristics
(Mean values with their standard errors of the mean for eight subjects)
Mean
SEM
Age (years) 26·3 2·6
Height (cm) 181·4 1·4
Body mass (kg) 74·3 1·8
V
O2max
(ml/kg per min) 68·1 0·6
W
max
(W) 376 12
HR
max
(beats/min) 185 4
HR
max
, maximal heart rate; W
max
, maximum power output.
R. L. P. G. Jentjens and A. E. Jeukendrup486
influence of circadian variance. On arrival in the laboratory, a
flexible 21-gauge Teflon catheter (Quickcath, Baxter) was
inserted in an antecubital vein of an arm and attached to a
three-way stopcock (Sims Portex, Kingsmead, UK) to allow for
repeated blood sampling during exercise. The catheter was kept
patent by flushing with 1·01·5 ml of isotonic saline (0·9 %;
Baxter) after each blood sample collection.
The subjects then mounted a cycle ergometer and a resting
breath sample was collected in 10 ml Exetainer tubes (Labco
Ltd, Brow Works, High Wycombe, UK), which were filled
directly from a mixing chamber in duplicate in order to determine
the
13
C:
12
C ratio in the expired air.
Next, a resting blood sample (8 ml) was taken and stored on ice
and later centrifuged. Subjects then started a 150 min exercise bout
at a work rate equivalent to 50 % W
max
(60^ 1% VO
2max
).
Additionally, blood samples were drawn at 15 min intervals
during exercise. Expiratory breath samples were collected every
15 min until the end of exercise. VO
2
, VCO
2
(CO
2
production)
and RER were measured every 15 min for periods of 4 min
using an online automated gas analysis system as previously
described.
During the first 3 min of exercise subjects drank an initial
bolus (600 ml) of one of the three experimental drinks: GLU,
GLUþFRUC or WAT. Thereafter, every 15 min a beverage
volume of 150 ml was provided. The total fluid provided during
the 150 min exercise bout was 1·95 litres. The average rate of glu-
cose intake in the GLU and GLUþ FRUC trial was 1·2 g/min. Fur-
thermore, in the GLUþ FRUC trial subjects ingested on average
1·2 g/min fructose which brought the total CHO intake rate in
the GLUþFRUC to 2·4 g/min.
Subjects were asked to rate their perceived exertion (RPE) for
whole body and legs every 30 min on a scale from 6 to 20 using
the Borg category scale (Borg, 1982). In addition, subjects were
asked every 30 min to fill in a questionnaire in order to rate
(possible) gastrointestinal problems (Jeukendrup et al. 2000). All
exercise tests were performed under normal and standard environ-
mental conditions (17218C dry bulb temperature and 55 65 %
relative humidity). During the exercise trials subjects were
cooled with standing floor fans in order minimize thermal stress.
Questionnaires
Subjects were asked to fill out a questionnaire every 30 min during
the exercise trials. The questionnaire contained questions regard-
ing the presence of gastrointestinal (GI) problems at that moment
and addressed the following complaints; stomach problems, gas-
trointestinal cramping, bloated feeling, diarrhoea, nausea, dizzi-
ness, headache, belching, vomiting, and urge to urinate/defecate.
While subjects were on the bike and continued their exercise
each question was answered by simply ticking a box on the ques-
tionnaire that corresponded to the severity of the GI problem
addressed. The items were scored on a 10-point scale (1 ¼ not at
all, 10 ¼ very, very much). The severity of the GI symptoms
was divided into two categories: severe and non-severe symptoms,
as was previously described by Jeukendrup et al. (2000). Severe
complaints included nausea, stomach problems, bloated feeling,
diarrhoea, urge to vomit, stomach and intestinal cramps because
these are symptoms that commonly impair performance and may
bring with them health risks. The above symptoms were only regis-
tered as severe symptoms when a score of 5 or higher out of 10 was
reported. When a score below 5 was given, they were registered
as non-severe. All other symptoms were registered as non-severe
regardless of the score reported.
Analyses
Blood samples were collected into pre-chilled EDTA-containing
tubes (Beckton Dickinson, Plymouth, UK) and centrifuged at
2300 g and 48C for 10 min. Aliquots of plasma were immediately
frozen in liquid nitrogen and stored at 2 258C until analyses for
glucose and lactate. Glucose (Glucose HK 125, ABX Diagnostics,
Shefford, UK) and lactate (Lactic Acid 10, ABX Diagnostics,
Shefford) were analysed on a COBAS MIRA semi-automatic ana-
lyser (ABX Diagnostics, Montpellier, France).
Breath samples were analysed for
13
C:
12
C ratio by gas chroma-
tography continuous flow isotope ratio mass spectrometry (GC-
IRMS; Europa Scientific). From indirect calorimetry (VO
2
and
VCO
2
) and stable isotope measurements (breath
13
CO
2
:
12
CO
2
ratio), oxidation rates of total fat, total CHO, endogenous CHO
and exogenous glucose were calculated.
Calculations
From VCO
2
and VO
2
(l/min), total CHO and fat oxidation rates
(g/min) were calculated using stoichiometric equations of Frayn
(1983) with the assumption that protein oxidation during exercise
was negligible:
CHO oxidation ¼ 4·55 VCO
2
2 3·21 VO
2
ð1Þ
Fat oxidation ¼ 1·67 VO
2
2 1·67 VCO
2
ð2Þ
The isotopic enrichment was expressed as d‰ difference between
the
13
C:
12
C ratio of the sample and a known laboratory reference
standard according to the formula of Craig (1957):
d
13
C ¼
13
C:
12
C sample
13
C:
12
C standard

2 1

£ 10
3
per mil ð3Þ
The d
13
C was then related to an international standard (PDB).
In the GLU and GLUþ FRUC trials, the rate of exogenous glu-
cose oxidation was calculated using the following formula
(Mosora et al. 1976):
Exogenous glucose oxidation
¼ VCO
2
£
dExp 2 dExp
bkg
dIng 2 dExp
bkg

1
k

ð4Þ
In which dExp is the
13
C enrichment of expired air during exer-
cise at different time points, dIng is the
13
C enrichment of the
ingested CHO solution, dExp
bkg
is the
13
C enrichment of expired
air in the WAT trial (background) at different time points and k is
the amount of CO
2
(in litres) produced by the oxidation of 1 g of
glucose (k ¼ 0·7467 litres CO
2
per g glucose).
Endogenous CHO oxidation was calculated by subtracting
exogenous CHO oxidation from total CHO oxidation.
A methodological consideration when using
13
CO
2
in expired
air to calculate exogenous substrate oxidation is the trapping of
13
CO
2
in the bicarbonate pool, in which an amount of CO
2
arising
from decarboxylation of energy substrates is temporarily trapped
(Robert et al. 1987). However, during exercise the CO
2
pro-
duction increases severalfold so that a physiological steady-state
condition will occur relatively rapidly, and
13
CO
2
in the
expired air will be equilibrated with the
13
CO
2
/H
13
CO
3
2
pool,
Exogenous oxidation of glucose and fructose 487
respectively. Recovery of
13
CO
2
from oxidation will approach
100 % after 60 min of exercise when dilution in the bicarbonate
pool becomes negligible (Robert et al. 1987; Pallikarakis et al.
1991). As a consequence of this, all calculations on substrate
oxidation were performed over the last 90 min of exercise
(60150 min).
Statistical analyses
Two-way ANOVA for repeated measures was used to compare
differences in substrate utilization and in blood-related parameters
over time between the trials. A Tukey post hoc was applied in the
event of a significant F ratio. Where appropriate, comparison of
variables between two conditions was conducted by using a Stu-
dent’s t test for paired samples. Data evaluation was performed
using SPSS for Windows version 10.0 software package (SPSS,
Chicago, IL, USA). All data are reported as means with their stan-
dard errors. Statistical significance was set at P, 0·05.
Results
Stable-isotope measurements
Changes in isotopic composition of expired CO
2
in response
to exercise with ingestion of water (WAT), glucose (GLU)
or a mixture of glucose and fructose (GLUþFRUC) are shown
in Fig. 1(A). In the GLU and GLUþFRUC trials,
13
CO
2
enrichment of expired breath increased (P, 0·01) from 225·87
(
SE 0·16) and 2 25·89 (SE 0·20) d v. PDB at rest to 2 20·88
(
SE 0·20) and 2 18·31 (SE 0·26) d v. PDB by the end of the
150 min exercise, respectively. From the 45 min point onwards,
breath
13
CO
2
enrichment in the GLUþ FRUC trial was signifi-
cantly (P, 0·01) higher compared with the GLU trial. During
the WAT trial, there was also a significant increase in
13
CO
2
enrichment of the expired air (P, 0·01). The rise in background
13
CO
2
enrichment during the WAT trial was relatively small
(approximately 10 14 %) compared with the rise in breath
13
CO
2
enrichment observed during the two CHO trials. Although
the background shift was small in the present study, a background
correction was made for the calculation of exogenous CHO oxi-
dation in the two CHO trials by using the data from the WAT
trial.
Oxygen uptake, rate of perceived exertion, total carbohydrate and
fat oxidation
Data for VO
2
, RER, total CHO and fat oxidation over the
60150 min exercise period are shown in Table 3. There was
no significant difference in VO
2
between the three experimental
trials. RER in the WAT trial was significantly lower (P, 0·01)
compared with the GLU and GLUþFRUC trial. During the
90120 min and the 120150 min exercise periods, RER was sig-
nificantly higher in GLUþFRUC compared with GLU. The aver-
age CHO oxidation rates during the last 90 min of exercise were
1·56 (
SE 0·13), 2·26 (SE 0·12) and 2·57 (SE 0·15) g/min for WAT,
GLU and GLUþ FRUC, respectively. The rate of CHO oxidation
was significantly higher (P, 0·01) after CHO ingestion compared
with WAT ingestion (Table 3). Furthermore, CHO oxidation
between 60 and 150 min was significantly higher (P, 0·05) in
GLUþFRUC compared with GLU. The ingestion of CHO
(GLU and GLUþ FRUC) resulted in significantly lower
(P, 0·01) fat oxidation rates compared with the WAT trial. Fur-
thermore, fat oxidation rates were significantly lower (P, 0·01)
in GLUþ FRUC compared with GLU. The average fat oxidation
rates over the 60150 min exercise period were 0·97 (
SE 0·05),
0·68 (
SE 0·05) and 0·51 (SE 0·04) g/min for WAT, GLU and
GLUþFRUC, respectively. The relative contribution of substrates
to total energy expenditure during the 60150 min period of exer-
cise is depicted in Fig. 2. Fat oxidation represented 61 (
SE 3), 43
(
SE 3) and 34 (SE 3) % of total energy expenditure in WAT, GLU
and GLUþ FRUC, respectively (WAT . GLU . GLUþ FRUC;
P, 0·05) (Fig. 2).
Exogenous and endogenous carbohydrate oxidation
In the GLU and GLUþ FRUC trials, the rate of exogenous CHO
oxidation increased significantly (P, 0·01) during exercise.
However, in GLU, exogenous CHO oxidation rates levelled
off after approximately 105120 min of exercise (Fig. 1(B)),
while the rate of exogenous CHO oxidation in GLUþ FRUC
increased until the end of exercise (no levelling off). Peak
exogenous CHO oxidation rates were reached at the end of exer-
cise (150 min) and were significantly higher (P, 0·01) in
the GLUþ FRUC trial (1·75 (
SE 0·11) g/min) compared with the
GLU trial (1·06 (
SE 0·04) g/min) (Fig. 1(B)). During the
60150 min exercise period, exogenous CHO oxidation rates
Fig. 1. Breath
13
CO
2
enrichment (A) and exogenous carbohydrate oxidation
(B) during exercise without ingestion of carbohydrate (WAT, B), with inges-
tion of glucose (GLU, W) or with ingestion of glucoseþ fructose (GLUþFRUC,
X). Values are means with their standard errors represented by vertical bars
(n 8). a, Significant difference between WAT and GLUþ FRUC (P, 0·05); b,
significant difference between WAT and CHO trials (P, 0·01); c, significant
difference between GLU and GLUþ FRUC (P, 0·01). PDB, Pee Dee Bellem-
nitella (international standard).
R. L. P. G. Jentjens and A. E. Jeukendrup488
were approximately 50 % higher (P, 0·01) in GLUþFRUC com-
pared with GLU (Table 2; Fig. 1(B) and Fig. 2).
The rate of endogenous CHO oxidation was significantly lower
(P, 0·05) in the two CHO trials compared with the WAT trial
(Table 3; Fig. 2). No significant difference was found in endogen-
ous CHO oxidation rates between the GLU and GLUþFRUC
trial. The average endogenous CHO oxidation rates over the
60150 min exercise period were 1·56 (
SE 0·13), 1·26 (SE 0·12)
and 1·07 (
SE 0·15) g/min for WAT, GLU and GLUþFRUC,
respectively. During the last 90 min of exercise, endogenous
CHO oxidation represented 39 (
SE 3), 32 (SE 3) and 28 (SE 4)
% of total energy expenditure in WAT, GLU and GLUþ FRUC,
respectively (WAT . GLU and GLUþFRUC; P, 0·05) (Fig. 2).
Plasma glucose and lactate
No differences were observed in fasting plasma glucose concen-
trations between trials (Fig. 3(A)). In the WAT trial, plasma
glucose concentrations decreased gradually during exercise,
reaching a nadir of 3·7 (
SE 0·2) mmol/l at the end of exercise
(t 150 min). In contrast, a large increase in plasma glucose was
observed following ingestion of GLU and GLUþFRUC, with
peak values of 5·8 (
SE 0·3) and 6·0 (SE 0·6) mmol/l respectively,
reached 15 min into the exercise period. Thereafter, plasma glu-
cose concentrations decreased to fasting levels and remained at
values varying between 4·6 and 5·0 mmol/l for the duration of
exercise. Plasma glucose concentrations were higher (P, 0·05)
throughout exercise in the two CHO trials compared with the
WAT trial. There were no significant differences in plasma glu-
cose concentrations between the GLU and GLUþFRUC trials.
Plasma lactate concentrations at rest in the WAT, GLU and
GLUþFRUC trials were 1·1 (
SE 0·2), 1·0 (SE 0·1) and 1·1 (SE
0·1) mmol/l, respectively (P. 0·05; Fig. 3(B)). At all time
points during exercise, plasma lactate concentrations were
higher (P, 0·01) in the GLUþ FRUC trial compared with the
WAT and GLU trials. No differences in plasma lactate concen-
trations were observed between the GLU and WAT trials.
Gastrointestinal discomfort and ratings of perceived exertion
The most frequently reported complaints were urge to urinate,
belching and bloated feeling. There were no differences (i.e.
number of complaints or number of subjects that reported com-
plaints) in GI discomfort between the three experimental trials,
apart from one subject who reported severe stomach problems
in the GLUþFRUC trial (stomach burn and bloated feeling).
No significant differences in RPE overall or RPE legs were
observed between the three conditions. The mean values for RPE
overall and RPE legs during 150 min of exercise were 11·7 (
SE
0·4) and 11·8 (SE 0·4) for WAT, 11·6 (SE 0·3) and 11·9 (SE 0·4)
for GLU, and 11·8 (
SE 0·4) and 11·8 (SE 0·4) for GLUþFRUC.
Discussion
The main finding of the present study was that combined inges-
tion of glucose and fructose at a rate of 1·2 and 1·2 g/min, respect-
ively, resulted in peak exogenous CHO oxidation rates of 1·75 g/
min (
SE 0·11).
In a recent study from our laboratory, we have shown that
ingestion of glucose at a rate of 1·2 g/min in combination with
fructose at a rate of 0·6 g/min leads to peak exogenous oxidation
Table 3. Mean oxygen uptake (VOd
2
), rate of perceived exertion (RER), total carbohydrate (CHO) oxidation (CHOtot), total fat oxidation (FATtot), endogenous
CHO oxidation and exogenous glucose oxidation during cycling exercise with ingestion of water, glucose and glucoseþ fructose.
(Mean values with their standard errors for eight subjects)
VO
2
(l/min) RER CHOtot (g/min) FATtot (g/min)
Endogenous
CHO oxidation
(g/min)
Exogenous
glucose oxi-
dation (g/min)
Time (min) Mean
SE Mean SE Mean SE Mean SE Mean SE Mean SE
WAT 6090 3·10 0·12 0·83 0·01
b
1·68 0·14
b
0·90 05
b
1·68 14
ae
90 120 3·14 0·12 0·81 0·01
b
1·54 0·13
b
0·98 06
b
1·54 13
ae
120 150 3·16 0·16 0·81 0·01
b
1·44 0·10
b
1·03 05
b
1·44 10
ae
GLU 60 90 3·03 0·09 0·87 0·01 2·28 0·13 0·65 0·05
d
1·36 13 0·91 0·07
c
90 120 3·06 0·09 0·87 0·01
d
2·27 0·11 0·67 0·05
c
1·25 0·12 1·03 0·07
c
120 150 3·10 0·09 0·86 0·07
c
2·23 0·11
d
0·70 0·04
c
1·18 0·10 1·06 0·06
c
GLUþ FRUC 60 90 2·94 0·10 0·89 0·01 2·49 0·15 0·53 0·05 1·18 0·15 1·31 0·07
90 120 2·96 0·10 0·90 0·01 2·57 0·15 0·51 0·04 1·04 0·15 1·53 0·08
120 150 2·98 0·10 0·90 0·01 2·64 0·18 0·50 0·04 0·97 0·16 1·67 0·10
GLU, ingestion of glucose; GLUþFRUC, ingestion of glucose and fructose; WAT, ingestion of water only.
abcde
Significant difference between
a
WAT and GLUþFRUC (P, 0·01);
b
WAT and CHO trials (P, 0·01);
c
GLU and GLUþFRUC (P, 0·01);
d
GLU and GLUþ FRUC (P, 0·05);
e
WAT and GLU
(P, 0·05).
Fig. 2. Relative contributions of substrates to total energy expenditure calcu-
lated for the 60 150 min period of exercise without ingestion of carbohydrate
(WAT), with ingestion of glucose (GLU) or with ingestion of glucoseþ fructose
(GLUþ FRUC). Values are means with their standard errors (n 8). b, Signifi-
cant difference between WAT and CHO trials (P, 0·05); d, significant differ-
ence between GLU and GLUþ FRUC (P, 0·05). p, Fat; B, exogenous
carbohydrate; A, endogenous carbohydrate.
Exogenous oxidation of glucose and fructose 489
rates of 1·26 (SE 0·07) g/min (Jentjens et al. 2004b). When a
mixture of glucose and sucrose was ingested at a rate of 1·2
and 0·6 g/min, respectively, almost similar rates of exogenous
CHO oxidation were found (1·25 (
SE 0·07) g/min; Jentjens et al.
2004c). More importantly, combined ingestion of glucoseþ
sucrose and glucoseþ fructose resulted in approximately 20
55 % higher exogenous CHO oxidation rates compared with the
ingestion of an isocaloric amount of glucose (Jentjens et al.
2004b,c). These findings support the data of Shi et al. (1995)
who demonstrated that a beverage containing two or three trans-
portable CHO (glucose, fructose and sucrose) resulted in higher
CHO and/or water absorption rates compared with an isoenergetic
glucose solution (Shi et al. 1995). Our previous findings and those
of Shi et al. (1995) might be explained by the fact that free fruc-
tose and most probably fructose released during sucrose hydroly-
sis uses a different intestinal transporter (GLUT-5) than glucose
(SGLT1; Davidson & Leese, 1977; Sandle et al. 1983; Burant
et al. 1992; Ferraris & Diamond, 1997) and hence intestinal
CHO absorption might be increased when a mixture of multiple
transportable CHO is consumed. Furthermore, studies in
humans and rats have indicated that fructose absorption is
enhanced by the presence of glucose (Holdsworth & Dawson,
1964; Fujisawa et al. 1991; Hoekstra & van den Aker, 1996;
Shi et al. 1997; Corpe et al. 1999). The facilitated fructose
absorption probably occurs as a result of glucose-induced water
streaming through the mucosal layer, also known as solvent
drag (Holdsworth & Dawson, 1964; Fine et al. 1994; Hoekstra
& van den Aker, 1996; Shi et al. 1997). This process requires
the opening of tight junctions by glucose absorption and the sub-
sequent movement of water through the paracellular pathway.
Small solutes, including fructose, will move passively with
water through the same pathway. In addition, glucose-induced
water absorption increases intraluminal fructose concentrations
and this might also lead to increased fructose transport (Holds-
worth & Dawson, 1964; Fine et al. 1994). Thus, in addition to
the different intestinal transport mechanisms for glucose and fruc-
tose, the stimulating effect of glucose on fructose absorption
might further contribute to an increased intestinal CHO absorp-
tion rate when mixtures of multiple transportable CHO are
ingested. It has been postulated that a faster intestinal CHO
absorption might increase the availability of exogenous CHO
for oxidation (Jentjens et al. 2004a,b,c, 2005) and this might
explain the high exogenous CHO oxidation rates (approximately
1·251·75 g/min) observed in the present study and in our pre-
vious studies in which mixtures of glucose, sucrose and/or fruc-
tose were ingested (Jentjens et al. 2004a,b,c, 2005).
Ingestion of fructose in combination with other carbohydrates
(present study; Jentjens et al. 2004a,b; L Moseley, GI Mainwar-
ing, S Samuels, S Perry, CH Mann and AE Jeukendrup, unpub-
lished results) or when ingested alone (Macdonald et al. 1978;
Koivisto et al. 1981) has been shown to result in elevated lactate
concentrations. The increased lactate concentrations following
fructose ingestion might be due to the high activity of fructoki-
nase, stimulation of pyruvate kinase and the fact that fructolysis
bypasses phosphofructokinase (the main rate-controlling step in
glycolysis). Fructose is therefore rapidly phosphorylated, resulting
in increased concentrations of glycolytic intermediates which will
lead to an increased glycolytic flux, evidenced by elevated plasma
lactate concentrations. Furthermore, studies in animals and
humans have shown that during absorption a considerable
amount of absorbed glucose (Hanson & Parsons, 1976; Porteous,
1978; Nicholls et al. 1983; Bjorkman et al. 1990) or absorbed
fructose (Bjorkman et al. 1984; Holloway & Parsons, 1984) is
converted in the intestine into lactate, most of which is secreted
into the portal vein. Most of the lactate will be converted into glu-
cose by the liver. However, some lactate might escape from the
liver into the systemic circulation and this could lead to increased
plasma lactate concentrations. Although speculative, the higher
plasma lactate concentrations following ingestion of GLUþ
FRUC may indicate faster intestinal CHO absorption and this
may have caused the higher exogenous CHO oxidation rates.
It has been shown that when equal amounts of glucose and
sucrose are ingested at a rate of 2·4 g/min (Jentjens et al. 2005),
exogenous CHO oxidation rates are not much different from the
oxidation rates found when glucose and sucrose are ingested at
a rate of 1·2 and 0·6 g/min, respectively (Jentjens et al. 2004c).
These findings indicate that the rate of exogenous CHO oxidation
does not increase when the rate of sucrose intake is increased
from 0·6 to 1·2 g/min and glucose is ingested simultaneously at
a rate of 1·2 g/min (Jentjens et al. 2004c, 2005). On the contrary,
the combined results from the present and a previous study
(Jentjens et al. 2004b) suggest that an increase in the rate of fruc-
tose ingestion from 0·6 to 1·2 g/min when coingested with glucose
at a rate of 1·2 g/min leads to higher peak oxidation rates
Fig. 3. Plasma glucose (A) and lactate (B) during exercise without ingestion
of carbohydrate (WAT, B), with ingestion of glucose (GLU, W) or with inges-
tion of glucoseþ fructose (GLUþ FRUC, X). Values are means with their
standard errors represented by vertical bars (n 8). a, Significant difference
between WAT and GLUþFRUC (P, 0·05); b, significant difference between
WAT and CHO trials (P, 0·01); e, significant difference between WAT and
GLU (P, 0·05); f, GLUþFRUC significantly different from GLU and WAT
(P, 0·05); g, GLUþ FRUC significantly different from GLU and WAT
(P, 0·01).
R. L. P. G. Jentjens and A. E. Jeukendrup490
(1·75 (SE 0·11) v. 1·26 (SE 0·07) g/min, respectively). These data
support the results of an earlier study from our laboratory, in
which a mixture of glucose, fructose and sucrose when ingested
at a rate of 1·2, 0·6 and 0·6 g/min, respectively, resulted in peak
exogenous CHO oxidation rates of 1·70 (
SE 0·07) g/min (Jentjens
et al. 2004a). The present data and previous findings from our
laboratory (Jentjens et al. 2004a) indicate that in order to achieve
high exogenous CHO oxidation rates (approximately 1·7 g/min) a
mixture of glucoseþ fructose (þsucrose) should be consumed at
high intake rates (i.e. 1·2 g/min glucoseþ 1·2 g/min fructose).
One potential limitation of our study is that we did not include
an isoenergetic glucose (only) trial and hence it may be difficult
to compare the results of the two CHO trials. However, it
should be noted that we and others have previously demonstrated
that the rate of exogenous CHO oxidation does not increase when
the rate of glucose or maltodextrin ingestion is increased from 1·2
to 1·8 g/min (Wagenmakers et al. 1993; Jentjens et al. 2004b).
Furthermore, we have recently shown that when glucose is
ingested at a rate of 2·4 g/min, average exogenous glucose oxi-
dation rates during the last 90 min of exercise are 1·01 (
SE 0·04)
g/min (Jentjens et al. 2004a). The rate of exogenous glucose oxi-
dation in the present study (GLU trial) is almost similar to the
oxidation rate observed in our previous study (Jentjens et al.
2004a), despite a 50 % lower glucose ingestion rate (1·2 v. 4 g/
min, respectively). The above findings indicate that maximal
glucose oxidation rates are reached when glucose is ingested at
a rate of approximately 1·2 g/min. In the present study, glucose
and fructose were both ingested at rates of 1·2 g/min and therefore
the higher exogenous CHO oxidation rates in the GLUþ FRUC
trial could be fully attributed to the oxidation of ingested fructose,
which supports our previous findings (Jentjens et al. 2004b). Of
note, previous studies have shown that when fructose is ingested
alone, average oxidation rates vary between 0·32 and 0·44 g/min
for exercise durations up to 180 min (Massicotte et al. 1986,
1989, 1990; Jandrain et al. 1993; Adopo et al. 1994). Unfortu-
nately most studies did not report ‘peak’ exogenous CHO
oxidation rates. In some studies it was found that the oxidation
rate of ingested fructose reached peak values of approximately
0·500·64 g/min at the end of 120180 min of cycling exercise
(Massicotte et al. 1986, 1990; Jandrain et al. 1993). During the
120150 min exercise period in the present study, the difference
in the rate of exogenous CHO oxidation between GLU and
GLUþFRUC was approximately 0·6 g/min. If it is assumed that
this oxidation rate represents the oxidation rate of ingested fruc-
tose then these results suggest that the ingested fructose and glu-
cose in the GLUþ FRUC trial were both oxidized at peak rates
(approximately 0·6 and approximately 1·1 g/min, respectively).
Therefore, the exogenous CHO oxidation rate observed in the
GLUþFRUC trial (approximately 1·75 g/min) could be the high-
est oxidation rate that is physiologically possible when multiple
transportable CHO (i.e. glucoseþfructose) are ingested orally.
It should be noted that in order to reach very high rates of
exogenous CHO oxidation, it may be important that both glucose
and fructose transporters (SGLT1 and GLUT-5, respectively) are
saturated. As mentioned earlier, intestinal glucose transporters
(SGLT1) may become saturated when glucose or glucose poly-
mers are ingested at a rate of . 1·2 g/min (Jentjens et al.
2004b). Therefore, in the present study and in our previous studies
(Jentjens et al. 2004a,b,c, 2005), glucose was ingested at a rate of
at least 1·2 g/min. The absorption rate of fructose is, however,
much lower than that of glucose or sucrose (Ravich et al. 1983;
Riby et al. 1993; Rumessen & Gudmand-Hoyer, 1986) and thus
ingestion of large amounts of fructose should be avoided as the
unabsorbed fructose might accumulate in the GI tract which
might increase the risk of GI discomfort (Murray et al. 1989;
Fujisawa et al. 1993). In our previous study, the maximum
amount of fructose theoretically available for absorption was
0·9 g/min (0·6 g/min fructose and 0·3 g/min fructose released
from sucrose hydrolysis) and glucose was ingested at a rate of
1·2 g/min (Jentjens et al. 2004a). In the present study, a higher
fructose intake rate (1·2 v. 0·9 g/min) did not lead to higher
exogenous CHO oxidation rates (1·75 (
SE 0·11) v. 1·70
(
SE 0·07)). Furthermore, previous studies have shown that oxi-
dation rates of ingested fructose (alone) are highest when fructose
is ingested at a rate of approximately 0·8 g/min (Massicotte et al.
1986, 1990). Although speculative, GLUT-5 transporters may
become ‘saturated’ at a fructose ingestion rate of 0·80·9 g/min
and therefore no increase in exogenous fructose oxidation is
observed when fructose is ingested at higher rates.
In conclusion, combined ingestion of large amounts of glucose
and fructose during 150 min of cycling exercise resulted in peak
exogenous CHO oxidation rates of approximately 1·75 g/min
and resulted in approximately 50 % higher exogenous CHO oxi-
dation rates compared with the ingestion of glucose alone. The
present findings are in agreement with our earlier findings and
suggest that intestinal CHO absorption could be a rate-limiting
factor for exogenous CHO oxidation.
Acknowledgements
The authors would like to thank Cerestar (Manchester, UK) for
donating glucose monohydrate and A.E. Staley Manufacturing
Company (USA) for donating fructose. This study was sup-
ported by a grant of GlaxoSmithKline Consumer Healthcare,
Brentford, UK.
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... Current consensus suggests that athletes should ingest CHO at 30-60 g hr −1 during exercises lasting 1-2.5 h and up to 90 g hr −1 during exercise lasting longer than 2.5 h [3]. Significant research has been performed with the aim of identifying the maximal rate at which exogenous CHO (ExCHO) is oxidised [4][5][6][7] with ~ 1.75 g min−1 as the highest reported within the literature [4]. To achieve these high rates of ExCHO, participants ingested a mixture of glucose and fructose at 2.4 g min −1 , far exceeding the recommended 1.5 g min −1 and also significantly higher than what has been reported to be ingested by athletes during a competitive marathon [8]. ...
... Current consensus suggests that athletes should ingest CHO at 30-60 g hr −1 during exercises lasting 1-2.5 h and up to 90 g hr −1 during exercise lasting longer than 2.5 h [3]. Significant research has been performed with the aim of identifying the maximal rate at which exogenous CHO (ExCHO) is oxidised [4][5][6][7] with ~ 1.75 g min−1 as the highest reported within the literature [4]. To achieve these high rates of ExCHO, participants ingested a mixture of glucose and fructose at 2.4 g min −1 , far exceeding the recommended 1.5 g min −1 and also significantly higher than what has been reported to be ingested by athletes during a competitive marathon [8]. ...
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Introduction Scientific and public interest in the potential ergogenic effects of sodium alginate added to a carbohydrate (CHO) beverage has increased in the last ~ 5 years. Despite an extensive use of this technology by elite athletes and recent research into the potential effects, there has been no meta-analysis to objectively elucidate the effects of adding sodium alginate to a CHO beverage on parameters relevant to exercise performance and to highlight gaps in the literature. Methods Three literature databases were systematically searched for studies investigating the effects of sodium alginate added to CHO beverage during prolonged, endurance exercise in healthy athletes. For the systematic review, the PROSPERO guidelines were followed, and risk assessment was made using the Cochrane collaboration’s tool for assessing the risk of bias. Additionally, a random-effects meta-analysis model was used to determine the standardised mean difference between a CHO beverage containing sodium alginate and an isocaloric control for performance, whole-body CHO oxidation and blood glucose concentration. Results Ten studies were reviewed systematically, of which seven were included within the meta-analysis. For each variable, there was homogeneity between studies for performance (n = 5 studies; I² = 0%), CHO oxidation (n = 7 studies; I² = 0%) and blood glucose concentration (n = 7 studies; I² = 0%). When compared with an isocaloric control, the meta-analysis demonstrated that there is no difference in performance (Z = 0.54, p = 0.59), CHO oxidation (Z = 0.34, p = 0.71) and blood glucose concentration (Z = 0.44, p = 0.66) when ingesting a CHO beverage containing sodium alginate. The systematic review revealed that several of the included studies did not use sufficient exercise intensity to elicit significant gastrointestinal disturbances or demonstrate any ergogenic benefit of CHO ingestion. Risk of bias was generally low across the included studies. Conclusions This systematic review and meta-analysis demonstrate that the current literature indicates no benefit of adding sodium alginate to a CHO beverage during exercise. Further research is required, however, before firm conclusions are drawn considering the range of exercise intensities, feeding rates and the apparent lack of benefit of CHO reported in the current literature investigating sodium alginate.
... h −1 ) (6, 7). To overcome this limitation, it was theorized that by combining multiple CHO sources, a higher ExCHO oxidation rate could be achieved (8). This was evidenced with a significantly higher maximal ExCHO rate (1.75 g . ...
... h −1 ) in comparison with an isocaloric, glucose beverage (64 g . h −1 ) in trained cyclists (8). To achieve this high ExCHO oxidation rate, CHO was ingested at a rate well in excess of the 90 g . ...
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PurposeThe purpose of this study is to quantify the effect of adding sodium alginate and pectin to a carbohydrate (CHO) beverage on exogenous glucose (ExGluc) oxidation rate compared with an isocaloric CHO beverage.Methods Following familiarization, eight well-trained endurance athletes performed four bouts of prolonged running (105 min; 71 ± 4% of VO2max) while ingesting 175 mL of one of the experimental beverages every 15 min. In randomized order, participants consumed either 70 g.h−1 of maltodextrin and fructose (10% CHO; NORM), 70 g.h−1 of maltodextrin, fructose, sodium alginate, and pectin (10% CHO; ENCAP), 180 g.h−1 of maltodextrin, fructose, sodium alginate, and pectin (26% CHO; HiENCAP), or water (WAT). All CHO beverages had a maltodextrin:fructose ratio of 1:0.7 and contained 1.5 g.L−1 of sodium chloride. Total substrate oxidation, ExGluc oxidation rate, blood glucose, blood lactate, serum non-esterified fatty acid (NEFA) concentration, and RPE were measured for every 15 min. Every 30 min participants provided information regarding their gastrointestinal discomfort (GID).ResultsThere was no significant difference in peak ExGluc oxidation between NORM and ENCAP (0.63 ± 0.07 and 0.64 ± 0.11 g.min−1, respectively; p > 0.5), both of which were significantly lower than HiENCAP (1.13 ± 0.13 g.min−1, p < 0.01). Both NORM and HiENCAP demonstrated higher total CHO oxidation than WAT from 60 and 75 min, respectively, until the end of exercise, with no differences between CHO trials. During the first 60 min, blood glucose was significantly lower in WAT compared with NORM and HiENCAP, but no differences were found between CHO beverages. Both ENCAP and HiENCAP demonstrated a higher blood glucose concentration from 60–105 min than WAT, and ENCAP was significantly higher than HiENCAP. There were no significant differences in reported GID symptoms between the trials.Conclusions At moderate ingestion rates (i.e., 70 g.h−1), the addition of sodium alginate and pectin did not influence the ExGluc oxidation rate compared with an isocaloric CHO beverage. At very high ingestion rates (i.e., 180 g.h−1), high rates of ExGluc oxidation were achieved in line with the literature.
... g/ min and fat oxidation of 0.50-0.70 g/min (Jentjens and Jeukendrup, 2005), the current study using a more modest (Miall et al., 2018), during steady-state running with CHO provision on P1 (○), P2 (•), and P3 (•). Mean ± SEM (n = 28): † p < 0.05 vs. pre-exercise (0 min) resting feeding tolerance. ...
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Using metadata from previously published research, this investigation sought to explore: (1) whole-body total carbohydrate and fat oxidation rates of endurance (e.g., half and full marathon) and ultra-endurance runners during an incremental exercise test to volitional exhaustion and steady-state exercise while consuming a mixed macronutrient diet and consuming carbohydrate during steady-state running and (2) feeding tolerance and glucose availability while consuming different carbohydrate regimes during steady-state running. Competitively trained male endurance and ultra-endurance runners ( n = 28) consuming a balanced macronutrient diet (57 ± 6% carbohydrate, 21 ± 16% protein, and 22 ± 9% fat) performed an incremental exercise test to exhaustion and one of three 3 h steady-state running protocols involving a carbohydrate feeding regime (76–90 g/h). Indirect calorimetry was used to determine maximum fat oxidation (MFO) in the incremental exercise and carbohydrate and fat oxidation rates during steady-state running. Gastrointestinal symptoms (GIS), breath hydrogen (H 2 ), and blood glucose responses were measured throughout the steady-state running protocols. Despite high variability between participants, high rates of MFO [mean (range): 0.66 (0.22–1.89) g/min], Fat max [63 (40–94) % V̇ O 2max ], and Fat min [94 (77–100) % V̇ O 2max ] were observed in the majority of participants in response to the incremental exercise test to volitional exhaustion. Whole-body total fat oxidation rate was 0.8 ± 0.3 g/min at the end of steady-state exercise, with 43% of participants presenting rates of ≥1.0 g/min, despite the state of hyperglycemia above resting homeostatic range [mean (95%CI): 6.9 (6.7–7.2) mmol/L]. In response to the carbohydrate feeding interventions of 90 g/h 2:1 glucose–fructose formulation, 38% of participants showed breath H 2 responses indicative of carbohydrate malabsorption. Greater gastrointestinal symptom severity and feeding intolerance was observed with higher carbohydrate intakes (90 vs. 76 g/h) during steady-state exercise and was greatest when high exercise intensity was performed (i.e., performance test). Endurance and ultra-endurance runners can attain relatively high rates of whole-body fat oxidation during exercise in a post-prandial state and with carbohydrate provisions during exercise, despite consuming a mixed macronutrient diet. Higher carbohydrate intake during exercise may lead to greater gastrointestinal symptom severity and feeding intolerance.
... TTE was performed to simulate the final end spurt, typically observed in the OWS competitions . No differences were observed in Csw, RPE, HR and SR during the 90 min race pace trial, despite several studies reported that the ingestion of a CHO drink increases performance (Jentjens & Jeukendrup, 2005;Smith et al., 2013) and reduces RPE (Burgess et al., 1991;Utter et al., 1999Utter et al., , 2004 during continuous endurance exercise. The ergogenic effect of glucose supplementation is often ascribed to a higher glucose uptake by the exercising muscles, thereby allowing a sufficient carbohydrate oxidation rate in exercise when muscle glycogen levels are low (Coyle et al., 1986;Nybo, 2003). ...
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Purpose The aim of present study was to test the effect of carbohydrate ingestion, simulating a 10-km open water race competition on energy cost (Csw), perceived exertion (RPE), heart rate (HR), stroke rate (SR) and performance. We hypothesized that carbohydrate ingestion would reduce Csw and RPE in elite open water swimmers (OW-swimmers) and improve performance. Methods Eight elite OW-swimmers swam for 3x30 minutes with 20-s of interval necessary to collect data in the swimming flume at a pre-set pace corresponding to their 10-km race pace, followed by a time to exhaustion test (TTE) at 100% of the peak oxygen uptake (V̇O2peak). During the set, OW-swimmers ingested 45-g of carbohydrates (CHO) in 550-mL of water (8% solution) during each of the two intervals or a placebo solution (PLA). HR, RPE, V̇O2 and SR were measured. Shapiro-Wilk test was used to verify the normal distribution of data. Two-way repeated measures ANOVA and t-test was performed (p<0.05). Results A significant difference emerged in TTE between the trials (169.00±91.06 s in CHO; 102.31±57.47 s in PLA). HR, RPE and SR increased during the TTE but did not differ between trials. Csw did not show a significant main effect between the two conditions and in time course in both conditions. Conclusions CHO ingestion significantly increased TTE at 100% of V̇O2peakafter 90-min of swimming at 10-km race pace. These findings indicate that CHO intake during a 10-km open water swimming competition should have a beneficial impact on performance in the final part of the race.
... Moreover, by ingesting mixtures of glucose and fructose, exogenous carbohydrate oxidation (CHO-O) rates have been demonstrated to increase 1.2-1.7-fold during prolonged exercise (Jentjens and Jeukendrup, 2005). Those studies indicate the efficacy of carbohydrate ingestion for enhancing performance during exercise. ...
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Background: This study examines the effects of sports drinks ingestion during high-intensity exercise for carbohydrate oxidation rate (CHO-O) among athletes. Methods: PubMed, Embase, and the Cochrane library were searched for available papers published up to November 2019. The primary outcome is the carbohydrate oxidation rate (CHO-O), and the secondary outcome is the fat oxidation rate (Fat-O). Statistical heterogeneity among the included studies was evaluated using Cochran's Q test and the I ² index. The random-effects model was used for all analyses, regardless of the I ² index. Results: Five studies are included, with a total of 58 participants (range, 8–14/study). All five studies are randomized crossover trials. Compared to the control beverages, sports drinks have no impact on the CHO-O of athletes [weighted mean difference (WMD) = 0.29; 95% CI, −0.06 to 0.65, P = 0.106; I ² = 97.4%, P < 0.001] and on the Fat-O of athletes (WMD = −0.074; 95% CI, −0.19 to 0.06, P = 0.297; I ² = 97.5%, P < 0.001). Carbohydrate–electrolyte solutions increase CHO-O (WMD = 0.47; 95% CI, 0.08–0.87, P = 0.020; I ² = 97.8%, P < 0.001) but not Fat-O (WMD = −0.14; 95% CI, −0.31 to 0.03, P = 0.103; I ² = 98.2%, P < 0.001). Caffeine has a borderline effect on Fat-O (WMD = 0.05; 95% CI, 0.00–0.10, P = 0.050). Conclusions: Compared with the control beverages, sports drinks show no significant improvement in CHO-O and Fat-O in athletes. Carbohydrate–electrolyte solutions increase CHO-O in athletes but not Fat-O.
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Davitt, PM, Saenz, C, Hartman, T, Barone, P, and Estremera, S. Physiological impact of a single serving slow absorption carbohydrate on metabolic, hemodynamic, and performance markers in endurance athletes during a bout of exercise. J Strength Cond Res 35(5): 1262-1272, 2021-The purpose of this study was to determine how a slow-absorbing carbohydrate affected markers of metabolism, hemodynamics, and performance in well-trained endurance athletes. We examined total and exogenous carbohydrate oxidation (CHO ox), glucose, and performance after consuming different glucose beverages, before a treadmill run. Ten male runners (32.4 years; V̇o2max, 55.9 ml·kg-1·min-1) participated on 3 occasions: slow digestion CHO (S), fast digestion CHO (F), and water (W). Subjects consumed a 50 g dose of either S or F before a 3-hour treadmill run at 57% V̇o2max. Variables were assessed at -15, 0, 30, 60, 90, 135, and 180 minutes. Immediately postrun, subjects completed a time-to-fatigue test at 110% V̇o2max. There was a significant difference in CHO ox for W vs. F and S (C,1.14; S,1.52; F,1.66 ± 0.2 g·min-1, p < 0.05). Fat ox was significantly higher in S vs. F (S,0.54; F,0.47 ± 0.08 g·min-1, p < 0.05). Exogenous CHO ox was significantly higher in F vs. S (F,0.26; S,0.19 + 0.04 g·min-1, p < 0.05). There was a significant difference in average blood glucose for trial (F,94.5; S,97.1 vs. W,88.4 + 2.1 mg·dl-1) and time × trial for F vs. S (0 minutes, p < 0.05). There were no significant performance differences. Consumption of a single bolus of CHO beverage before a 3-hour run elicits significant alterations in energy metabolism compared with just water, with S CHO oxidizing significantly more fat than a rapidly digested carbohydrate. These findings suggest that slow-digesting modified starch provides a consistent blood glucose level and sustained exogenous energy supply during a sustained, 3-hour endurance run. Significance was set at p < 0.05.
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Purpose Carbohydrates (CHO) are one of the fundamental energy sources during prolonged steady state and intermittent exercise. The consumption of exogenous CHO during exercise is common place, with the aim to enhance sporting performance. Despite the popularity around exogenous CHO use, the process by which CHO is regulated from intake to its use in the working muscle is still not fully appreciated. Recent studies utilizing the hyperglycaemic glucose clamp technique have shed light on some of the potential barriers to CHO utilisation during exercise. The present review addresses the role of exogenous CHO utilisation during exercise, with a focus on potential mechanisms involved, from glucose uptake to glucose delivery and oxidation at the different stages of regulation. Methods Narrative review. Results A number of potential barriers were identified, including gastric emptying, intestinal absorption, blood flow (splanchnic and muscle), muscle uptake and oxidation. The relocation of glucose transporters plays a key role in the regulation of CHO, particularly in epithelial cells and subsequent transport into the blood. Limitations are also apparent when CHO is infused, particularly with regards to blood flow and uptake within the muscle. Conclusion We highlight a number of potential barriers involved with the regulation of both ingested and infused CHO during exercise. Future work on the influence of longitudinal training within the regulation processes (such as the gut) is warranted to further understand the optimal type, dose and method of CHO delivery to enhance sporting performance.
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Purpose To critically examine the research on novel supplements and strategies designed to enhance carbohydrate delivery and/or availability. Methods Narrative review. Results Available data would suggest that there are varying levels of effectiveness based on the supplement/supplementation strategy in question and mechanism of action. Novel carbohydrate supplements including multiple transportable carbohydrate (MTC), modified carbohydrate (MC), and hydrogels (HGEL) have been generally effective at modifying gastric emptying and/or intestinal absorption. Moreover, these effects often correlate with altered fuel utilization patterns and/or glycogen storage. Nevertheless, performance effects differ widely based on supplement and study design. MTC consistently enhances performance, but the magnitude of the effect is yet to be fully elucidated. MC and HGEL seem unlikely to be beneficial when compared to supplementation strategies that align with current sport nutrition recommendations. Combining carbohydrate with other ergogenic substances may, in some cases, result in additive or synergistic effects on metabolism and/or performance; however, data are often lacking and results vary based on the quantity, timing, and inter-individual responses to different treatments. Altering dietary carbohydrate intake likely influences absorption, oxidation, and and/or storage of acutely ingested carbohydrate, but how this affects the ergogenicity of carbohydrate is still mostly unknown. Conclusions In conclusion, novel carbohydrate supplements and strategies alter carbohydrate delivery through various mechanisms. However, more research is needed to determine if/when interventions are ergogenic based on different contexts, populations, and applications.
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We recently reported that the glucose transporter isoform, GLUT5, is expressed on the brush border membrane of human small intestinal enterocytes (Davidson, N. O., Hausman, A. M. L., Ifkovits, C. A., Buse, J. B., Gould, G. W., Burant, C. F., and Bell, G. I. (1992) Am. J. Physiol. 262, C795-C800). To define its role in sugar transport, human GLUT5 was expressed in Xenopus oocytes and its substrate specifiicity and kinetic properties determined. GLUT5 exhibits selectivity for fructose transport, as determined by inhibition studies, with a K(m) of 6 mM. In addition, fructose transport by GLUT5 is not inhibited by cytochalasin B, a competitive inhibitor of facilitative glucose transporters. RNA and protein blotting studies showed the presence of high levels of GLUT5 mRNA and protein in human testis and spermatozoa, and immunocytochemical studies localize GLUT5 to the plasma membrane of mature spermatids and spermatozoa. The biochemical properties and tissue distribution of GLUT5 are consistent with a physiological role for this protein as a fructose transporter.
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David B. Duncan [2] has formulated a new multiple range test making use of special protection levels based upon degrees of freedom. Duncan [Tables II and III] has also tabulated the critical values (significant studentized ranges) for 5 percent and 1 percent level new multiple range tests, based upon tables by Pearson and Hartley [8] and by Beyer [1]. Unfortunately, there are sizable errors in some of the published critical values. This fact was discovered and reported by the author [4], who instigated the computation at Wright-Patterson Air Force Base of more accurate tables of the probability integrals of the range and of the studentized range than those published by Pearson and Hartley [7, 8]. This extensive computing project, of which one of the primary objectives was the determination of more accurate critical values for Duncan's test, has now been completed. The purpose of this paper is to report critical values (to four significant figures) which have been found by inverse interpolation in the new table of the probability integral of the studentized range. Included are corrected tables for significance levels α = 0.05, 0.01 and new tables for significance levels α = 0.10, 0.005, 0.001-all with sample sizes n = 2(1)20(2)40(10)100 and degrees of freedom ν = 1(1)20, 24, 30, 40, 60, 120, ∞.
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Five healthy young male volunteers were given isocaloric meals composed of glucose alone or in combination with protein, fat, or dietary fiber. Glycemic response was blunted in case of all mixed meals, the glucose level at 2.0 h and the area under the 2-h glucose curve being significantly lower (p<0.05) as compared to the glucose-only meal. Insulin responses to various meals were not significantly different from one another. The data point to an improved efficiency of insulin when nutrients other than carbohydrate are incorporated in a glucose meal.
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Tolerance tests using glucose, sucrose, fructose, or sorbitol each at 4 dose levels, were carried out in nine healthy young men and during the 90 min after ingestion the plasma serum concentrations of glucose, insulin, fructose, triglyceride, glycerol, uric acid, lactate, and pyruvate were estimated. It was confirmed that serum glucose levels are unaffected by the amount of glucose given. Little fructose seems to be converted to glucose judging by the serum fructose levels following sucrose and fructose, and by the small insulin response to oral fructose. The insulin response to a sucrose meal is half of that after an equivalent amount of glucose. The fall in serum triglyceride seen after carbohydrate meals is not related to insulin. Only glucose is not associated with a rise in serum uric acid, lactate, and pyruvate concentrations after ingestion.
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1. The absorption of glucose and fructose derived from sucrose has been studied using in vitro and in vivo loops of the rat jejunum.2. At low sucrose concentrations (1 and 10 mM) glucose appeared in the serosal compartment of the in vitro preparation at a faster rate than fructose, but at high sucrose concentrations (50 and 100 mM) the rates of serosal transfer of the two sugars were similar. Glucose and fructose appeared in the mucosal compartment, with the rate of fructose appearance exceeding that of glucose, at all the sucrose concentrations studied.3. Phlorizin (5 x 10(-5)M) added to the mucosal medium of the in vitro preparation abolished the serosal transfer of glucose derived from 50 mM sucrose, and reduced that of fructose by 75%.4. In the absence of sodium ions, the in vitro preparation failed to transfer glucose and fructose derived from 50 mM sucrose, into the serosal compartment.5. Glucose was actively accumulated in the whole gut wall of the in vivo preparation to concentrations higher than those in the plasma at 50 and 100 mM, but not at 10 mM sucrose concentrations. Fructose was also actively accumulated to about half the extent of glucose, but reached tissue concentrations greater than those in the plasma, at each sucrose concentration.6. The whole wall concentrations of glucose and fructose derived from sucrose added to the lumen continued to rise when the blood supply to the in vivo preparation was terminated.7. No increase in the in vivo whole wall concentrations of glucose and fructose were detected when sucrose was added to the lumen together with concentrations of glucose sufficient to saturate the monosaccharide transport systems.8. The results favour the view that disaccharide hydrolysis and resulting hexose transfer are sequential, separate events.