| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Exercise Physiology and Metabolism Laboratory, Department of Physiology, The University of Melbourne, Parkville, Victoria 3052; and 2 Exercise Metabolism Group, Department of Human Biology and Movement Science, Royal Melbourne Institute of Technology University, Bundoora, Victoria 3083, Australia
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
We investigated the effect of carbohydrate (CHO) ingestion before and during exercise and in combination on glucose kinetics, metabolism and performance in seven trained men, who cycled for 120 min (SS) at ~63% of peak power output, followed by a 7 kJ/kg body wt time trial (TT). On four separate occasions, subjects received either a placebo beverage before and during SS (PP); placebo 30 min before and 2 g/kg body wt of CHO in a 6.4% CHO solution throughout SS (PC); 2 g/kg body wt of CHO in a 25.7% CHO beverage 30 min before and placebo throughout SS (CP); or 2 g/kg body wt of CHO in a 25.7% CHO beverage 30 min before and 2 g/kg of CHO in a 6.4% CHO solution throughout SS (CC). Ingestion of CC and CP markedly (>8 mM) increased plasma glucose concentration ([glucose]) compared with PP and PC (5 mM). However, plasma [glucose] fell rapidly at the onset of SS so that after 80 min it was similar (6 mM) between all treatments. After this time, plasma [glucose] declined in both PP and CP (P < 0.05) but was well maintained in both CC and PC. Ingestion of CC and CP increased rates of glucose appearance (Ra) and disappearance (Rd) compared with PP and PC at the onset of, and early during, SS (P < 0.05). However, late in SS, both glucose Ra and Rd were higher in CC and PC compared with other trials (P < 0.05). Although calculated rates of glucose oxidation were different when comparing the four trials (P < 0.05), total CHO oxidation and total fat oxidation were similar. Despite this, TT was improved in CC and PC compared with PP (P < 0.05). We conclude that 1) preexercise ingestion of CHO improves performance only when CHO ingestion is maintained throughout exercise, and 2) ingestion of CHO during 120 min of cycling improves subsequent TT performance.
glucose uptake; glycogen
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
IT IS WELL ESTABLISHED THAT carbohydrate (CHO) feeding during prolonged (>120 min) exercise can increase work capacity by maintaining power output or speed (1, 5, 23) or by prolonging the time to fatigue at a fixed, submaximal workload (7, 21, 28). In contrast, studies that have examined the effect of preexercise CHO feedings on performance have produced conflicting results. This practice has been demonstrated to increase (11, 30), decrease (6, 10), or have no effect (9, 27) on exercise performance. This may, in part, be due to the hyperinsulinemia resulting from preexercise CHO ingestion. Rises in circulating insulin increase muscle glucose uptake at the onset of exercise but subsequently result in rebound hypoglycemia after ~30 min (18), thereby decreasing peripheral glucose availability. Increases in plasma insulin concentration during exercise also act to reduce lipolysis (32) and fat availability (27), which are likely to lead to increased intramuscular glycogen use (2) and a consequent reduction in exercise performance. Nonetheless, preexercise CHO ingestion has been demonstrated to increase both liver (24) and muscle (8) glycogen stores, and, therefore, this practice has the capacity to increase exercise performance.
If CHO ingestion during exercise is undertaken in conjunction with a preexercise CHO feeding, it is possible that the resulting hyperinsulinemia and increased muscle glucose uptake will be sustained as a result of a better maintenance of blood glucose concentration. Indeed, CHO feeding during exercise has been shown to increase muscle glucose uptake compared with the ingestion of a sweet placebo (19). Such an increase in blood glucose availability could, theoretically, more than compensate for any hyperinsulinemia-induced reduction in lipolysis while also reducing the reliance on intramuscular glycogen stores. Such a metabolic scenario is likely to lead to an enhanced exercise performance.
In this regard, Wright et al. (33) have previously demonstrated that a combination of CHO feeding before and during exercise has an additive effect on performance compared with when CHO is ingested only before, or only during, exercise. In that study (33), however, subjects ingested different amounts of CHO before and during exercise, and, therefore, the relative importance of each practice could not be elucidated. In addition, neither muscle glycogen nor glucose kinetics were determined in the study of Wright et al. (33), so it was impossible to determine the underlying mechanism behind their observed performance enhancement.
The aim of the present study was to determine the effect of CHO ingestion before, during, or in combination on exercise metabolism and performance. We conducted a comprehensive study by obtaining glucose kinetic data throughout exercise, which allowed us to determine the rate of glucose disposal when different CHO feeding strategies are adopted. We hypothesized that a combination of CHO feeding before and throughout exercise would maintain euglycemia, and a modest hyperinsulinemia, thereby preserving high rates of glucose uptake by the contracting muscles. By reducing the reliance on muscle glycogen, we hypothesized that performance would be significantly improved when feeding was combined before and during exercise.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Subjects.
Seven endurance-trained men [age 26.9 ± 6.4 (SD) yr; weight
74.7 ± 9.0 kg; peak oxygen uptake
(
O2 peak) 63.0 ± 4.4 ml · kg
1 · min1; height
181 ± 6 cm] were recruited as subjects for this study after
being fully informed of the risks associated with the procedures and
signing a letter of informed consent. The project was approved by the
Research and Ethics Committees of the University of Melbourne and Royal
Melbourne Institute of Technology University.
Preliminary testing.
O2 peak was determined during an
incremental cycling test to volitional fatigue on an electrically
braked cycle ergometer (Lode, Groningen, The Netherlands). Expired air
was directed via a Hans Rudolph valve and plastic tubing into Douglas
bags. The oxygen and carbon dioxide content of the Douglas bags was
analyzed using Applied Electrochemistry (Ametek, Pittsburgh, PA)
S-3A/II and CD-3A gas analyzers, respectively, calibrated before each test with a commercially prepared gas mixture of known composition. The
volume of expired gases was determined using a gas meter
(Parkinson-Cowan, Manchester, UK).
Experimental trials. Subjects reported to the laboratory on four occasions after an overnight fast, having abstained from alcohol, caffeine, tobacco, and strenuous exercise for the previous 24 h. To minimize differences in resting muscle and liver glycogen concentration, subjects were provided with preprepared food packages (~15.6 J, 71% CHO, 15% protein, 14% fat) for 24 h before each trial. Such a dietary-exercise regimen has previously been shown to minimize differences in preexperimental metabolism and substrate availability (1). Each experiment was separated by a minimum of 7 days.
During each trial, subjects cycled for 120 min (SS) at a workload (~64 ± 2% of peak power output) equivalent to ~70% ofO2 peak, followed by a performance
cycle (TT) in which subjects completed 7 kJ/kg body wt as fast as
possible. Trials were performed in random order using a double-blind
protocol, and the identity of each trial was not revealed until after
analyses. Subjects received either no CHO-electrolyte before or during
SS (PP); a placebo-electrolyte beverage 30 min before and 2 g/kg body
wt of CHO in a 6.4% CHO-electrolyte beverage (Lucozade Sport)
throughout SS (PC); 2 g/kg body wt of CHO in a 25.7% CHO-electrolyte
beverage (Lucozade) 30 min before and a placebo-electrolyte beverage
throughout SS (CP); or 2 g/kg body wt of CHO in a 25.7%
CHO-electrolyte beverage 30 min before and 2 g/kg body wt of CHO in a
6.4% CHO-electrolyte beverage throughout SS (CC). The CHO and
placebo beverages were matched for electrolyte content. They were
provided at the onset and at 15-min intervals during SS. During the TT,
subjects had access to water ad libitum.
On arrival in the laboratory, the subjects voided, were weighed, and
catheters (Terumo 20 gauge) were inserted into a vein in the
antecubital space of each arm for blood sampling and infusion of the
tracer (described subsequently). After a basal blood sample was
collected, the catheter was flushed with 0.5 ml of saline containing
heparin (10 IU/ml). A primed (3.3 mmol) continuous (~44 µmol/min)
infusion of sterile [6,6-2H]glucose (Cambridge Isotope
Laboratories, Cambridge, MA) commenced and was maintained for the 120 min of rest and throughout SS. The infusate was delivered via a
peristaltic pump (Gilson, Minipuls 3, Villiers Le Bel, France) that was
calibrated before and after each experiment. At the completion of SS,
subjects rested for 1 min before they commenced the TT.
Heart rate (HR), ratings of perceived exertion (RPE),
O2, carbon dioxide production
(CO2), and respiratory exchange ratio (RER) were measured at 15-min intervals during SS. In addition to the
basal blood sample, further samples were obtained 10, 20, and 30 min
postprandial and at 20-min intervals during SS.
Analytic techniques.
HR was measured by telemetry (Polar, Kempele, Finland), and RPE was
estimated using a 19-point scale (3).
O2, CO2, and RER values were analyzed using Douglas bags as previously described, and the values were used to estimate rates of whole body CHO
and fat oxidation according to the equations of Peronnet and Massicotte
(25). Because estimated rates of substrate oxidation were
contingent on precise pulmonary gas measures, the analyzers were
calibrated before each measure, and the Douglas bags were analyzed on collection.
80°C and later analyzed for
plasma glucose concentration using an automated method (EML-105,
Electrolyte Metabolite Laboratory, Radiometer, Copenhagen, Denmark) and
plasma insulin concentration by radioimmunoassay (Incstar, Stillwater,
MN). A further aliquot of blood was mixed in a tube containing lithium
heparin and spun in a centrifuge. Two hundred and fifty microliters of
plasma were placed into a tube containing 250 µl of ice-cold 3 M
perchloric acid, mixed vigorously on a vortex mixer, and spun. Four
hundred microliters of this supernatant were added to a tube containing
100 µl of 6 M KOH, mixed, and spun. The resultant supernatant was
analyzed for plasma glycerol concentration using an enzymatic
spectrophotometric analysis as previously described (1).
The further aliquot of this plasma was stored for measurement of
[6,6-2H]glucose enrichment as previously described
(12). Briefly, 500 µl of plasma were mixed with 500 µl
of 0.3 M Ba(OH)2 and 500 µl of ZnSO4 and
spun. The supernatant was passed down an ion-exchange column (Dowex
2 × 8, 200-400 mesh, Bio-Rad, Richmond, CA) washed with
distilled water (3 × 1-ml aliquots), and dried. The samples were
then resuspended with distilled water, placed in glass vials, dehydrated overnight, and derivatized with the addition of pyridine and
acetic anhydride. The derivatized samples were measured using a gas
chromatograph-mass spectrometer (5890 series 2 gas chromatograph, 5971 mass spectrometer detector, Hewlett-Packard, Avondale, PA). The rates
of glucose appearance (Ra) and glucose disappearance (Rd) were determined from changes in the percent enrichment
in the plasma of [6,6-2H]glucose, calculated using the
one-pool non-steady-state model (29), assuming a pool
fraction of 0.65 and estimating the apparent glucose space as 25% of
body mass. Glucose oxidation was estimated by assuming that glucose
Rd during exercise was approximately equal to the amount of
glucose oxidized (16). An estimate of glycogen oxidation
was then calculated by subtracting glucose oxidation from total CHO
oxidation obtained from pulmonary measures.
Two milliliters of whole blood were added to an aliquot of preservative
consisting of EGTA and reduced glutathione in normal saline, mixed
gently, and spun in a centrifuge. Plasma was decanted, placed in vials
and stored at 80°C. These samples were later analyzed for plasma
free fatty acids (FFAs) using an enzymatic colorimetric method
(22). The remaining blood (2 ml) was added to a lithium
heparin tube containing 200 µl of a protease inhibitor (10%
Trasylol), mixed gently, and spun in a centrifuge. Plasma was decanted,
placed in vials, and stored at 80°C until analysis of plasma
glucagon concentration by immunoradiometric assay (Bioclone, Marrickville, Australia) as previously described (12).
Statistical analyses. The metabolic data from the four trials was compared using two-factor (time and treatment) ANOVA with repeated measures. A one-way ANOVA was used to compare time to complete the performance cycle. Newman-Keuls post hoc tests were used to locate differences when ANOVA revealed a significant interaction. A Statistica computer software program was used to compute these statistics. The alpha level to reject the null hypothesis was set at P < 0.05. All values are expressed as means ± SE.
| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Mean O2,
CO2, RER, HR, and RPE during SS were not
different between trials (Table 1).
However, RER was higher (P < 0.05) in CC compared with
other trials at 105 and 120 min (data not shown). Preexercise CHO
consumption resulted in a higher (P < 0.01) plasma
glucose concentration 10, 20, and 30 min postingestion in CC and CP
compared with PC and PP (Fig. 1). During
the first 90 min of SS, no differences in plasma glucose concentration
were observed between trials. However, during the last 30 min of SS, plasma glucose concentration was higher in CC and PC compared with CP
and PP (Fig. 1). Neither plasma FFA nor glycerol concentrations were
different between trials during the first 60 min of SS. However, during
the final 60 min of SS, both plasma FFA and glycerol concentrations were elevated (P < 0.05) in PP compared with CC, CP,
and PC (Fig. 2). Plasma FFA
concentrations during this period were not different between CC, CP, or
PC (Fig. 2), although plasma glycerol was higher (P < 0.05) when comparing PP with PC at 120 min. Preexercise CHO ingestion
resulted in a higher (P < 0.01) plasma insulin
concentration 10, 20, and 30 min postingestion in CC and CP compared
with PC and PP. However, shortly after the start of exercise, plasma
insulin concentrations were similar between trials (Fig.
3). Although plasma glucagon
concentration increased (P < 0.05) as exercise progressed, this hormone was not different between trials (Fig. 3).
Glucose Ra and Rd were higher
(P < 0.05) in CC and CP compared with PC and PP after
beverage ingestion and at the onset of SS. In addition, for reasons not
readily apparent, glucose Ra was higher (P < 0.05) in CC compared with CP 10 min after ingestion. No differences
in glucose Ra or Rd were observed between
trials during the first 105 min of SS. However, during the last 15 min of SS, glucose Ra and Rd were higher
(P < 0.05) in CC and PC compared with CP and PP (Fig.
4). The rates of total CHO oxidation were not different between trials for the first 105 min of SS but were higher (P < 0.05) in CC compared with other trials at
105 and 120 min. Because we assumed that glucose Rd during
exercise was approximately equal to the amount of glucose oxidized, we
were able to obtain an indirect measure of glucose oxidation and CHO oxidation derived from other sources (i.e., glycogen). These
calculations demonstrated that glucose oxidation was different
(P < 0.05) when comparing the four trials, with
CC > CP > PC > PP. However, the contribution of
glucose to total substrate oxidation was minimal, ranging from 38 to
43 g (8-11% of total energy). Hence, estimated total
glycogen oxidation and fat utilization were not different when
comparing the four trials (Fig. 5).
Despite this, the time taken to complete 7 kJ/kg was lower
(P < 0.05) when comparing CC and PC with PP. No
difference in exercise performance was observed when comparing PP with
CP (Fig. 6).
|
|
|
|
|
|
|
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The results from this study demonstrate that even when relatively high amounts of CHO are fed in combination before and during exercise, the contribution of CHO and fat to total substrate use were not affected when compared with ingestion of a placebo. Nonetheless, when CHO was ingested both before and during exercise, endurance performance was increased compared with the ingestion of a placebo. In addition, when equal amounts of CHO were consumed either 30 min before or throughout exercise, endurance performance was increased only when CHO was consumed throughout exercise, despite the fact that the contribution of glucose to energy turnover was higher when glucose was ingested before exercise.
In the present study, ~150 g of glucose were fed before exercise and an equal amount was fed during exercise in CC. Despite this high oral glucose load and the fact that plasma insulin concentration increased markedly (Fig. 2), providing an added stimulus other than muscle contraction for glucose disposal, the estimated contribution from glucose to total substrate oxidation was only 11%, representing an average rate of oxidation of only 0.4 g/min. This result was somewhat unexpected but demonstrates that, in endurance-trained humans, the contribution of glucose to total energy turnover during exercise is relatively minor. These data support those of Juekendrup et al. (17), who observed that the ingestion of 354 g of CHO during 120 min of low-intensity (50% maximal oxygen uptake) cycling resulted in glucose contributing <1 g/min to the total substrate turnover. In fact, several studies have demonstrated that glucose oxidation is limited during exercise despite marked hyperglycemia and hyperinsulinemia (13, 14, 17, 26, 31). In the present study, we were unable to determine what percentage of glucose Ra came from exogenous glucose. Nonetheless, even if hepatic glucose production was completely suppressed, as is possible when large amounts of glucose are ingested during exercise (17), we cannot account for all of the ingested glucose appearing in the plasma and/or being taken up by tissue. Therefore, our data are in agreement with the previous suggestion that the rate of exogenous glucose oxidation may be limited by digestion, absorption, and glucose Ra into the bloodstream (16). It must be noted that, in the present study, we assumed that glucose Rd matches glucose oxidation because we were unable to directly measure glucose oxidation using 6,6-2H. However, we are confident that this assumption is valid because it has been previously demonstrated that ~98% of glucose Rd is oxidized during exercise (16).
It is important to note that the calculated rate of glucose oxidation was higher in CP compared with PC, even though the amount of glucose ingested during both of these trials was equal. It is likely that the small, but nonetheless significant, increase in glucose uptake and oxidation during exercise was due to marked hyperinsulinemia after ingestion in CP, which was not apparent in PC (Fig. 3). Insulin and contraction have a synergistic effect on muscle glucose uptake (4). Despite this observation, exercise performance was increased in PC, but not CP, when compared with PP (Fig. 6). These data support the previous investigations that have demonstrated that the ergogenic benefit of CHO consumption during prolonged exercise is a consistent and reproducible finding (1, 5, 7, 21, 23, 28) but that the efficacy of preexercise CHO ingestion on performance is equivocal (6, 9-11, 27, 30). It has been suggested that the differences seen when comparing the effect of preexercise CHO ingestion with feeding throughout exercise are related to the negative effects of hyperinsulinemia associated with preexercise CHO ingestion. Increased insulin reduces the lipolytic rate and limits the availability of plasma FFAs in the circulation (32). Such a reduction in FFA availability augments muscle glycogen utilization (2). However, in the present study, despite the relative hyperinsulinemia when comparing CP with PC (Fig. 2), we found no evidence of impaired fat availability (Fig. 2) or fat utilization (Fig. 4). Furthermore, CHO utilization was not different between these two trials (Fig. 4). Hence, we found no evidence that the superior exercise performance in PC compared with CP and PP was related to substrate metabolism. It is important to note, however, that, in the two trials that produced increased exercise performance, plasma glucose concentration was better maintained in the final hour of SS (Fig. 1). It is possible that this better maintenance of plasma glucose concentration had a positive effect on mechanisms other than those associated with substrate turnover. It has been previously demonstrated that CHO ingestion can increase exercise performance during a 60-min TT (15) or when CHO is ingested throughout, as opposed to only during the final 30 min of a 120-min cycle (20). Similar to the present observations, the authors of these respective studies found little evidence of a metabolic bases for their observed performance improvement. Hence, it appears that the maintenance of high (i.e., 6 mM) plasma glucose concentrations typically associated with the ingestion of CHO throughout exercise may improve exercise performance by mechanisms other than alterations in substrate utilization, such as negative central nervous system changes, as previously suggested (20).
In summary, our data demonstrate that, even when CHO is ingested in large quantities before and during exercise, the amount of glucose disappearance is relatively minor. However, the maintenance of high plasma glucose concentrations throughout exercise appears to increase exercise performance.
| |
ACKNOWLEDGEMENTS |
|---|
We acknowledge the excellent technical assistance of Rebecca Starkie and Dr. Dominic Caridi from the School of Life Sciences of Victoria University of Technology (Footscray, Victoria, Australia) for the use of the gas chromatography-mass spectrometer.
| |
FOOTNOTES |
|---|
This study was supported by a grant from SmithKline Beecham Consumer Healthcare (UK).
Address for reprint requests and other correspondence: J. A. Hawley, Dept. of Human Biology and Movement Science, Royal Melbourne Institute of Technology University, PO Box 71, Bundoora, Victoria 3083, Australia (E-mail: john.hawley{at}rmit.edu.au).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 3 April 2000; accepted in final form 7 July 2000.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Angus, DJ,
Hargreaves M,
Dancey J,
and
Febbraio MA.
Effect of carbohydrate or carbohydrate plus medium-chain triglyceride ingestion on cycling time trial performance.
J Appl Physiol
88:
113-119,
2000
2.
Bergstrom, J,
Hultman E,
Jorfeldt L,
Pernow B,
and
Wahren J.
Effect of nicotinic acid on physical work capacity and on metabolism of muscle glycogen in man.
J Appl Physiol
26:
170-176,
1969
3.
Borg, G.
Simple rating methods for estimation of perceived exertion.
In: Physical Work and Effort, edited by Borg G.. New York: Pergamon, 1973, p. 39-46.
4.
Bourey, RE,
Coggan AR,
Kohrt WM,
Kirwan JP,
King DS,
and
Holloszy JO.
Effect of exercise on glucose disposal: response to a maximal insulin stimulus.
J Appl Physiol
69:
1689-1694,
1990
5.
Coggan, AR,
and
Coyle EF.
Reversal of fatigue during prolonged exercise by carbohydrate infusion or ingestion.
J Appl Physiol
63:
2388-2395,
1987
6.
Costill, DL,
Coyle E,
Dalsky G,
Evans W,
Fink W,
and
Hoopes D.
Effects of plasma FFA and insulin on muscle glycogen usage during exercise.
J Appl Physiol
43:
693-699,
1977.
7.
Coyle, EF,
Coggan AR,
Hemmert MK,
and
Ivy JL.
Muscle glycogen utilization during prolonged strenuous exercise when fed carbohydrate.
J Appl Physiol
61:
165-172,
1986
8.
Coyle, EF,
Coggan AR,
Hemmert MK,
Lowe RC,
and
Walters TJ.
Substrate use during prolonged exercise following a preexercise meal.
J Appl Physiol
59:
429-433,
1985
9.
Febbraio, MA,
and
Stewart KL.
CHO feeding before prolonged exercise: effect of glycemic index on muscle glycogenolysis and exercise performance.
J Appl Physiol
81:
1115-1120,
1996
10.
Foster, C,
Costill DL,
and
Fink WJ.
Effects of preexercise feedings on endurance performance.
Med Sci Sports Exerc
11:
1-5,
1979.
11.
Gleeson, M,
Maughan RJ,
and
Greenhaff PL.
Comparison of the effects of preexercise feeding of glucose, glycerol and placebo on endurance and fuel homeostasis in man.
Eur J Appl Physiol
55:
645-653,
1986.
12.
Hargreaves, M,
Angus DJ,
Howlett K,
Marmy Conus N,
and
Febbraio MA.
Effect of heat stress on glucose kinetics during exercise.
J Appl Physiol
81:
1594-1597,
1996
13.
Hawley, JA,
Bosch AN,
Weltan SM,
Dennis SC,
and
Noakes TD.
Glucose kinetics during prolonged exercise in euglycaemic and hyperglycaemic subjects.
Pflügers Arch
426:
378-386,
1994[Web of Science][Medline].
14.
Horowitz, JF,
Mora-Rodriguez R,
Byerley LO,
and
Coyle EF.
Substrate metabolism when subjects are fed carbohydrate during exercise.
Am J Physiol Endocrinol Metab
276:
E828-E835,
1999
15.
Jeukendrup, AE,
Brouns F,
Wagenmakers AJM,
and
Saris WHM
Carbohydrate-electrolyte feedings improve 1 h time trial cycling performance.
Int J Sports Med
18:
125-129,
1997[Web of Science][Medline].
16.
Jeukendrup, AE,
Raben A,
Gijsen A,
Stegen JH,
Brouns F,
Saris WH,
and
Wagenmakers AJM
Glucose kinetics during prolonged exercise in highly trained human subjects: effect of glucose ingestion.
J Physiol (Lond)
515:
579-589,
1999
17.
Jeukendrup, AE,
Wagenmakers AJ,
Stegen JH,
Gijsen AP,
Brouns F,
and
Saris WH.
Carbohydrate ingestion can completely suppress endogenous glucose production during exercise.
Am J Physiol Endocrinol Metab
276:
E672-E683,
1999
18.
Marmy Conus, N,
Fabris S,
Proietto J,
and
Hargreaves M.
Preexercise glucose ingestion and glucose kinetics during exercise.
J Appl Physiol
81:
853-857,
1996
19.
McConell, G,
Fabris S,
Proietto J,
and
Hargreaves M.
Effect of carbohydrate ingestion on glucose kinetics during exercise.
J Appl Physiol
77:
1537-1541,
1994
20.
McConell, G,
Kloot K,
and
Hargreaves M.
Effect of timing of carbohydrate ingestion on endurance exercise performance.
Med Sci Sports Exerc
28:
1300-1304,
1996[Web of Science][Medline].
21.
McConell, G,
Snow RJ,
Proietto J,
and
Hargreaves M.
Muscle metabolism during prolonged exercise in humans: influence of carbohydrate availability.
J Appl Physiol
87:
1083-1086,
1999
22.
Miles, J,
Glasscock R,
Aikens J,
Gerich J,
and
Haymond M.
A microfluorometric determination of free fatty acids in plasma.
J Lipid Res
24:
96-99,
1983[Abstract].
23.
Mitchell, JB,
Costill DL,
Houmard JA,
Fink WJ,
Pascoe DD,
and
Pearson DR.
Influence of carbohydrate dosage on exercise performance and glycogen metabolism.
J Appl Physiol
67:
1843-1849,
1989
24.
Nilsson, LH,
and
Hultman E.
Liver glycogen in man
the effects of total starvation or a carbohydrate-poor diet followed by carbohydrate refeeding.
Scand J Clin Lab Invest
32:
325-330,
1973[Web of Science][Medline].
25.
Peronnet, F,
and
Massicotte D.
Table of nonprotein respiratory quotient: an update.
Can J Sport Sci
16:
23-29,
1991[Web of Science][Medline].
26.
Rehrer, NJ,
Wagenmakers AJM,
Beckers EJ,
Halliday D,
Leiper JB,
Brouns F,
Maughan RJ,
Westerterp K,
and
Saris WHM
Gastric emptying, absorption, and carbohydrate oxidation during prolonged exercise.
J Appl Physiol
72:
468-475,
1992
27.
Sparks, MJ,
Selig S,
and
Febbraio MA.
Pre-exercise carbohydrate ingestion: effect of the glycaemic index on endurance exercise performance.
Med Sci Sports Exerc
30:
844-859,
1998[Web of Science][Medline].
28.
Spencer, MK,
Yan Z,
and
Katz A.
Carbohydrate supplementation attenuates IMP accumulation in human muscle during prolonged exercise.
Am J Physiol Cell Physiol
261:
C71-C76,
1991
29.
Steele, R,
Wall JS,
Debodo RC,
and
Altszuler N.
Measurement of the size and turnover rate of body glucose pool by isotope dilution method.
Am J Physiol
187:
15-24,
1956.
30.
Thomas, DE,
Brotherhood JR,
and
Brand JC.
Carbohydrate feeding before exercise: effect of the glycemic index.
Int J Sports Med
12:
180-186,
1991[Web of Science][Medline].
31.
Wagenmakers, AJM,
Brouns F,
Saris WHM,
and
Halliday D.
Oxidation rates of orally ingested carbohydrates during prolonged exercise in men.
J Appl Physiol
75:
2774-2780,
1993
32.
Wolfe, RR,
Nadel ER,
Shaw JHF,
Stephenson LA,
and
Wolfe MH.
Role of changes in insulin and glucagon in glucose homeostasis in exercise.
Metabolism
77:
900-907,
1986.
33.
Wright, DA,
Sherman M,
and
Dernbach AR.
Carbohydrate feedings before, during, or in combination improve cycling performance.
J Appl Physiol
71:
1082-1088,
1991
This article has been cited by other articles:
|
|
 |
|
  E. J. Stevenson, N. M. Astbury, E. J. Simpson, M. A. Taylor, and I. A. Macdonald Fat Oxidation during Exercise and Satiety during Recovery Are Increased following a Low-Glycemic Index Breakfast in Sedentary Women J. Nutr., May 1, 2009; 139(5): 890 - 897. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. De Bock, W. Derave, B. O. Eijnde, M. K. Hesselink, E. Koninckx, A. J. Rose, P. Schrauwen, A. Bonen, E. A. Richter, and P. Hespel Effect of training in the fasted state on metabolic responses during exercise with carbohydrate intake J Appl Physiol, April 1, 2008; 104(4): 1045 - 1055. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. R. Harvey, R. Frew, D. Massicotte, F. Peronnet, and N. J. Rehrer Muscle glycogen oxidation during prolonged exercise measured with oral [13C]glucose: comparison with changes in muscle glycogen content J Appl Physiol, May 1, 2007; 102(5): 1773 - 1779. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. De Bock, W. Derave, M. Ramaekers, E. A. Richter, and P. Hespel Fiber type-specific muscle glycogen sparing due to carbohydrate intake before and during exercise J Appl Physiol, January 1, 2007; 102(1): 183 - 188. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. J Stevenson, C. Williams, L. E Mash, B. Phillips, and M. L Nute Influence of high-carbohydrate mixed meals with different glycemic indexes on substrate utilization during subsequent exercise in women. Am. J. Clinical Nutrition, August 1, 2006; 84(2): 354 - 360. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. A. Wallis, R. Dawson, J. Achten, J. Webber, and A. E. Jeukendrup Metabolic response to carbohydrate ingestion during exercise in males and females Am J Physiol Endocrinol Metab, April 1, 2006; 290(4): E708 - E715. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. S. Fulco, K. W. Kambis, A. L. Friedlander, P. B. Rock, S. R. Muza, and A. Cymerman Carbohydrate supplementation improves time-trial cycle performance during energy deficit at 4,300-m altitude J Appl Physiol, September 1, 2005; 99(3): 867 - 876. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. Watt, P. Krustrup, N. H. Secher, B. Saltin, B. K. Pedersen, and M. A. Febbraio Glucose ingestion blunts hormone-sensitive lipase activity in contracting human skeletal muscle Am J Physiol Endocrinol Metab, January 1, 2004; 286(1): E144 - E150. [Abstract] [Full Text]
|
|
|
|
|
|
A. D. Karelis, F. Peronnet, and P. F. Gardiner Insulin does not mediate the attenuation of fatigue associated with glucose infusion in rat plantaris muscle J Appl Physiol, July 1, 2003; 95(1): 330 - 335. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Baldwin, R. J. Snow, M. J. Gibala, A. Garnham, K. Howarth, and M. A. Febbraio Glycogen availability does not affect the TCA cycle or TAN pools during prolonged, fatiguing exercise J Appl Physiol, June 1, 2003; 94(6): 2181 - 2187. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. Watt, G. J. F. Heigenhauser, and L. L. Spriet Intramuscular triacylglycerol utilization in human skeletal muscle during exercise: is there a controversy? J Appl Physiol, October 1, 2002; 93(4): 1185 - 1195. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. R. Cox, B. Desbrow, P. G. Montgomery, M. E. Anderson, C. R. Bruce, T. A. Macrides, D. T. Martin, A. Moquin, A. Roberts, J. A. Hawley, et al. Effect of different protocols of caffeine intake on metabolism and endurance performance J Appl Physiol, September 1, 2002; 93(3): 990 - 999. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. E. Campbell and M. A. Febbraio Effect of the ovarian hormones on GLUT4 expression and contraction-stimulated glucose uptake Am J Physiol Endocrinol Metab, May 1, 2002; 282(5): E1139 - E1146. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. Arkinstall, C. R. Bruce, V. Nikolopoulos, A. P. Garnham, and J. A. Hawley Effect of carbohydrate ingestion on metabolism during running and cycling J Appl Physiol, November 1, 2001; 91(5): 2125 - 2134. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. E. Campbell, D. J. Angus, and M. A. Febbraio Glucose kinetics and exercise performance during phases of the menstrual cycle: effect of glucose ingestion Am J Physiol Endocrinol Metab, October 1, 2001; 281(4): E817 - E825. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. L. Carey, H. M. Staudacher, N. K. Cummings, N. K. Stepto, V. Nikolopoulos, L. M. Burke, and J. A. Hawley Effects of fat adaptation and carbohydrate restoration on prolonged endurance exercise J Appl Physiol, July 1, 2001; 91(1): 115 - 122. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
), CP (
), PC
(
), and PP (
) were ingested. Values are
means ± SE for 7 subjects. Open bar, feeding 30 min before
exercise; filled bar, exercise. * Difference when comparing PP with
CC, P < 0.05. # Difference when comparing PP with
CC and PC, P < 0.05. ** Difference when comparing
PP with CC, CP, and PC, P < 0.05.
Difference when comparing CC with CP,
P < 0.05.
Difference compared with PP, P < 0.05.
