| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Département d'Éducation Physique, Université de Montréal, Montréal, Province of Quebec, Canada H3C 3J7
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Péronnet, F., Y. Burelle, D. Massicotte, C. Lavoie,
and C. Hillaire-Marcel. Respective oxidation of
13C-labeled lactate and glucose
ingested simultaneously during exercise. J. Appl.
Physiol. 82(2): 440-446, 1997.
The purpose of
this experiment was to measure, by using
13C labeling, the oxidation rate
of exogenous lactate (25 g, as Na+,
K+,
Ca2+, and
Mg2+ salts) and glucose (75 g)
ingested simultaneously (in 1,000 ml of water) during prolonged
exercise (120 min, 65 ± 3% maximum oxygen uptake in 6 male subjects). The percentage of exogenous glucose and lactate
oxidized were similar (48 ± 3 vs. 45 ± 5%, respectively). However, because of the small amount of oral lactate that could be tolerated without gastrointestinal discomfort, the amount
of exogenous lactate oxidized was much smaller than that of exogenous
glucose (11.1 ± 0.5 vs. 36.3 ± 1.3 g, respectively) and
contributed to only 2.6 ± 0.4% of the energy yield
(vs. 8.4 ± 1.9% for exogenous glucose). The cumulative amount of
exogenous glucose and lactate oxidized was similar to that observed
when 100 g of
[13C]glucose were
ingested (47.3 ± 1.8 vs. 50.9 ± 1.2 g, respectively). When
[13C]glucose was
ingested, changes in the plasma glucose
13C/12C
ratio indicated that between 39 and 61% of plasma glucose derived from
exogenous glucose. On the other hand, the plasma glucose 13C/12C
ratio remained unchanged when
[13C]lactate was
ingested, suggesting no prior conversion into glucose before oxidation.
exogenous lactate; prolonged exercise; substrate oxidation; stable
isotopes; insulin
INTRODUCTION INGESTION OF CARBOHYDRATES during prolonged exercise
has been shown to improve performance in endurance events (8, 16, 30),
and this could be due to the maintenance of a higher rate of
carbohydrate oxidation (10, 13). Indeed, by using labeling with
13C and
14C, several studies have shown
that exogenous carbohydrates ingested during exercise are oxidized at a
high rate (16, 24, 26). These observations have led to the development
of many sports drinks containing mixtures of hexoses, dissaccharides,
and glucose polymers of various lengths (22). Recently, some
manufacturers have also added lactate to sports drinks (2, 7, 15, 33). Lactate supplementation during exercise is based on the observation that during prolonged moderate exercise carbon skeletons originating from muscle glycogen are shuttled among the working muscles under the
form of lactate (5). Most of this lactate released from one muscle
appears to be oxidized within another muscle, with only a small portion
being recycled into glucose by the liver (21, 32), and the plasma
lactate flux appears to be larger than the plasma glucose flux (6).
Compared with exogenous glucose provided by carbohydrates in sports
drinks, exogenous lactate could have the advantages of introducing
fewer disturbances in the endocrine response to exercise, to be
independent of insulin for entering the working muscle fiber through a
transporter distinct from that of glucose (28, 29), and to be readily
available for entering the tricarboxylic acid cycle and providing
reducing equivalents. In addition, complete oxidation of the lactate
ion consumes one proton. Accordingly, exogenous lactate oxidation during exercise could increase muscle buffering capacity. On the other
hand, because of poor gastrointestinal tolerance (33), lactate can be
provided only in limited amounts during prolonged exercise and should
be associated with other carbohydrates, such as glucose polymers, in
sports drinks.
Only a limited number of studies have described the effect of ingesting
lactate supplements on the metabolic response and performance during
prolonged exercise (15, 33), and no data are available on the actual
metabolic fate of ingested lactate at rest or during exercise. The
purpose of the present experiment was to measure the oxidation rate of
exogenous lactate (25 g) ingested along with glucose (75 g) during
prolonged exercise. The oxidation rate of each of the two substrates in
the mixture was measured separately by using selective
13C labeling of lactate or glucose
(1), and the rate was compared with the oxidation rate of an isocaloric
amount of glucose. In addition, change in plasma glucose
13C/12C
ratio when
[13C]lactate was
ingested was used to estimate the extent of possible conversion of
lactate into glucose by the liver.
METHODS
O2 max) on a
cycle ergometer were 21 ± 1 yr, 65 ± 2 kg, 172 ± 2 cm, and
4.40 ± 0.06 l/min, respectively (mean ± SE). All subjects had a
normal fasting plasma glucose concentration (4.71 ± 0.29 mM).
O2 max and
experimental workloads on the cycle ergometer (Ergomeca, La Bayette,
France) were determined for each subject during a preliminary test
session using open-circuit spirometry (1100 medical gas analyzer,
Marquette Electronics, Milwaukee, WI). Subsequently, at 1-wk intervals,
all subjects performed four exercises of 120-min duration at a workload
corresponding to 65 ± 3%
O2 max (218.3 ± 10.6 W). The exercises were performed at 1:00
P.M. in a laboratory with controlled
temperature (21 ± 1°C) and humidity (45 ± 5%). The last
evening meal [at 7:00 P.M.,
1,300 kcal (55% carbohydrates, 30% fat, and 15% proteins)],
the morning breakfast [at 7:30
A.M., 800 kcal (60% carbohydrates,
30% fat, and 10% proteins)], and a small snack [at 11:00
A.M., 500 kcal (50% carbohydrates,
35% fat, and 15% proteins)] were provided to the subjects. In
addition, to keep a low background of
13C enrichment of plasma glucose
and expired CO2 during the period of experiments, ingestion of carbohydrates from plants with the C4 photosynthetic cycle, which are
naturally enriched in 13C (20),
was avoided. Subjects also refrained from exercising and from drinking
coffee and alcohol for 2 days before each experiment.
During the exercise period, the subjects ingested 1,000 ml of water at
room temperature, containing 100 g of glucose (trial 1) or a mixture of 75 g of glucose and 25 g of
lactate (trials 2 and
3). The solutions were given in five
equal volumes (20 g of substrates in 200 ml) taken immediately after
the beginning of exercise and at 20, 40, 60, and 80 min during the
exercise period. In trials 1 and
2, the glucose ingested was
artificially labeled with 13C,
whereas in trial 3 the lactate was
artificially labeled with 13C to
separately measure the oxidation rate of exogenous glucose when
ingested alone or in combination with lactate and the oxidation rate of
lactate when ingested in combination with glucose. Glucose, naturally
poor in 13C [Dextrosport,
Vitagermine, Villenave-d'Ornon, France; 
25.2
[
-13C] Pee Dee
Belemnitella1
(PDB1)], was
enriched with
[U-13C]glucose
(13C/C >99%, Isotec,
Miamisburg, OH) to achieve a final isotopic composition close to
+25
[-13C]PDB1
(actual value measured by mass spectrometry: +24.5 and +24.3
[-13C]PDB1,
in trials 1 and
2, respectively). Lactate was
administered as a mixture of four salts (12 g sodium lactate, 4.5 g
potassium lactate, 13 g calcium lactate, and 3.4 g magnesium lactate,
kindly provided by PURAC America, Lincolnshire, IL;
27.4
[-13C]PDB1),
to reduce the amount of each cation ingested. In addition, the presence
of calcium and magnesium with two negative charges allowed
us to somewhat reduce the osmotic pressure of the
solution, which, however, remained very high (933 mM taking into
account the glucose present in the solution, compared with 556 mM when 100 g of glucose were ingested). The total dose of lactate salts that
could be tolerated was determined from preliminary experiments. As
reported in previous studies of lactate ingestion during exercise (15,
33), gastrointestinal discomfort was experienced by about one-half of
the subjects, who developed mild diarrhea in the evening after the
test. The lactate was traced with
[U-13C]-labeled sodium
lactate (13C/C >99%, Isotec),
the final
13C/12C
ratio in the mixture of lactate salts being +62.5
[-13C]PDB1.
Finally, to correct for the shift in
13C background enrichment of
expired CO2 observed in response
to exercise (25), the subjects were submitted to an additional exercise
session without ingestion of any exogenous substrate.
Measurements and computations.
Observations were made at rest, immediately before exercise, and every
15 min during the exercise period. Carbohydrate and fat oxidation were
computed from carbon dioxide production
(CO2) and oxygen
consumption (O2) by using
open-circuit spirometry (20- and 5-min collection periods at rest and
exercise, respectively). For the measurement of
13C/12C ratios in
expired CO2, 80-ml samples of
expired gases were collected and stored in vacutainers
(Becton-Dickinson, Franklin Lakes, NJ). Finally, 8-ml blood samples
were withdrawn through a catheter (Baxter Health Care, Valencia, CA)
inserted into an antecubital vein 30 min before the beginning of
experiment for the measurement of plasma glucose lactate (Sigma
Diagnostics, Sigma, Mississauga, Canada), and insulin (KTSP-11001,
Immunocorp Sciences, Montreal, Canada) concentrations, and for the
measurement of
13C/12C
ratios in plasma glucose (at 40 and 80 min only). Plasma samples were stored at 80°C until analysis.
For the measurement of glucose enrichment, glucose was extracted from
plasma according to the method described and validated by Wolfe et al.
(35). The plasma (1 ml) was first deproteinized with barium hydroxide
(1.5 ml, 0.3 N) and zinc sulfate (1.5 ml, 0.3 N). The soluble phase was
separated from the protein precipitate by centrifugation (20 min, 3,000 g, 4°C), and the remaining protein precipitate was washed with 3 ml of distilled water. The glucose was
then separated by double-bed ion exchange chromatography by running the
combined supernatants (7 ml) through superposed columns (0.5 × 2 cm) of AG 50W-X8 H+ (200-400
mesh) and (0.5 × 2 cm) of AG 1-X8 chloride (200-400 mesh)
resins (Bio-Rad, Mississauga, Canada) equilibrated and eluted with
distilled water. The solution obtained (~10 ml) was evaporated to
dryness (Virtis Research Equipment, New York, NY). The average recovery
of glucose was 86 ± 3%. The glucose was then combusted for 60 min
at 400°C in presence of copper oxide (20 mg), and the CO2 recovered was analyzed by mass
spectrometry. This procedure for purification of plasma glucose has
been demonstrated to yield values for
[13C]glucose
enrichment similar to those obtained using the more specific isolation
procedure of plasma glucose by crystallization as potassium gluconate
(35). In the present experiment, the material obtained after
evaporation was resuspended in 0.5 ml of distilled water for screening
for possible contamination by nonglucose carbons. Compared with the
amount of glucose present (8.2 mM), the amounts of glycerol
(0.07-0.09 mM) and lactate (0-0.04 mM) present were
negligible, and no proteins were detectable.
When [13C]glucose was
ingested (trials 1 and
2), the percentage of plasma glucose
derived from exogenous glucose was computed as follows
![% *Glu = [<IT>R</IT><SUB>spl</SUB> − <IT>R</IT><SUB>ref</SUB>/<IT>R</IT><SUB>exo</SUB> − <IT>R</IT><SUB>ref</SUB> ] × 100](/content/vol82/issue2/fulltext/440/img001.gif)
|
(1) |
O2 and
CO2 as follows (27)
|
(2) |
|
(3) |
![‰ [&dgr;-<SUP>13</SUP>C]PDB<SUB>1</SUB> = [(<IT>R</IT><SUB>spl</SUB>/<IT>R</IT><SUB>std</SUB> ) − 1] × 1,000](/content/vol82/issue2/fulltext/440/img004.gif)
|
|
(4) |
CO2 is in liters/min
STPD,
Rexp
is the
13C/12C
ratio observed in expired CO2,
Rref
is the
13C/12C
ratio in expired CO2 in the
control trial,
Rexo
is the
13C/12C
ratio in the artificially labeled exogenous glucose or lactate ingested, and k (0.7426 l/g) is the volume of
CO2 provided by the complete
oxidation of glucose or lactate (27). The computation of the amounts of
exogenous substrate oxidized is made assuming that, in response to
exercise,
13CO2
recovery in expired gases is complete or almost complete (11, 17, 19).
In addition, the total volume of
CO2 produced during exercise is
large compared with the labile bicarbonate pool. Accordingly, the
influence of this pool on the amount of exogenous glucose oxidized that
is computed from
13CO2
recovered at the mouth can be neglected (23).
The amount of unlabeled glucose (endogenous + exogenous unlabeled
glucose in trial 2) oxidized was
computed by difference between total glucose oxidation computed from
O2 and
CO2 and the amount of
labeled glucose or lactate oxidized computed from 13CO2
at the mouth (Eq. 4). The
contribution of the oxidation of the various substrates to the energy
yield was computed from their respective energy potentials at 37°C
[3.87, 9.75, and 3.76 kcal/g for glucose, fatty acid, and
lactate, respectively (27, 34)].
Statistics.
Data are presented as means ± SE. The main effects of time and
exogenous substrate ingested (glucose vs. glucose+lactate) as well as
time-substrate interactions were tested by repeated-measures analysis
of variance (Statistica package). Tukey wholly significant difference
tests were used to identify the location of significant differences
(P 
0.05) when analysis of variance
yielded a significant F ratio.
RESULTS
No significant difference was observed between the four trials for
heart rate at rest before exercise (72 ± 3 beats/min,
n = 18) and during the final 5 min of
the exercise period (152 ± 3 beats/min,
n = 18). The average
CO2 observed was also similar during the four trials (2.44 ± 0.08; 2.55 ± 0.09; 2.51 ± 0.08 and 2.47 ± 0.09 l/min, in the control trial and in
trials 1,
2, and
3, respectively). When no exogenous
substrate was ingested during exercise, the
13C/12C
ratio in expired CO2 increased and
reached a plateau after ~30 min of exercise (Fig.
1). The observed increase in
13C/12C
ratio was much higher and did not plateau when
13C-enriched substrates were
ingested during the exercise.
) and when
[13C]glucose was
ingested alone (
; 100 g of
[13C]glucose) or in
combination with unlabeled lactate (
, 75 g of [13C]glucose with 25 g
of lactate), or when unlabeled glucose was ingested in combination with
[13C]lactate (
, 75 g of glucose with 25 g of
[13C]lactate). Data
are means ± SE of observations made over corresponding 30-min
exercise period (e.g., at 30, 45, and 60 min for the 30- to 60-min
period). PDB1, Pee Dee Belemnitella1.
As shown in Fig. 2, no significant
difference was observed between the oxidation rate of glucose
(endogenous + exogenous, including lactate when lactate was ingested;
see METHODS) and fatty acids,
respectively, when glucose or the mixture of glucose and lactate was
ingested. When 100 g of glucose were ingested, the oxidation rate of
exogenous glucose increased steadily and significantly from an average
of 0.12 ± 0.04 g/min during the first 30 min of exercise to 0.72 ± 0.03 g/min during the last 30 min of exercise (Fig.
3). When 75 g of
[13C]glucose were
ingested along with unlabeled lactate, the oxidation rate of exogenous
glucose was slightly but not significantly lower than that observed
when 100 g of glucose were ingested during the first 90 min. However,
this difference reached statistical signifiance during the
last 30 min of exercise (0.47 ± 0.06 vs. 0.72 ± 0.03 g/min).
When 25 g of
[13C]lactate were
ingested along with 75 g of glucose, the oxidation rate of exogenous
lactate which was very low at the beginning of exercise (0-30 min:
0.03 ± 0.01 g/min) steadily increased thereafter and reached 0.16 ± 0.01 g/min between 90 and 120 min. The percentage of exogenous
lactate that was oxidized over the exercise period was close to that of
exogenous glucose (45 ± 5 vs. 51 ± 5 and 48 ± 3% for 100 and 75 g of glucose, respectively). When 75 g of glucose were ingested
in combination with lactate, the total amount of exogenous glucose
oxidized during exercise was significantly lower than when 100 g of
glucose were ingested alone (36.3 ± 1.3 vs. 50.9 ± 1.2 g,
respectively). However, the cumulative amount of exogenous glucose and
lactate oxidized was similar to the amount of glucose oxidized that was
observed when 100 g of glucose were ingested (47.3 ± 1.8 vs. 50.9 ± 1.2 g, respectively; Fig. 3). Over the exercise period, the
oxidation of exogenous glucose and lactate contributed 11.1 ± 2.1%
to the energy yield, compared with 10.9 ± 1.7% for 100 g of
exogenous glucose (not significantly different). On the other hand, the
contribution of exogenous lactate oxidation to the energy yield was
significantly lower (2.6 ± 0.4%).
), when glucose was ingested alone (, 100 g of glucose) or
in combination with lactate (
, 75 g of glucose with 25 g of lactate;
average values of observations in trials 2 and 3). Data are
means ± SE of observations made over corresponding 30-min exercise
period (e.g., at 30, 45, and 60 min for the 30- to 60-min period).
aSignificantly different from the
first 30 min of exercise; P 0.05.
) or in combination with unlabeled lactate (; 75 g of [13C]glucose with
25 g of lactate), or when unlabeled glucose was ingested in combination
with [13C]lactate
(, 75 g of glucose with 25 g of
[13C]lactate).
Cumulative oxidation of exogenous glucose + lactate () computed from
trials 2 and
3 is also shown. Values are means ± SE. aSignificantly different
from preceding 30-min period, P 0.05; bsignificantly
different from
[13C]glucose,
P 0.05;
csignificantly different from
first 30-min period;
dsignificantly different from 100 g of [13C]glucose,
P 0.05.
Plasma glucose concentration remained stable throughout the exercise
period, and no significant difference was observed between trial 1 (100 g of glucose) and
trials 2 and
3 (75 g of glucose + 25 g of lactate;
Fig. 4). Plasma lactate concentration also remained stable at ~1.5 mM during the exercise period when glucose alone was ingested and was slightly but not significantly higher when
the mixture of glucose and lactate was ingested. The small and not
significant decrease in plasma insulin concentration in response to
exercise was similar with ingestion of glucose and the mixture of
glucose and lactate.
), when glucose was
ingested alone (, 100 g of glucose) or in combination with lactate
(, 75 g of glucose with 25 g of lactate; values are means ± SE of observations in trials 2 and 3). cSignificantly
different from first 30-min period, P 0.05.
Resting plasma glucose
13C/12C
ratio was similar in the three trials (21.8 ± 0.45
[-13C]PDB1;
pooled data, n = 18; Fig.
5). Ingestion of
[13C]glucose alone or
in combination with unlabeled lactate during exercise resulted in
significant rises in plasma glucose
13C/12C
ratio. When 75 g of glucose were ingested, the percentage of plasma
glucose deriving from exogenous glucose was slightly lower than when
100 g of glucose were ingested at 40 min (39 ± 3 and 47 ± 5%,
respectively), and this difference reached statistical significance at
80 min during the exercise (51 ± 5 and 61 ± 6%, respectively).
When [13C]lactate was
ingested along with unlabeled glucose, no significant change was
observed in plasma glucose
13C/12C
ratio (Fig. 5).
, 100 g) or in combination with unlabeled lactate
(, 75 g of
[13C]glucose with 25 g
of lactate), or when unlabeled glucose was ingested in combination with
[13C]lactate (, 75 g of glucose with 25 g of
[13C]lactate). Values
are means ± SE. aSignificantly
different from rest, P 0.05;
bsignificantly different from
[13C]glucose;
csignificantly different from 100 g of [13C]glucose,
P 0.05.
DISCUSSION
Results from the present experiment indicate that, during prolonged exercise, about one-half of the exogenous lactate ingested in the form of a mixture of various salts was oxidized. This percentage was similar to that observed when exogenous glucose was ingested. However, the amount of lactate that could be ingested without intestinal discomfort was much smaller than that of exogenous glucose. Accordingly, lactate ingestion did not significantly modify the metabolic response to exercise, including plasma lactate concentration, and the rate of exogenous lactate oxidation and its contribution to the energy yield remained small. Finally, no significant amounts of exogenous lactate appeared to be converted into glucose before being oxidized. This observation suggests that direct oxidation was the predominant metabolic fate of the exogenous lactate that was absorbed from the gastrointestinal tract.
The rate of lactate ingestion that was tolerated with minor intestinal
discomfort by the subjects in the present experiment (4.3 mg · kg
1 · min1)
was larger than those used by Swensen et al. (33) and by Fahey et
al. (15) (1.6 and 2.6 mg · kg1 · min1,
respectively) but remained well below the rate of ingestion of glucose
(13-17
mg · kg1 · min1).
Much higher ingestion rates of glucose or glucose polymers have
actually been reported without any major gastrointestinal discomfort in
some previous studies (50-95
mg · kg1 · min1;
Refs. 3, 9, 13). The adverse effects of lactate on the gastrointestinal
function is related to the much higher osmolality of lactate salt
solutions compared with those of isocaloric carbohydrate solutions,
particularly when ingested in the form of polymers, both because of the
smaller molar mass of lactate and because of the presence of positively
charged molecules and/or ions associated with the lactate
anion.
This high osmolality of lactate solutions, which severely limits the amounts that can be administered orally, appears to be the major drawback for their use as energy supplements in sports drinks. In fact, except for the small increase in plasma pH and bicarbonate concentration reported by Fahey et al. (15), the limited amounts of lactate that can be ingested have no noticeable effect on the endocrine and metabolic response to exercise. In the studies by Fahey et al. (15) and by Swensen et al. (33), the response of plasma insulin, glucose, free fatty acid, and glycerol concentrations to exercise was similar when glucose polymers and a mixture of glucose polymers and lactate was ingested in isocaloric amounts. In addition, there was no effect of lactate ingestion on the response of plasma lactate concentration in both studies. Results from the present experiment are in line with these previous findings: compared with the observation made when 100 g of glucose were ingested, ingestion of the mixture of glucose (75 g) and lactate (25 g) did not significantly modify plasma glucose and insulin concentration or significantly increase plasma lactate concentration. The lack of effect of lactate ingestion on plasma lactate concentration during exercise could be due to the fact that the amount of lactate ingested remains small compared with the large plasma lactate turnover observed during exercise (5). It also suggests that lactate might not be absorbed from the gastrointestinal tract in significant amounts.
In the present experiment, the increase in 13C/12C ratio in expired CO2 after [13C]lactate ingestion confirms that at least a portion of the lactate ingested during prolonged exercise was actually absorbed from the gastrointestinal tract and was available for oxidation. The amount of 13CO2 recovered at the mouth indicates that 11.1 ± 0.5 g of the lactate ingested was oxidized or 45 ± 5% of the load. When 100 g of glucose were ingested alone or when 75 g of glucose were ingested in combination with 25 g of lactate, the percentages of the glucose loads that were actually oxidized were not significantly different (51 ± 5 and 48 ± 3%). However, the much larger amounts ingested without any gastrointestinal disturbance or discomfort translated into much larger amounts oxidized (50.9 ± 1.2 and 36.3 ± 1.3 g over the entire period of exercise). As a consequence, the contribution of exogenous glucose oxidation to the energy yield, which ranged between 8.4 ± 1.9 and 11.4 ± 2.1%, as previously reported (1) was much higher than that observed with exogenous lactate (2.6 ± 0.4%). The small contribution of exogenous lactate ingested orally during exercise to the energy yield, which is due to its poor gastrointestinal tolerance, probably explains why this energy supplement has not been shown to improve endurance performance (33).
Two major pathways exist for the oxidation of plasma lactate during prolonged exercise. The first pathway is the direct oxidation of lactate that can occur in any tissue where oxygen in consumed, including exercising muscles and the heart (4). The second pathway involves the conversion of lactate into glucose, which mainly occurs in the liver. The neoformed glucose could, in turn, be released into the blood and could be oxidized in peripheral tissues (4). Data from Mazzeo et al. (21) and Stanley et al. (31) suggest that lactate released from exercising muscles during prolonged exercise is oxidized mainly in other tissues, with only a small portion being converted into glucose in the liver (~20%). Results from the present experiment are in line with these data and suggest that oral lactate is also probably directly oxidized without being first converted into glucose. When [13C]glucose was ingested, the large increase in plasma glucose 13C/12C ratio observed at 40 and 80 min of exercise indicates that between 39 and 61% of plasma glucose was derived from exogenous glucose. These figures are within the range of data reported between 40 and 90 min of exercise by Costill et al. (12) after [14C]glucose ingestion and by Jandrain et al. (18) after [13C]fructose ingestion (~45 and 40-60%, respectively). In contrast, when [13C]lactate was ingested, the plasma glucose 13C/12C ratio remained unchanged from preexercise value. This observation suggests that only a small portion, if any, of the lactate ingested was converted into glucose before being oxidized, and, accordingly, that exogenous lactate did not significantly contribute to the maintenance of plasma glucose through gluconeogenesis.
ACKNOWLEDGEMENTS
The authors thank Rinske Potjewijd from PURAC America, Lincolnshire, IL, for kindly providing the lactate salts.
FOOTNOTES
Address for reprint requests: F. Péronnet, Dept. d'Éducation Physique, Université de Montréal, CP 6128-Centre Ville, Montréal PQ, Canada H3C 3J7 (E-mail: peronnet{at}ere.umontreal.ca).
Received 29 May 1996; accepted in final form 21 October 1996.
REFERENCES
| 1. |
Adopo, E.,
F. Péronnet,
D. Massicotte,
G. R. Brisson,
and
C. Hillaire-Marcel.
Respective oxidation of exogenous glucose and fructose given in the same drink during exercise.
J. Appl. Physiol.
76:
1014-1019,
1994.
|
| 2. | Anderson, O. Can CYTOMAX really help you "beat the burn"? Running Res. 9: 1-6, 1993. |
| 3. | Brooke, J. D., G. J. Davies, and L. F. Green. The effects of normal and glucose syrup work diets on the performance of racing cyclists. J. Sports Med. 15: 257-265, 1975. |
| 4. | Brooks, G. A. Current concepts in lactate exchange. Med. Sci. Sports Exercise 23: 895-906, 1991. [Medline] |
| 5. | Brooks, G. A. The lactate shuttle during exercise and recovery. Med. Sci. Sports Exercise 18: 360-368, 1986. [Medline] |
| 6. |
Brooks, G. A.,
and
C. M. Donovan.
Effect of endurance training on glucose kinetics during exercise.
Am. J. Physiol.
244 (Endocrinol. Metab. 7):
E505-E512,
1983.
|
| 7. | Brouns, F., M. Fogelholm, G. Van Hall, A. Wagenmakers, and W. H. M. Saris. Chronic oral lactate supplementation does not affect lactate disappearance from blood after exercise. Int. J. Sport Nutr. 5: 117-124, 1995. [Medline] |
| 8. | Coggan, A., and E. F. Coyle. Carbohydrate ingestion during prolonged exercise: effects on metabolism and performance. Exercise Sport Sci. Rev. 19: 1-40, 1991. [Medline] |
| 9. |
Coggan, A. R.,
and
E. F. Coyle.
Effect of carbohydrate feedings during high-intensity exercise.
J. Appl. Physiol.
65:
1703-1709,
1988.
|
| 10. |
Coggan, A. R.,
and
E. F. Coyle.
Reversal of fatigue during prolonged exercise by carbohydrate infusion or ingestion.
J. Appl. Physiol.
63:
2388-2395,
1987.
|
| 11. |
Coggan, A. R.,
D. L. Habash,
L. A. Mendenhall,
S. C. Swanson,
and
C. L. Kien.
Isotopic estimation of CO2 production during exercise before and after endurance training.
J. Appl. Physiol.
75:
70-75,
1993.
|
| 12. |
Costill, D. L.,
A. Bennett,
G. Branam,
and
D. Eddy.
Glucose ingestion at rest and during prolonged exercise.
J. Appl. Physiol.
34:
764-769,
1973.
|
| 13. |
Coyle, E. F.,
A. R. Coggan,
M. K. Hemmert,
and
J. L. Ivy.
Muscle glycogen utilization during prolonged strenous exercise when fed carbohydrate.
J. Appl. Physiol.
61:
165-172,
1986.
|
| 14. | Craig, H. The geochemistry of stable isotopes. Geochim. Cosmochim. Acta 3: 53-92, 1953. |
| 15. | Fahey, T. D., J. D. Larsen, G. A. Brooks, W. Colvin, S. Henderson, and D. Lary. The effect of ingesting polylactate or glucose polymer drinks during prolonged exercise. Int. J. Sport Nutr. 1: 249-256, 1991. [Medline] |
| 16. | Hawley, J. A., S. C. Dennis, and T. D. Noakes. Oxidation of carbohydrate ingested during prolonged endurance exercise. Sports Med. 14: 27-42, 1992. [Medline] |
| 17. |
Hoerr, R. A.,
Y.-M. Yu,
D. A. Wagner,
J. F. Burke,
and
V. R. Young.
Recovery of 13C in breath from NaH13CO3 infused by gut and vein: effect of feeding.
Am. J. Physiol.
257:
E426-E438,
1989.
|
| 18. |
Jandrain, B. J.,
N. Pallikarakis,
S. Normand,
F. Pirnay,
M. Lacroix,
F. Mosora,
C. Pachiaudi,
J. F. Gautier,
A. J. Scheen,
J. P. Riou,
and
P. J. Lefèbvre.
Fructose utilization during exercise in men: rapid conversion of ingested fructose to circulating glucose.
J. Appl. Physiol.
74:
2146-2154,
1993.
|
| 19. | Leese, G. P., A. E. Nicoll, M. Varnier, J. Thompson, and M. J. Rennie. 13C-bicarbonate elimination kinetics during different exercise and metabolic conditions. Eur. J. Clin. Invest. 24: 818-823, 1994. [Medline] |
| 20. | Lefèbvre, P. J. From plant physiology to human metabolic investigations. Diabetologia 28: 255-263, 1985. [Medline] |
| 21. |
Mazzeo, R. S.,
G. A. Brooks,
D. A. Schoeller,
and
T. F. Budinger.
Disposal of blood[1-13C] lactate in humans during rest and exercise.
J. Appl. Physiol.
60:
232-241,
1986.
|
| 22. | Mora, J. Refueling, the facts and myths about fluid and energy replacement. Triathlete (July): 42-46, 1991. |
| 23. | Pallikarakis, N., N. Sphiris, and P. Lefèbvre. Influence of the bicarbonate pool and the occurrence of 13CO2 in exhaled air. Eur. J. Appl. Physiol. Occup. Physiol. 63: 179-183, 1991. [Medline] |
| 24. | Péronnet, F., E. Adopo, and D. Massicotte. Exogenous substrate utilization during prolonged exercise: studies with 13C-labeling. In: Muscle Fatigue Mechanisms in Exercise and Training, edited by P. Marconnet, P. V. Komi, B. Saltin, and O. M. Sejersted. Basel: Karger, 1992, vol. 34, p. 195-206. (Medicine and Sport Science Ser.) |
| 25. | Péronnet, F., E. Adopo, D. Massicotte, G. Brisson, and C. Hillaire-Marcel. Comparison of two methods for computing exogenous substrate oxidation using 13C-labeling. Med. Sci. Sports Exercise 25: 297-302, 1993. [Medline] |
| 26. | Péronnet, F., E. Adopo, D. Massicotte, and C. Hillaire-Marcel. Exogenous substrate oxidation during exercise: studies using isotopic labeling. Int. J. Sport Med. 13, Suppl.: S123-S125, 1992. |
| 27. | Péronnet, F., and D. Massicotte. Table on nonprotein respiratory quotient: an update. Can. J. Sport Sci. 16: 23-29, 1991. [Medline] |
| 28. |
Pilegaard, H.,
J. Bangsbo,
E. A. Richter,
and
C. Juel.
Lactate transport studied in sarcolemmal giant vesicles from human muscle biopsies: relation to training status.
J. Appl. Physiol.
77:
1858-1862,
1994.
|
| 29. | Roth, D. A. The sarcolemmal lactate transporter: transmembrane determinants of lactate flux. Med. Sci. Sports Exercise 23: 925-934, 1991. [Medline] |
| 30. | Sherman, W. M., and D. R. Lamb. Nutrition during prolonged exercise. In: Perspective in Exercise Science and Sports Medecine. Prolonged Exercise, edited by D. R. Lamb, and R. Murray. Indianapolis, IN: Benchmark, 1988, vol. 1, p. 213-280. |
| 31. |
Stanley, W. C.,
E. W. Gertz,
J. A. Wisneski,
D. L. Morris,
R. Neese,
and
G. A. Brooks.
Lactate extraction during net lactate release in legs of humans during exercise.
J. Appl. Physiol.
60:
1116-1120,
1986.
|
| 32. | Stanley, W. C., J. A. Wisneski, E. W. Gertz, R. A. Neese, and G. A. Brooks. Glucose and lactate interrelations during moderate-intensity exercise in humans. Metabolism 37: 850-858, 1988. [Medline] |
| 33. | Swensen, T., G. Crater, D. R. Bassett, Jr., and E. T. Howley. Adding polylactate to a glucose polymer drink does not improve endurance. Int. J. Sports Med. 15: 430-434, 1994. [Medline] |
| 34. | Weast, R. C. (Editor). CRC Handbook of Chemistry and Physics. Boca Raton, FL: CRC, 1989-1990, p. D-278. |
| 35. | Wolfe, R. R., J. R. Allsop, and J. F. Burke. Glucose metabolism in man: responses to intravenous glucose infusion. Metabolism 28: 210-220, 1979. [Medline] |
This article has been cited by other articles:
|
|
 |
|
  M. Korach-Andre, Y. Burelle, F. Peronnet, D. Massicotte, C. Lavoie, and C. Hillaire-Marcel Differential metabolic fate of the carbon skeleton and amino-N of [13C]alanine and [15N]alanine ingested during prolonged exercise J Appl Physiol, August 1, 2002; 93(2): 499 - 504. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Burelle, D. Massicotte, M. Lussier, C. Lavoie, C. Hillaire-Marcel, and F. Peronnet Oxidation of [13C]glycerol ingested along with glucose during prolonged exercise J Appl Physiol, May 1, 2001; 90(5): 1685 - 1690. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Burelle, F. Peronnet, S. Charpentier, C. Lavoie, C. Hillaire-Marcel, and D. Massicotte Oxidation of an oral [13C]glucose load at rest and prolonged exercise in trained and sedentary subjects J Appl Physiol, January 1, 1999; 86(1): 52 - 60. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
