REVIEW ARTICLE Sports Med 2000 Jun; 29 (6): 407-424

0112-1642/00/0006-0407/$20.00/0

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Oxidation of Carbohydrate Feedings

During Prolonged Exercise
Current Thoughts, Guidelines and Directions for
Future Research
Asker E. Jeukendrup and Roy Jentjens
Human Performance Laboratory, School of Sport and Exercise Sciences, University of Birmingham,
Edgbaston, Birmingham, England

Contents
Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 407
1. Methodological Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 408
1.1 Radioactive Isotopes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 409
1.2 Stable Isotopes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 409
2. Feeding Strategies and Exogenous Carbohydrate (CHO) Oxidation . . . . . . . . . . . . . . . . . 410
2.1 Feeding Schedule . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 410
2.2 Types of CHO . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 411
2.2.1 Fructose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 411
2.2.2 Galactose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 412
2.2.3 Maltose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 412
2.2.4 Sucrose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 413
2.2.5 Glucose Polymers – Maltodextrins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 413
2.2.6 Starch . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 413
2.2.7 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 414
2.3 Multiple Transportable CHOs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 414
2.4 Osmolality and Concentration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 415
2.5 Amount of CHO . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 415
3. Factors Affecting Exogenous CHO Oxidation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 416
3.1 Exercise Intensity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 416
3.2 Muscle Glycogen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 417
3.3 Training . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 418
4. Limitations of Exogenous CHO Oxidation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 419
5. Directions for Future Research . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 421
6. Practical Implications, Guidelines and Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . 422

Abstract Although it is known that carbohydrate (CHO) feedings during exercise im-
prove endurance performance, the effects of different feeding strategies are less
clear. Studies using (stable) isotope methodology have shown that not all carbo-
hydrates are oxidised at similar rates and hence they may not be equally effective.
Glucose, sucrose, maltose, maltodextrins and amylopectin are oxidised at high
rates. Fructose, galactose and amylose have been shown to be oxidised at 25 to
50% lower rates. Combinations of multiple transportable CHO may increase the
total CHO absorption and total exogenous CHO oxidation. Increasing the CHO
408 Jeukendrup & Jentjens

intake up to 1.0 to 1.5 g/min will increase the oxidation up to about 1.0 to 1.1
g/min. However, a further increase of the intake will not further increase the
oxidation rates. Training status does not affect exogenous CHO oxidation. The
effects of fasting and muscle glycogen depletion are less clear.
The most remarkable conclusion is probably that exogenous CHO oxidation
rates do not exceed 1.0 to 1.1 g/min. There is convincing evidence that this
limitation is not at the muscular level but most likely located in the intestine or
the liver. Intestinal perfusion studies seem to suggest that the capacity to absorb
glucose is only slightly in excess of the observed entrance of glucose into the
blood and the rate of absorption may thus be a factor contributing to the limitation.
However, the liver may play an additional important role, in that it provides
glucose to the bloodstream at a rate of about 1 g/min by balancing the glucose
from the gut and from glycogenolysis/gluconeogenesis. It is possible that when
large amounts of glucose are ingested absorption is a limiting factor, and the liver
will retain some glucose and thus act as a second limiting factor to exogenous
CHO oxidation.

The number of studies concluding that carbohy- The purpose of this review is not to review the
drate (CHO) feedings during exercise improve ex- effects of CHO on exercise performance per se, but
ercise capacity or exercise performance is so large to summarise the factors that determine the efficacy
that, from a scientific point of view, we can con- (i.e. oxidation) of ingested CHO. With the conclu-
sider this relationship true. In the last few years, sions from this overview, guidelines will be formu-
studies have accumulated to show that CHO feed- lated for the use of CHO supplements during exer-
ings during exercise can positively affect perfor- cise. Finally, some of the remaining questions and
mance when the exercise duration is about 45 min- directions for future research will be discussed.
utes or longer.[1,2] The mechanism by which these
CHO feedings exert their effect is believed to be a 1. Methodological Considerations
maintenance of blood glucose and increased rates
of CHO oxidation during exercise.[2] It has also been The oxidation of ingested CHO can be measured
shown that CHO feedings during exercise ‘spare’ by using isotope techniques. Costill et al.[10] were
liver glycogen.[3-5] However, whether CHO feedings probably the first to study the oxidation of ingested
CHO. They labeled the CHO in a drink with a ra-
‘spare’muscle glycogen is still controversial, as some
dioactive tracer ([U-14C]glucose) and reported that
studies reported glycogen ‘sparing’[6,7] whereas oth-
only a small amount of an ingested CHO load was
ers did not.[2,8] This debate has recently been re-
oxidised during exercise. As a result, they concluded
viewed by Tsintzas and Williams.[9] Several studies that CHO feedings were of limited importance for
have also addressed the questions of which CHO was muscle metabolism. However, this result was prob-
most effective, what the most effective feeding ably the result of methodological problems, since
schedule was and the optimal amount of CHO to many studies in the following years have shown
be ingested. Additional studies have looked at fac- significant contributions of ingested CHO to energy
tors that can possibly influence the oxidation of expenditure during exercise. Most studies today use
ingested CHO, such as muscle glycogen levels, diet, stable isotopes for the measurement of exogenous
and exercise intensity. More recently, studies have CHO oxidation, since this does not provoke any
attempted to detect the factors that limit the maxi- health hazards in contrast to the potential negative
mal rates of exogenous CHO oxidation. effects of radioactive isotopes. The advantages and

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Oxidation of Carbohydrate Feedings During Exercise 409

disadvantages of these techniques will be discussed In many experimental conditions, the entrapment
in sections 1.1 and 1.2. of 14CO2 or 13CO2 in the bicarbonate pool may cause
a marked underestimation of the true exogenous
1.1 Radioactive Isotopes CHO oxidation, especially during the first hour of
exercise.
The oldest method to trace ingested CHO is to There are a few ways around this problem. One
add a [U-14C]glucose tracer to a CHO beverage and way is to prime the bicarbonate pool with H14CO3 –
measure 14C in expired gases using a scintillation or H13CO3 –. This would bring the bicarbonate pool
counter. The advantage of this technique is that it into equilibrium within the first 15 minutes of ex-
is relatively inexpensive compared with the use of ercise.[5,8] A second way is to avoid calculating ex-
stable isotopes. In addition, shifts in background ogenous CHO oxidation rates in the first hour.[14]
enrichments which may occur when using stable Finally, it is possible to use an acetate correction
isotopes (see section 1.2) are not a problem, be- factor as suggested recently.[15] In addition to the
cause the background level of 14C is negligible. temporary label loss in the bicarbonate pool, it has
An obvious disadvantage of this technique is the also been reported that, in studies using a 13C-tracer
fact that it exposes the volunteer to radioactivity. for studying fatty acid metabolism, part of the tracer
Although the radiation dose given is usually low may be trapped in exchange reactions with the tri-
(<40 uCi/L is consumed), and is calculated to cor- carboxylic acid (TCA)-cycle.[15,16] For example,
respond to 0.02 to 0.03 rem, 200 to 250 times lower some 13C-carbons may be incorporated into the glu-
than the permissible dose, the actual risks may of- tamate/glutamine pool via α-ketoglutarate (α-KG),
ten be underestimated.[11] Glucose is not only used or into phosphoenolpyruvate (PEP) via oxaloace-
for oxidation, but is also a substrate for other me- tate (OAA).[16] This label fixation results in a de-
tabolic pathways, including pathways that result in creased recovery of label in the expired gases and,
the formation of DNA. Incorporation of radioac- in order to correct for this loss, the acetate correc-
tivity in a DNA molecule is of course dangerous tion factor has been proposed.[15] This correction
because it may damage genetic material. It is there- is based on the assumption that acetate has immediate
fore advisable to use stable isotopes rather than access to the TCA-cycle and is instantly oxidised.
radioactive isotopes to study metabolism. The percentage of label (13C or 14C) not recovered
One potential problem with using isotopes (ra- in expired CO2 represents the amount of CO2
dioactive or stable) is that part of the CO2 (includ- trapped in exchange reactions with TCA-cycle in-
ing 14CO2 or 13CO2) may not appear in the expired termediates (TCAI) and the bicarbonate pool. The
gases because it is temporarily trapped in the bicar- label loss is dependent on the metabolic rate. At
bonate pool. high oxygen uptakes (>35 ml/kg/min) less label is
CO2 + H2O ↓à H2CO3 ↓à HCO3 – + H+ (Eq. 1) trapped and recovery of the 1-14C-acetate label was
found to be 85 to 90%.[15] Similar results were ob-
This is a very large and only slowly exchanging tained by Schrauwen et al.[16] when [U-13C]palmi-
pool, in which CO2, arising from various decarbox- tate was used. This implies that studies performed
ylation reactions, is retained. In resting conditions, at low absolute exercise intensities may have under-
it may take hours before there is an equilibrium estimated exogenous CHO oxidation rates.
between 14CO2 and H14CO3 – (or 13CO2 and H13CO3 –).
However, during exercise the turnover of this pool 1.2 Stable Isotopes
increases severalfold and, especially at high absolute
workloads, equilibrium may be reached within 60 Studies in which stable isotope methodology
minutes. It has been reported that recovery of 13CO2 was used to measure exogenous CHO oxidation
approached 100% after 60 minutes of exercise at have used 13C-enriched substrates. Some of these
.
60 to 70% maximal oxygen uptake (VO2max).[10,12,13] studies have used naturally enriched CHO (derived

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410 Jeukendrup & Jentjens

from C4 plants such as corn and cane sugar). These can then be used to correct the calculated exoge-
plants have a naturally high abundance of 13C. nous CHO oxidation.
When ingesting these CHOs during exercise, breath .
13CO will become enriched and, together with a
Exogenous CHO oxidation = VCO2 • (ECO2 –
2 Ebkg)/(Eing – Ebkg) • 1/k (Eq. 2)
measure of the total CO2 production rate, exoge- .
nous CHO oxidation rates can be quantified. In ad- where VCO2 is the total CO2 production rate, ECO2
dition to the problems described above, there is an- is the 13 C-enrichment of CO 2 , Eing is the 13 C-
other complication with this technique: shifts in enrichment of the ingested CHO, Ebkg is the back-
substrate utilisation may result in a change in back- ground enrichment determined in a separate exper-
ground enrichment.[17,18] Because CHO is usually iment with the same conditions, and k is the amount
more 13C-enriched than fat, glycogen stores may of CO2 that will arise from the oxidation of 1g of
display higher 13C-enrichments than endogenous glucose (0.7466L CO2/g glucose).
fat stores. Any change in shift in endogenous sub- It is possible to obtain accurate and reliable
measures of exogenous CHO oxidation using (ra-
strate utilisation can therefore cause a change in the
dioactive or stable) isotopes. However, as was just
background 13C-enrichment independent of ingested
discussed, there are several errors that can be made
CHO. These changes occur for instance in the tran-
and have been made in the past. This is important
sition from rest to exercise, and typically an increase
when interpreting results, especially from some of
in 13CO2 in the expired gases is observed. The mag- the earlier studies. The absolute values reported in
nitude of the error depends on the 13C-enrichment several trials may be overestimated in studies using
of the ingested CHO relative to the 13C-enrichment CHO with a naturally high 13C-abundance because
of endogenous glycogen stores. It has been shown no corrections were made for background enrich-
that individuals with a diet in which most CHOs ment. Other studies may have underestimated ex-
are derived from C4 plants (a typical northern Amer- ogenous CHO oxidation because no correction was
ican or Canadian diet) have higher 13C-enrichments made for label loss or label fixation. We would like
in their muscle glycogen stores compared with Euro- the reader to keep this in mind when interpreting
peans, whose diet is typically derived from C3 plants the results of various studies. Here, we will present
such as potato and beet sugar. the data of different studies as presented in the orig-
.
In a comparative study at 60% VO2max at Ball inal papers. We have not tried to correct for the
State University (Indiana, USA) and Maastricht Uni- possible methodological errors because there were
versity (The Netherlands), we have observed that too many unknown variables (e.g. diet, background
in northern America, shifts in background enrich- enrichments) and often papers did not report suffi-
ment may be 3 to 5 times higher than in Europe cient information (e.g. enrichment data) to allow
(unpublished data). Several investigators have there- these corrections to be made. Nevertheless, in most
fore instructed their study participants not to con- cases the error will be small (5 to 10%) and correc-
sume products with a high natural 13C-abundance, tion would not have altered the conclusions of these
or have reduced the error by artificially increasing papers since typically 2 or 3 trials are compared in
the same experimental conditions.
the 13C-enrichment of the CHO ingested during the
experiment (typically by adding [U-13C]glucose to
2. Feeding Strategies and Exogenous
a CHO beverage). By adding a tracer to the CHO,
Carbohydrate (CHO) Oxidation
the shift in background remains the same but the
relative error is reduced. Another way around the
2.1 Feeding Schedule
problem is to perform control trials with an identi-
cal protocol but with ingestion of CHO with a low The typical pattern of exogenous glucose oxida-
natural abundance. The background 13C-enrichments tion rates is shown in figure 1. The first appearance

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Oxidation of Carbohydrate Feedings During Exercise 411

of label from ingested CHO can already be ob-

Exogenous CHO oxidation (g/min)

1.2
served in the first 5 minutes (unpublished observa- HI-GLU
tions). During the first 75 to 90 minutes of exercise, 1.0

exogenous CHO oxidation will continue to rise as 0.8

more and more CHO will be emptied from the 0.6

stomach and absorbed in the intestine. After 75 to 0.4
90 minutes a leveling-off will occur and the exog- 0.2 LO-GLU
enous CHO oxidation rate will reach its maximum 0
value and will not further increase. The timing of 0 30 60 90 120

CHO feedings seemed to have very little effect on Time (min)

the slope of this curve or the plateau value. In sev- Fig. 1. Typical pattern of exogenous carbohydrate (CHO) oxi-
dation during exercise when beverages are consumed at the
eral studies[19-23] the oxidation of a single glucose onset of exercise and at regular intervals thereafter. HI-GLU =
load (100g) given at the onset of exercise (90 to high glucose ingestion; LO-GLU = low glucose ingestion.
120 minutes) was investigated. They all reported a
very similar oxidation pattern for ingested glucose;
an increase in oxidation rates during the first 75 to impact on the maximal exogenous CHO oxidation
90 minutes and a plateau thereafter. Maximal ex- rates or the time to reach this maximum. However,
ogenous CHO oxidation rates in these studies var- the feeding schedule should be such that high exo-
ied between 0.48 and 0.65 g/min. These rates are genous CHO oxidation rates are achieved as soon
similar to those observed when ingesting similar as possible after the onset of exercise and the amount
amounts of glucose (90 to 100g in 90 to 120 min- of CHO ingested should be sufficient to maintain
utes) as repetitive feedings during exercise.[24-28] high rates of exogenous CHO oxidation.
In a study by Krzentowski et al.,[20] volunteers McConell et al.[32] compared the effects of CHO
. ingestion throughout exercise with ingestion of an
walked at a 10% grade (45% VO2max) for 4 hours.
equal amount of CHO late in exercise. In this study,
They ingested 100g of glucose after 15 or 120 min-
performance was improved relative to the control
utes. Exogenous CHO oxidation rates followed an
trial only when CHO was ingested throughout ex-
identical pattern from the time of ingestion until 2
ercise. CHO ingestion late in exercise did not im-
hours later. The amount of ingested glucose ox-
prove performance despite increases in plasma glu-
idised was similar in the 2 hours following inges-
cose and insulin levels.
tion (55g when CHO was ingested after 15 minutes
and 54g when ingested after 120 minutes). This 2.2 Types of CHO
study showed that the time of ingestion has no ef-
fect on exogenous CHO oxidation. Often repetitive In figure 2, different types of dietary CHO are
feeding schedules are adopted because it has been depicted. Different types of CHO may have differ-
shown that this accelerates the rate of gastric emp- ent properties. Differences in osmolality and struc-
tying and hence the delivery of CHO to the intes- ture have effects on taste, digestion, absorption, the
tine.[29,30] However, since gastric emptying does release of various hormones, and the availability
not usually limit exogenous CHO oxidation,[27,31] of glucose for oxidation in the muscle. A number
the feeding schedule may have little effect on the of studies have compared the oxidation rates of
maximum oxidation rates or the time to reach these various types of ingested CHO with the oxidation
high rates of oxidation. Thus, although there are no of glucose during exercise.[26,27,31,33-38] The results
studies available that have directly studied the ef- will be discussed in the following sections.
fect of different feeding schedules on the rate of 2.2.1 Fructose
exogenous CHO oxidation, the literature seems to There has been considerable interest in fructose
suggest that the feeding schedule has very little for a variety of reasons.[23,39,40] The first reason is

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412 Jeukendrup & Jentjens

C OH Glucose Fructose Galactose

C
C O
OH OH Maltose Sucrose Lactose
C C
C
OH
OH

Amylopectin
starch
Maltodextrin Amylose
starch
Fig. 2. Overview of different carbohydrates and their structure. There are 3 monosaccharides (glucose, fructose and galactose) and
3 disaccharides (maltose, sucrose and lactose). Glucose polymers (maltodextrins) and starch consist of a series of coupled glucose
molecules.

that adding fructose will generally improve the pal- 2.2.2 Galactose
atability of a drink. Secondly, fructose will cause a Only one study has investigated the oxidation
20 to 30% smaller increase in plasma insulin levels rates of ingested galactose during exercise. Leijssen
compared with glucose,[41] and hence it will reduce et al.[35] fed 8 volunteers, who exercised for 2 hours
.
lipolysis to a smaller extent. Fructose has also been at 70% VO2max, 155g of galactose or glucose and
used as a pre-exercise feeding to prevent exercise- calculated the oxidation rates of the exogenous CHO.
induced rebound hypoglycaemia.[23,39,40] Massicotte While glucose was oxidised at a rate of 0.85 g/min
and colleagues[26,33] studied the oxidation of fruc- during the last hour, galactose oxidation was only
tose compared with an isoenergetic glucose solution half of that (0.41 g/min). It was suggested that the
and found 25% lower oxidation rates for fructose. absorption or the conversion into glucose in the
Jandrain et al.[42] studied exogenous CHO oxida- liver was limiting. Galactose on its own therefore
tion rates in 10 healthy but untrained volunteers seemed an inappropriate source of CHO for sports
.
during 3 hours of exercise at 45% VO2max while drinks.
ingesting 150g glucose or fructose. The peak oxi-
dation rates for the ingested glucose were 0.67 g/min 2.2.3 Maltose
and fructose oxidation peaked at 0.50 g/min (25% Hawley et al.[36] investigated the oxidation of
lower). Similar findings were reported by oth- maltose and glucose during 90 minutes of exercise
.
ers.[23,34,43,44] The lower oxidation rates of fructose at 70% VO2max. Trained volunteers ingested 180g
are probably due to a lower rate of absorption and of glucose or maltose during exercise and exogen-
the fact that fructose has to be converted into glu- ous CHO oxidation was measured using radioactive
cose in the liver before it can be metabolised. The isotopes. High peak oxidation rates were reached
latter is usually a relatively slow process. Interest- at the end of exercise and equaled 0.9 g/min for
ingly, during fasting when gluconeogenic pathways glucose and 1.0 g/min for maltose. These differ-
are activated, similar rates of oxidation were found ences were not statistically significant and it was
for glucose and fructose.[25,34] concluded that maltose and glucose are oxidised at

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Oxidation of Carbohydrate Feedings During Exercise 413

similar rates. In addition, these authors found no Table I. Amylose and amylopectin content of various plant starches
differences in the absorption rates of these CHOs. Plant starches Amylose (%) Amylopectin (%)
Maize 24 76
2.2.4 Sucrose Potato 20 80
Few studies have investigated the oxidation of Rice 19 81
ingested sucrose. In a study by Moodley et al.,[27] Tapioca 17 83
volunteers ingested 90g of sucrose during 90 min- Wheat 25 75
.
utes of exercise at 70% VO2max. Sucrose oxidation
rates peaked at approximately 0.4 g/min. Although
these rates may seem quite low, similar oxidation Wagenmakers et al.[37] found similar results when
rates were reported for glucose and the low values feeding volunteers maltodextrin solutions ranging
may therefore be a result of the methodology used from 4 to 16%. Increasing rates of CHO ingestion
in that study. Wagenmakers et al.[37] gave their seemed to increase oral CHO oxidation up to a rate
study participants an 8% sucrose solution during 2 of 1.0 to 1.1 g/min. Ingestion of more than 1.2 g/min
. had very little or no additional effect on the oxida-
hours of cycling exercise at 65% VO2max. The total
amount of sucrose ingested during the 2 hours was tion rates.[37] However, these high rates of inges-
145g, and it was estimated that 81g was oxidised. tion did result in high oral CHO oxidation rates
The peak oxidation rate was 0.87 g/min, a value (0.53 to 1.07 g/min) that were similar to the rates
similar to that observed after glucose ingestion in observed with glucose ingestion in other studies.
other studies.[8,14,25-28,36,45] It can therefore be con-
2.2.6 Starch
cluded that sucrose can be oxidised at similar rates
There are 2 major types of starch: amylopectin
as glucose and the efficacy of these 2 CHOs may
and amylose. Amylopectin is a highly branched mol-
be similar.
ecule, whereas amylose is a long straight chain of
2.2.5 Glucose Polymers – Maltodextrins glucose molecules (fig. 2) twisted into a helical
Because of their neutral taste and their relatively coil. Branches in starch are created by 1,6 bonds
low osmotic value, maltodextrins have been used between glucose units, whereas 1,4 glucosidic bonds
by many manufacturers of sports drinks to increase will result in a straight chain of glucose units.
the CHO content of these beverages. In a study by Starches with a relatively large amount of amylo-
Rehrer et al.,[31] a 17% maltodextrin solution was pectin are rapidly digested and absorbed, whereas
compared with a 17% glucose solution. The total those with a high amylose content will have a slow
amount of CHO that was ingested during 80 min- rate of hydrolysis. Starches make up approximately
.
utes of exercise at 70% VO2max was 220g. Oral 50% of our total daily CHO intake and most natu-
CHO oxidation was measured and was found to be rally occurring starches are a mixture of amylose
similar for the glucose and the maltodextrin drink and amylopectin (see table I). One study[38] com-
(42 and 39g for glucose and maltodextrin, respec- pared the rate of gastric emptying and the oxidation
tively). A peak oxidation rate of 0.78 g/min was rate of an insoluble starch consisting of 23% amy-
reported for glucose and 0.75 g/min for malto- lose and 77% amylopectin with a soluble starch
dextrins. These results indicate that there is no dif- consisting of 100% amylopectin. Volunteers ingested
ference in the oxidation of maltodextrins and glu- 316g during 2.5 hours of cycling exercise at 68%
.
cose. In addition, it was found that the rates of VO2max. The amount of CHO delivered to the in-
gastric emptying and thus the rate of delivery of testine seemed somewhat lower in the case of the
CHO to the intestine was similar between glucose insoluble starch, but this difference did not reach
and the glucose polymer. These results also imply statistical significance. However, the insoluble starch
that the digestion (hydrolysis of the bonds between was oxidised at a lower rate (75g of insoluble starch
glucose molecules of a glucose polymer) is not a compared with 126g of soluble starch). Peak oxi-
rate-limiting step for exogenous CHO oxidation. dation rates were 1.1 and 0.8 g/min for the soluble

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414 Jeukendrup & Jentjens

3 Glucose
Fructose
Galactose
Sucrose
Maltose
MD
Oral CHO oxidation rate (g/min)

Starch
2

0
0 1 2 3
CHO ingestion rate (g/min)

Fig. 3. Peak oxidation rates of oral carbohydrates (CHOs) are depicted against the CHO ingestion rate of different types of CHO.
Fructose and galactose appear to be oxidised at relatively low rates whereas glucose, sucrose, maltose, maltodextrins and soluble
starch seem to be oxidised at relatively high rates. The horizontal line depicts the absolute maximum for oral CHO oxidation. The
dotted line represents the line of identity, where CHO ingestion equals CHO oxidation.

starch and the insoluble starch, respectively, while high rates. Maximal oral CHO oxidation seems to
the insoluble starch seemed to cause some gastro- be around 1 g/min. The horizontal line depicts the
intestinal discomfort.[38] The oxidation of amylose absolute maximum just below 1.1 g/min. The dot-
only was not measured but can be assumed to be ted line represents the line of identity, where CHO
very low. Although one study reported a very high ingestion equals CHO oxidation. From this graph
rate of oxidation for insoluble starch,[46] this has it can be concluded that oral CHO oxidation may
been shown to be due to a methodological error.[38] be optimal at rates of ingestion around 1.0 to 1.5
In conclusion, amylopectin is oxidised at higher g/min. This implies that athletes should ensure a
rates than amylose and is therefore a more appro- CHO intake of about 60 to 70g per hour for optimal
priate energy source in CHO beverages for athletes. CHO delivery. Adopting an ingestion rate of 60 to
Furthermore, insoluble starch may provoke gastro- 70 g/h will optimise exogenous CHO oxidation.
intestinal symptoms.[38]
2.3 Multiple Transportable CHOs
2.2.7 Summary
The results of various studies are summarised in A study by Shi and colleagues[47] suggested that
figure 3. This figure shows the peak oxidation rates, the inclusion of 2 or 3 CHOs (glucose, fructose and
which may depend on a variety of factors including sucrose) in a drink may increase water and CHO
the exercise intensity, the amount of CHO ingested, absorption despite increased osmolality. This effect
and the timing of these feedings. Fructose and ga- was attributed to the separate transport mechanisms
lactose appear to be oxidised at relatively low rates, across the intestinal wall for glucose, fructose and
whereas glucose, sucrose, maltose, maltodextrins sucrose.[47] Interestingly, fructose absorption from
and soluble starch seem to be oxidised at relatively sucrose is also more rapid than the absorption of an

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Oxidation of Carbohydrate Feedings During Exercise 415

.
equimolar amount of fructose. In an elegant study, during 4 hours of exercise at 45% VO2max. This
Adopo et al.[44] fed 6 volunteers CHO at the onset of study suggests that the total amount of CHO seems
.
2 hours of exercise at 61% VO2max. The CHO feed- to be a more important determinant of exogenous
ings were 50g of glucose, 50g of fructose, 100g of CHO oxidation than osmolality or CHO concentra-
glucose, 100g of fructose or 50g of glucose plus tion.
50g of fructose. It was found that adding fructose
to a glucose solution increases the oral CHO oxi- 2.5 Amount of CHO
dation by 21% compared with an iso-energetic glu-
cose solution (fig. 3). The oxidation rate of 50g The amount of CHO that needs to be ingested
glucose plus 50g fructose in a combined drink was in order to obtain optimal performance is important
higher than the oxidation rate of either 100g glu- from a practical point of view. The optimal amount
cose or 100g fructose. However, amounts ingested is likely to be the amount of CHO resulting in max-
were relatively small and it remains to be estab- imal exogenous CHO oxidation rates. Pallikarakis
lished whether combined ingestion of glucose and et al.[51] found that doubling the amount of CHO
ingested from 200 to 400g during 285 minutes of
fructose can increase exogenous CHO oxidation .
more than the ingestion of large amounts of a single exercise at 45% VO2max increased exogenous CHO
CHO. Whether addition of galactose to a glucose oxidation. However, exogenous CHO oxidation rates
drink can increase total exogenous CHO oxidation did not double and the percentage of the CHO in-
in a similar way to glucose and fructose needs to gested that was oxidised was slightly lower (59.5
be determined. and 56.8%, respectively). Here we will refer to this
These data suggest that it might be useful to phenomenon as a lower oxidation efficiency with
include multiple types of CHO in CHO drinks for the larger dose of CHO.
athletes. More studies are needed to identify opti- Oxidation efficiency = exogenous CHO
mal combinations of different CHOs. oxidation rate/ingestion rate • 100% (Eq. 3)

2.4 Osmolality and Concentration Rehrer et al.[31] studied the oxidation of differ-
ent amounts of CHO ingested during 80 minutes of
.
Gastric emptying and absorption may depend cycling exercise at 70% VO2max. In a randomised
on the concentration and osmolality and hence the cross-over design, volunteers received a 4.5% glu-
type and amount of CHO, and the volume of the cose solution (a total of 58g glucose during 80 min-
ingested beverage. Recent studies seem to suggest utes of exercise) or a 17% glucose solution (220g
that CHO content is a more important determinant during 80 minutes of exercise). Exogenous CHO
of gastric emptying than osmolality.[48] Therefore, oxidation was measured and these were slightly
the CHO type may have little or no effect on the higher with the larger CHO dose (42 and 32g in 80
rate of gastric emptying.[49] It has become clear that minutes, respectively). Thus, even though the am-
the CHO type and osmolality of a solution can in- ount of CHO ingested was increased almost 4-fold,
fluence intestinal absorption of fluid and CHO. Rel- the oxidation rates were barely affected. The oxi-
atively large amounts of glucose in the form of glu- dation efficiency was much lower with the large
cose polymers introduced to the gastrointestinal tract amount of CHO (19% for the 17% glucose solution
without changing the osmotic load can increase the versus 55% for the 4.5% glucose solution). Inges-
glucose delivery and induce greater water absorp- tion of a 17% maltodextrin solution lead to the same
tion.[50] Jandrain et al.[19] investigated the oxidation conclusion (i.e. there was a lower oxidation effi-
of a 50g glucose load dissolved in either 200, 400 ciency with the more concentrated solution). In a
or 600ml of water. Although both the concentration study by Wagenmakers et al.,[37] participants exer-
.
and osmolality were different in these drinks, no dif- cised for 120 minutes at 65% VO2max on 5 occa-
ferences were observed in exogenous CHO oxidation sions and received 4 doses of maltodextrin ranging

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416 Jeukendrup & Jentjens

from 72 to 289g. Calculated average ingestion rates CHO as a source of energy. Both an increased mus-
were 0.6, 1.2, 1.8 and 2.4 g/min. Although oxida- cle glycogenolysis and increased plasma glucose
tion rates increased with increasing intake, exoge- oxidation will contribute to the increased energy
nous CHO oxidation seemed to level off after an demands.[52] It is therefore reasonable to suspect
intake of 1.2 g/min. Oxidation rates were 0.53, that exogenous CHO oxidation might increase with
0.86, 1.00 and 1.07 g/min, respectively. Also in this increasing exercise intensities. Indeed, an early study
study, the oxidation efficiency decreased with in- by Pirnay et al.[53] reported lower exogenous CHO
creasing intake (72, 52, 39 and 32%, respectively). oxidation rates at low exercise intensities compared
More recently, Jeukendrup et al.[5] investigated with moderate intensities, but exogenous CHO ox-
the oxidation rates of even larger CHO intakes on idation tended to level off between 51 and 64%
exogenous CHO oxidation. In this study, well trained .
VO2max. In this study, participants exercised for 90
volunteers exercised at a relatively low exercise
. minutes on a treadmill on 4 different occasions at
intensity of 50% VO2max for 120 minutes while in-
different percentages of their maximal aerobic ca-
gesting 70 or 360g of glucose. With the low dose
of glucose (average ingestion rate of 0.58 g/min) pacity. They ingested 100g of glucose during exer-
exogenous CHO oxidation rates averaged 0.34 cise. The average oxidation rates of the ingested
glucose were 0.18, 0.36, 0.46 and 0.49 g/min at 22,
g/min, while with the high dose (average ingestion .
rate 3.00 g/min) these rates increased up to 0.94 39, 51, and 64% VO2max, respectively. The exoge-
g/min. This study also demonstrated a decreased nous CHO oxidation rates did not further increase
CHO oxidation efficiency with increasing inges- when the exercise intensity was increased from 51
.
tion rates (59 vs 31%). It is interesting to note that to 64% VO2max.
although ingestion rates increased up to 2.4 to 3.0 Recently, the same group of researchers found
g/min,[5,37] in none of these studies did CHO oxi- an almost similar relationship between the exoge-
dation rates exceed 1.1 g/min. nous CHO oxidation rate and the power output on
The results of all studies currently available in the a cycle ergometer.[54] The oxidation rate of the in-
literature were used to construct figure 3. Although gested CHO increased with increasing metabolism
.
this graph needs to be interpreted with caution (it for intensities below 60% VO2max. However, when
includes studies at different exercise intensities, the exercise intensity was increased from 60 to 75%
different feeding schedules, different volunteer .
VO2max the oxidation rate leveled off or even de-
populations, etc.), it must be concluded that the creased (0.51 and 0.42 g/min, respectively). One
maximal rate at which ingested CHO can be oxi- possible explanation for the reduced exogenous oxi-
dised is 1.0 to 1.1 g/min. Increasing the CHO intake dation rate during high exercise intensities (>70 to
during exercise may increase oxidation rates until .
75% VO2max) might be the limitation of intestinal
the intake exceeds 1.0 to 1.2 g/min. Clearly, the rate digestion and/or absorption, although to our knowl-
of oxidation of ingested CHO is limited. However,
edge such a limitation has not been shown at exer-
the factors limiting exogenous CHO oxidation are .
cise intensities below 80% VO2max. Massicotte et
still largely unknown. Possible mechanisms will be
al.[28] examined a group of individuals with a wide
discussed in section 3.
variety of fitness levels during exercise at 60% of
.
their individual VO2max. Although volunteers exer-
3. Factors Affecting Exogenous .
cised at the same relative workload (60% VO2max),
CHO Oxidation
there were large differences in the metabolic rate
(absolute workload). In agreement with the find-
3.1 Exercise Intensity
ings of Pirnay et al.,[53,54] a linear relationship be-
With increasing exercise intensity, the exercis- tween the metabolic rate and the oxidation rate of
ing muscle becomes more and more dependent on 100g ingested CHO was found.

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Oxidation of Carbohydrate Feedings During Exercise 417

.
However, it could be argued that these findings for 2 hours at 40% VO2max on a cycle ergometer, 1
are an artifact caused by the stable isotopic meth- hour after ingestion of 100g of glucose. The oxida-
ods used, rather than a physiological phenomenon. tion rates of the ingested CHOs were similar: 41g
As discussed in section 1, some label may be lost in the group with normal glycogen availability and
in exchange reactions with the TCA-cycle. It was 38g in the group with reduced glycogen availabil-
also shown that at low metabolic rates recovery of ity. However, the study had no cross-over design,
the label was only 60 to 70%, whereas at high work which may have influenced the results. Although
rates recovery of the label can be 90% or more.[13] the absolute rates of exogenous CHO were not dif-
Because no correction was made for label loss in ferent between groups, due to the 20% higher en-
the studies cited above, the calculated exogenous ergy expenditure observed in the group of glycogen-
CHO oxidation rates could have been underesti-
depleted individuals, exogenous CHO oxidation
mated, especially at lower metabolic rates. We
provided only 16% of the energy yield versus 20%
therefore corrected the values for label loss accord-
in the group with normal glycogen levels. Thus, the
ing to Sidossis et al.[13] However, although the dif-
ferences were less pronounced after correction, lower glycogen level was associated with a decreased
they were still present. Van Loon et al.[55] did not contribution of exogenous CHO oxidation to en-
observe differences in exogenous CHO oxidation ergy expenditure during moderate intensity exercise.
rates when trained cyclists exercised at 38 or 55% More recently, Jeukendrup et al.[45] manipulated
. pre-exercise glycogen levels by glycogen lowering
VO2max. It is therefore possible that lower exoge-
nous CHO oxidation rates are only observed at very exercise in combination with CHO restriction (LG
low exercise intensities when the reliance on CHO trial) or rest in combination with CHO loading (HG
as an energy source is minimal. In this situation, trial). In a randomised cross-over design, volun-
part of the ingested CHO may be directed towards teers received an average of 127g glucose during
.
non-oxidative glucose disposal (storage in the liver 120 minutes of exercise at 57% VO2max. In contrast
or muscle) rather than towards oxidation. Studies to the conclusion of Ravussin et al.,[57] it was found
with CHO ingestion during intermittent exercise that exogenous glucose oxidation was 28% lower
have suggested that glycogen can be resynthesised in the LG trial compared with the HG trial: 36g of
during low intensity exercise.[56] glucose was oxidised during 60 to 120 minutes of
It seems fair to conclude that at exercise inten-
. exercise during LG, whereas 50g was oxidised with
sities below 50 to 60% VO2max, exogenous CHO HG. Péronnet et al.[58] studied the effect of endog-
oxidation will increase with increasing total CHO enous CHO availability, after high and low CHO
oxidation rates, whereas above approximately 50
. diets, on the oxidation of exogenous CHOs during
.
to 60% VO2max, oxidation rates will not usually 120 minutes of exercise at 64% VO2max. Volunteers
increase further. relied more on exogenous CHO oxidation after the
low CHO diet, when glycogen availability was pre-
3.2 Muscle Glycogen sumably low, than after the high CHO diet, when
Although determinants of exogenous CHO ox- glycogen availability was presumably high. Between
idation have been intensively investigated for al- 40 and 80 minutes of the exercise period, exoge-
most 30 years, the effect of pre-exercise glycogen nous CHO oxidation was significantly higher after
levels on exogenous CHO oxidation during exer- the low CHO diet compared with the high CHO
cise are still largely unknown and studies have pro- diet (0.63 vs 0.52 g/min, respectively). These re-
duced different results. In a study conducted by sults are inconsistent with the results of Ravussin
Ravussin et al.,[57] the oxidation rate of exogenous et al.[57] and Jeukendrup et al.,[45] and are likely
glucose was studied in individuals with normal and attributed to differences in experimental conditions
low glycogen levels. The 2 groups were observed of exercise and the amounts of CHO ingestion.

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418 Jeukendrup & Jentjens

Because of the higher relative workload in the 3.3 Training

.
study of Péronnet et al.[58] (64 vs 40 and 57% VO2max
in the studies by Ravussin et al.[57] and Jeukendrup Endurance training has a marked effect on sub-
et al.,[45] respectively) and the larger amount of glu- strate utilisation and generally results in a shift from
cose ingested (200 vs 100 and 127g in the studies CHO towards fat metabolism. There is a decreased
reliance on CHO metabolism after training at the
by Ravussin et al.[57] and Jeukendrup et al.,[45] re-
same absolute workload.[61-64] However, some con-
spectively) volunteers relied more on CHO oxida-
troversy still exists regarding whether the reliance
tion and less on fat oxidation after both diets. The on CHO as a fuel is also decreased at the same
increased reliance on CHO oxidation at this higher relative exercise intensity. Several studies suggest
exercise intensity, when glycogen levels are reduced, that even though the exercise after training is per-
might explain why exogenous CHO oxidation was formed at the same relative intensity (and thus a
higher. higher absolute intensity), there is a decreased re-
Another explanation could be that the extent to liance on blood glucose and muscle glycogen.[63-65]
which glycogen levels were reduced was responsi- However, some studies did not find a change in
ble for the different findings between the studies. glucose uptake after training when compared at the
Although none of the above studies measured gly- same relative exercise intensity,[61,62] although
cogen levels, the glycogen depletion protocol used plasma glucose oxidation was decreased.[62] Train-
in the study by Jeukendrup et al.[45] has previously ing induces several adaptations at the muscular level
been shown to result in very low muscle glycogen including an increased GLUT-4 content,[66] increased
insulin action[67] and an increased capillary bed.
levels (<140 mmol/kg dry weight),[59] and to lead
All these adaptations would favour glucose uptake
to low plasma insulin levels and high plasma free
and could possibly alter the handling of blood glu-
fatty acids. The 2 to 3 times higher plasma free fatty
cose and thus of exogenous glucose.
acid level and the lower plasma insulin level when A few studies have investigated the effects of
glycogen levels were low[45,57] could have reduced training (or training status) on exogenous CHO ox-
plasma glucose uptake and oxidation.[60] Péronnet idation rates.[24,55,68,69] In an early study by Krzen-
et al.[58] found a smaller difference in free fatty acid towski et al.,[68] volunteers trained for 6 weeks and
levels between their experimental trials, whereas substrate utilisation was measured at the same ab-
insulin levels were not different. This was possibly solute exercise intensity before and after the train-
due to the moderate glycogen depletion regimen ing programme. The authors concluded that exog-
applied in their study, which might therefore ex- enous CHO oxidation was increased by 17% after
plain why exogenous CHO oxidation did not de- training. However, the results seem difficult to in-
.
crease when glycogen availability was low. terpret. Firstly, the VO2max of the participants was
The effect of muscle glycogen on exogenous CHO increased by an unphysiological amount (29%). Sec-
oxidation per se is unknown at present. Studies have ondly, in contrast to the literature and despite the
improved aerobic capacity after training, no differ-
attempted to manipulate muscle glycogen stores by
ence in total CHO and fat oxidation was observed.
altering the dietary CHO intake and employing ex-
More recently, van Loon et al.[55] reported that the
ercise programmes but, by doing so, other vari-
contribution of CHO to energy expenditure was
ables (i.e hormonal changes, high free fatty acid lower in well trained cyclists compared with healthy
levels) have been changed as well and these changes untrained controls at the same absolute intensity.
may have been responsible for the variable results The reduction in CHO oxidation was due to a re-
in different studies. More studies are required to duction in muscle glycogen oxidation (0.10 and 0.75
elucidate the role of muscle glycogen on the oxida- g/min) and endogenous glucose production (0.20
tion rate of ingested CHO. and 0.13 g/min), respectively (fig. 4). However, de-

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Oxidation of Carbohydrate Feedings During Exercise 419

spite these differences in substrate utilisation, ex- 1.2 Glucose from liver
ogenous glucose oxidation rates were unaffected Glucose from feedings
1.0
(0.7 g/min in trained and untrained cyclists).

Ra glucose (g/min)
Burelle et al.[24] also compared exogenous CHO 0.8
oxidation in trained and sedentary individuals dur-
0.6
ing exercise at the same absolute workload. Volun-
teers cycled for 90 minutes at 140W and received 0.4
100g 13C-enriched glucose during exercise. Sur-
0.2
prisingly, no differences were found in total CHO
and fat oxidation between trained and untrained 0
volunteers. However, although blood glucose oxi- Fast LO-GLU HI-GLU
dation rates were not different, exogenous CHO Fig. 4. Glucose delivery to the blood from the liver and gastro-
intestinal tract (feedings) during exercise. During a fast, no glu-
oxidation rates were higher in trained individuals. cose feedings were provided and all glucose appearing in the
Differences in the results of van Loon et al.[55] and blood stream was derived from the liver. When a small amount
Burelle et al.[24] may also be caused by differences of glucose was provided (LO-GLU) the total delivery of carbo-
hydrate (CHO) increased but the contribution of liver glucose
in the experimental protocol (amount of CHO in- declined. When large amounts of CHO were ingested (HI-GLU),
gested, exercise intensity and timing of feedings). the total delivery of CHO was further increased. Liver glucose
For instance, Burelle et al.[24] gave their first feed- output was negligible and all glucose was derived from the feed-
ings. Ra = rate of appearance (adapted from Jeukendrup et
ing (25g glucose) 30 minutes before exercise, which al.,[70] with permission).
means that glycogen stores may have been pre-la-
beled, particularly in the trained volunteers who
are more insulin sensitive and will have an increased creased muscle glycogen use, which is in contrast
muscle glucose uptake after an oral glucose load. with most of the literature showing either no change
This would result in an overestimation of exoge- or a decreased intramuscular glycogen breakdown
nous CHO oxidation rates during exercise in the after training at the same relative intensity.[61,62]
trained volunteers. If trained individuals stored 20% In section 4 of this review we will discuss how
more of the initial glucose gift (5g) than the un- maximal exogenous CHO oxidation rates are reg-
trained individuals, this could explain the entire ulated. This concept, which is based on the premise
observed difference in exogenous CHO oxidation. that the liver and intestine play a crucial role in
This seems a reasonable assumption since it has glucose homeostasis, describes that a maximal glu-
been shown that post-exercise, glycogen resynthe- cose output by the liver controls maximal exogenous
sis can be twice as fast after endurance training.[71] CHO oxidation rates. This concept would predict that
Three studies have investigated the effects of exogenous CHO oxidation rates are similar in trained
exogenous CHO oxidation during exercise at the and untrained individuals at the same absolute and
same relative exercise intensity.[24,55,69] Two stud- relative workload. Higher exogenous CHO oxida-
ies showed no effect of training on the oxidation of tion rates in trained individuals would suggest a
superior absorption or more exogenous glucose
ingested CHO, whereas Burelle et al.[24] reported
would escape from the liver. There are currently no
higher oxidation rates in trained compared with un-
. data available to support these potential differences
trained individuals at 68% VO2max.
between trained and untrained individuals.
The difference between these studies may be
related to the fact that the latter study showed an
4. Limitations of Exogenous
increase in total CHO oxidation in trained individ-
CHO Oxidation
uals, whereas no changes in CHO oxidation were
found in the studies by van Loon et al.[55] and Jeu- As depicted in figure 3, exogenous CHO oxida-
kendrup et al.[69] Burelle et al.[24] also reported in- tion seems to be limited to rates of 1.0 to 1.1 g/min.

 Adis International Limited. All rights reserved. Sports Med 2000 Jun; 29 (6)
420 Jeukendrup & Jentjens

CHO and feeding schedules.[27,38] Because in these studies

ingestion rate only 32 to 48% of the CHO delivered to the intes-
Gastrointestinal tract
>2.0 g/min tine was oxidised, it was concluded that gastric emp-
tying was not limiting exogenous CHO oxidation.
? g/min
Glucogen Liver Another potential rate-limiting factor is intesti-
1.2-1.7 g/min
nal absorption of CHO. Studies using a triple lu-
1.0 g/min 0-1.0 g/min men technique have measured duodenojejunal glu-
cose absorption and estimated whole body intestinal
1.0 g/min absorption rates of a 6% glucose-electrolyte solu-
Glucose tion.[72] It was estimated that the maximal absorp-
Blood
tion rate of the intestine ranged from 1.3 to 1.7
1.0 g/min g/min. Recent studies using stable isotope method-
Muscle ology have tried to quantify the appearance of glu-
cose from the gut into the systemic circulation (Ra
1.0 g/min gut). When a low dose of CHO was ingested during
exercise, the rate of appearance of glucose from the
CO2
gut equaled the rate of CHO ingestion during the
Fig. 5. Regulation of hepatic glucose production and the control
of glucose appearance into the systemic circulation with carbo- second hour (both 0.43 g/min).[5] This implies that
hydrate (CHO) ingestion. CHO can be ingested at fairly high at low ingestion rates absorption is not limiting and
rates up to about 3 g/min before causing gastrointestinal symp- there is no net storage of glucose in the liver. In-
toms. This CHO will then be digested and absorbed at a rate of
1.2 to 1.7 g/min, which has been suggested to be the maximal stead, all ingested glucose appears in the blood
absorptive capacity of the intestine. CHO will then enter the liver stream. It was also found that the glucose appearing
through the portal vein. A maximum of 1 g/min will escape from in the bloodstream was taken up at similar rates to
the liver and enter the bloodstream. The CHO entering the
bloodstream may be derived from ingested CHO (in extreme its Ra and 90 to 95% of this glucose was oxidised
conditions 1 g/min), can be derived from the liver (glycogenoly- during exercise. When a larger dose of CHO was
sis and gluconeogenesis) at a rate of 0 to 1 g/min, or can be
derived from a combination of both. Whether glucose from in-
ingested (3 g/min), Ra gut was one-third the rate of
gested CHO can be directed towards liver glycogen during ex- CHO ingestion (0.96 to 1.04 g/min). Thus, only
ercise has not been established. Glucose will be taken up by part of the ingested CHO entered the systemic cir-
the muscle and can be oxidised at virtually similar rates. This
graph was composed with results from various studies.[5,8,72]
culation. However, the glucose appearing in the blood
was taken up and 90 to 95% was oxidised. It was
therefore concluded that entrance into the systemic
This finding seems supported by the vast majority circulation is a limiting factor for exogenous glu-
of studies using either radioactive[3,36] or sta- cose oxidation, rather than intramuscular factors.
ble[5,37,45,53,69] isotopes to quantify exogenous CHO This is further supported by glucose infusion stud-
oxidation during exercise. One of the limiting fac- ies. Hawley et al.[73] bypassed both intestinal ab-
tors could be gastric emptying. However, Rehrer et sorption and hepatic glucose uptake by infusing
.
al.[31] showed that gastric emptying is unlikely to glucose in volunteers exercising at 70% VO2max.
affect exogenous CHO oxidation rates. In their study, When large amounts of glucose were infused and
participants ingested 220g glucose during 80 min- volunteers were hyperglycemic (10 mmol/L), it was
.
utes of exercise at 70% VO2max. After 80 minutes, possible to raise blood glucose oxidation rates above
100g of glucose was present in the stomach and 1 g/min.
thus 120g was delivered to the duodenum. How- These studies provide evidence that exogenous
ever, at 80 minutes only 38g of the ingested CHO CHO oxidation is limited by the rate of digestion,
was oxidised. These results were later confirmed absorption and subsequent transport of glucose into
by others using slightly different exercise protocols the systemic circulation rather than the rate of up-

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Oxidation of Carbohydrate Feedings During Exercise 421

take and oxidation by the muscle. The maximal Fat

Muscle glycogen
rates of intestinal absorption seem to be slightly in Hepatic glucose output
excess of the maximal appearance of glucose from 3 Exogenous carbohydrate
the gut into the bloodstream.[5] It is important to
note that during high intensity exercise, a reduced

Substrate utilisation (g/min)

mesenteric blood flow may result in a decreased *
2
absorption of glucose and water[50] and hence a low *
Ra gut relative to the rate of ingestion. However,
this may only apply to exercise at very high inten- *
sities.[50] Taken together, this suggests that intesti- 1
nal absorption is a factor contributing to the limi- *
tation to oxidise ingested CHO at rates higher than
1.0 to 1.1 g/min, but it may not be the sole factor. 0
The liver may play an additional important role. T1 UT T2
Hepatic glucose output is highly regulated and it is Fig. 6. Substrate utilisation in untrained (UT) and trained indi-
possible that the glucose output derived from the viduals at the same absolute (T1) and relative exercise intensity
intestine and from hepatic glycogenolysis and glu- (T2). UT and T1 .
is exercise at 148W [55 and 38% maximal
oxygen. uptake (V O2max), respectively] and T2 is exercise at 200W
coneogenesis will not exceed 1.0 to 1.1 g/min even (55% V O2max).
though the absorption is slightly in excess of this
rate (fig. 5). If supply from the intestine is too large
very high rates, may not enter the systemic circu-
(>1.0 g/min), glycogenesis may be activated in the
lation at these high rates. The relative role of ab-
liver. Recent findings by Jeukendrup et al.[5] support
sorption and the liver retaining glucose remain to
the role of the liver. Ingestion of small CHO doses
be determined. With the recent developments in
during exercise suppressed endogenous (mainly
nuclear magnetic resonance spectroscopy it should
liver) glucose production (fig. 6). Very high rates
be possible to more accurately determine the role
of CHO intake (3 g/min) completely suppressed en-
dogenous glucose production. However, despite of the liver.[78]
these high rates of ingestion the total Ra did not Another question, which may be beyond the scope
exceed 1 g/min. Assuming that CHO was absorbed of this review, is related to the performance effects
at a rate slightly in excess of 1 g/min, this would of glucose feedings during exercise. It has been
suggest glycogenesis in the liver during exercise. shown that CHO feeding during exercise can im-
The hormonal profile as observed after ingesting prove performance when the exercise duration is
large amounts of glucose during exercise (higher only about 60 minutes.[1,79,80] It was calculated that
plasma insulin and lower plasma glucagon levels) by this time only 5 to 15g of the ingested glucose
would support glycogenesis by activating hepatic could have been oxidised,[1] and it is therefore un-
glycogen synthase activity,[74] GLUT-2 transporter likely that this small contribution causes the rela-
expression,[75] increased glucose kinase expres- tively large effect on performance. However, alter-
sion[76] or liver cell swelling.[77] native mechanisms are currently unknown. Other
questions, which may have important practical im-
5. Directions for Future Research plications, are related to exercise in extreme con-
ditions (heat, altitude). Formulated guidelines are
Although many advances have been made in the primarily based on studies in thermoneutral and
last few years, several questions remain to be an- sea level conditions.
swered. One of the intriguing questions is the fate However, it is possible that these guidelines are
of excess amounts of ingested CHO. Recent stud- not suitable for exercise in the heat or at high alti-
ies have revealed that glucose, when ingested at tude. Both conditions have been shown to result in

 Adis International Limited. All rights reserved. Sports Med 2000 Jun; 29 (6)
422 Jeukendrup & Jentjens

marked changes in substrate utilisation at rest and Acknowledgements

during exercise.[81,82] Prolonged exercise in the heat
The authors want to acknowledge the invaluable support
will lead to distribution of blood to the skin to allow from and fruitful discussions with Dr Anton Wagenmakers,
for evaporative cooling.[83] As a consequence, blood Professor Wim Saris and Dr Fred Brouns at Maastricht
flow to other organs such as the liver, kidney, inac- University in The Netherlands. We also want to thank Pro-
tive tissue and the gut will be reduced.[84,85] A re- fessor Mike Gleeson for his careful and critical reviewing of
duced blood flow to the gut may impair gut func- this manuscript.
tion, especially during ultra-endurance exercise, as
recently suggested.[70] Absorption of CHO (and other References
1. Jeukendrup AE, Brouns F, Wagenmakers AJM, et al. Carbohydrate
nutrients) may be impaired, which may finally lead feedings improve 1 h time trial cycling performance. Int J
to a reduced oxidation rate of ingested CHO. This Sports Med 1997; 18: 125-9
2. Coyle EF, Coggan AR, Hemmert MK, et al. Muscle glycogen
may also partly explain why CHO feeding during utilization during prolonged strenuous exercise when fed car-
exercise in the heat has no effect on endurance per- bohydrate. J Appl Physiol 1986; 61: 165-72
formance.[86-88] Future studies are therefore needed 3. Bosch AN, Dennis SC, Noakes TD. Influence of carbohydrate
ingestion on fuel substrate turnover and oxidation during pro-
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