The Human Performance Laboratory, Department of Kinesiology and Health Education and Division of Nutritional Sciences, The University of Texas at Austin, Austin, Texas 78712
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ABSTRACT |
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This study
determined the effect of carbohydrate ingestion during exercise on the
lipolytic rate, glucose disappearance from plasma
(Rd Glc), and fat
oxidation. Six moderately trained men cycled for 2 h on four separate
occasions. During two trials, they were fed a high-glycemic
carbohydrate meal during exercise at 30 min (0.8 g/kg), 60 min (0.4 g/kg), and 90 min (0.4 g/kg); once during low-intensity exercise
[25% peak oxygen consumption (O2 peak)] and
once during moderate-intensity exercise (68%
O2 peak). During two
additional trials, the subjects remained fasted (12-14 h)
throughout exercise at each intensity. After 55 min of low-intensity
exercise in fed subjects, hyperglycemia (30% increase) and a threefold
elevation in plasma insulin concentration (P < 0.05) were associated with a
22% suppression of lipolysis compared with when subjects were fasted
(5.2 ± 0.5 vs. 6.7 ± 1.2 µmol · kg
1 · min
1,
P < 0.05), but fat oxidation was not
different from fasted levels at this time. Fat oxidation when subjects
were fed carbohydrate was not reduced below fasting levels until
80-90 min of exercise, and lipolysis was in excess of fat
oxidation at this time. The reduction in fat oxidation corresponded in
time with the increase in
Rd Glc. During
moderate-intensity exercise, the very small elevation in plasma insulin
concentration (~3 µU/ml; P < 0.05) during the second hour of exercise when subjects were fed vs. when they were fasted slightly attenuated lipolysis
(P < 0.05) but did not increase
Rd Glc or suppress fat
oxidation. These findings indicate that despite a suppression of
lipolysis after carbohydrate ingestion during exercise, the lipolytic
rate remained in excess and thus did not limit fat oxidation. Under
these conditions, a reduction in fat oxidation was associated in time
with an increase in glucose uptake.
insulin; lipolysis; glucose uptake; exercise intensity; glycogen; stable isotopes
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INTRODUCTION |
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FAT AND CARBOHYDRATE are the two primary substrates
oxidized by skeletal muscle during exercise (17). Carbohydrate
ingestion during exercise can modify the relative contribution of these substrates to total energy production (1). However, the influence of
carbohydrate ingestion on substrate oxidation depends on the intensity
of exercise (24). Carbohydrate ingestion during low-intensity exercise
[25-45% peak oxygen consumption
(O2 peak)]
reduces fat oxidation ~40% below fasted levels (1, 15). In contrast, carbohydrate ingestion during moderate-intensity exercise
(65-75%
O2 peak)
does not reduce fat oxidation during the first 120 min of
exercise (5, 6).
The differential effects of carbohydrate ingestion during low and moderate-intensity exercise may be related to differences in insulin response. During low-intensity exercise, carbohydrate ingestion increases plasma insulin concentration two- to threefold above fasting levels (1, 15) and increases glucose uptake by skeletal muscle (1). Furthermore, the increase in plasma insulin concentration is associated with a reduction in plasma free fatty acid (FFA) concentration (1, 15, 24) and probably a suppression of triglyceride hydrolysis (i.e., lipolysis; Ref. 3). These events favor an increase in carbohydrate oxidation and a decrease in fat oxidation (1). Unlike low-intensity exercise, the insulin response to carbohydrate ingestion during moderate-intensity exercise is almost completely suppressed (5, 12). This may explain why carbohydrate ingestion during moderate-intensity exercise does not affect fat oxidation, carbohydrate oxidation, muscle glycogen utilization (5, 12), or presumably blood glucose oxidation during the first 2 h of exercise at moderate intensity (2). Interestingly, carbohydrate ingestion during moderate-intensity exercise does not reduce fat oxidation despite a significant suppression in plasma FFA and glycerol concentrations (5, 6).
Because there is only a very small pool of unesterified fatty acids
within the human body (10-40 µmol/kg), the rate of fat oxidation
cannot exceed the rate of lipolysis for more than a few minutes during
exercise. Therefore, a low lipolytic rate can limit fat oxidation by
reducing the amount of FFA available for oxidation. In a recent study,
we reported that carbohydrate ingestion 1 h before exercise (45%
O2 peak) and a
subsequent modest elevation in plasma insulin concentration (10-30
µU/ml) suppressed lipolysis sufficiently to reduce fat oxidation
during exercise (13). However, when exercise is initiated while
subjects are fasted, lipolysis increases rapidly to relatively high
levels and exceeds fat oxidation by as much as 50% (25); thus
lipolysis does not limit fat oxidation in this condition. The principal
aim of this study was to determine whether an elevation in plasma
insulin concentration during exercise, after lipolysis has been
increased to relatively high rates while subjects are fasted, will
allow the lipolytic rate to remain in excess and therefore not limit
fat oxidation.
It seems that in addition to suppressing lipolysis, preexercise
carbohydrate ingestion and the resultant increase in plasma insulin
concentration also can suppress fat oxidation during exercise by a
phenomenon specific to the exercising muscle (8, 13), whereby increased
glycolytic flux may directly reduce fat oxidation within muscle (8, 10,
26). An additional aim of this study was to determine whether an
increase in glucose uptake and glycolytic flux after carbohydrate
ingestion during exercise is associated with a reduction in fat
oxidation. We measured the rate of glycerol appearance in plasma
(Ra glycerol; an index of
whole body lipolysis) and the rate of glucose disappearance from plasma
(Rd Glc) after carbohydrate ingestion during exercise. Carbohydrate was ingested during low-intensity exercise (25%
O2 peak) to elicit a
modest elevation in plasma insulin concentration (10-20 µU/ml)
and during moderate-intensity exercise (68%
O2 peak) to elicit a
very small insulin response (<5 µU/ml).
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METHODS |
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Subjects. Six moderately trained males
participated in this experiment. Their
O2 peak, blood
lactate threshold
(%
O2 peak at lactate
threshold), body weight, and age were 4.5 ± 0.7 l/min (60.3 ± 4.9 ml · kg
1 · min
1),
74.3 ± 3.1 %
O2 peak, 75.1 ± 7.3 kg, and 25 ± 2 yr, respectively. Subjects were informed of the
possible risks, and each signed a consent form approved by the Internal
Review Board of the University of Texas at Austin.
Experimental design. On four separate
occasions, subjects arrived at the laboratory in the morning after an
overnight fast (12 h) and cycled continuously for 2 h. On two
occasions, subjects ingested a high-glycemic sports bar (glycemic
index = 99 ± 4; Gator Bar; Quaker Oats, Barrington, IL)
at 30 min (0.8 g/kg body wt), 60 min (0.4 g/kg), and 90 min (0.4 g/kg) during either low-intensity exercise
[trial
1; 25%
O2 peak
(Low-Fed)] to elicit a modest elevation in plasma insulin
concentration (10-20 µU/ml) or moderate-intensity exercise
[trial
2; 5% below lactate threshold; 68%
O2 peak
(Mod-Fed)] to elicit a very small insulin response (<5
µU/ml). During the other two trials, Low-Fast
(trial
3) and Mod-Fast
(trial
4), the subjects remained fasted
throughout the exercise bout at each intensity. During all trials,
water (2.8 ml/kg body wt; ~200 ml) was provided at 30, 60, and 90 min
of exercise. Trials were separated by
3 days, and the order of the
trials was counterbalanced.
Isotope infusion. On the arrival of
the subjects at the laboratory, Teflon catheters were inserted into
veins of both forearms (one for isotope infusion and the other for
blood sampling). A heating pad was affixed to the hand and forearm of
the sampling arm. A blood sample was then withdrawn for determination
of background isotopic enrichment. This was followed by a primed,
constant rate infusion of
[6,6,-2H2]glucose
(0.41 µmol · kg1 · min
1;
prime of 35 µmol/kg) and
[2H5]glycerol
(0.22 µmol · kg
1 · min
1;
prime of 3.2 µmol/kg) with calibrated syringe pumps (Harvard Apparatus, South Natick, MA). Subjects received isotope infusions for
1 h before exercise.
Blood sampling and analysis. For
determination of resting glucose and glycerol kinetics, blood samples
(8 ml) were withdrawn 10 min before and immediately before exercise.
During exercise, blood samples were drawn every 10 min for the first 90 min and then at 105 and 120 min of exercise. Each blood sample was
divided into three different tubes for subsequent analysis and
immediately placed in an ice bath until the end of the trial. Three
milliliters of each blood sample were placed in evacuated tubes
containing 143 USP units of sodium heparin (Vacutainer;
Becton-Dickinson, Rutherford, NJ). These samples were later analyzed
for isotopic enrichment of the aldonitrile acetate derivative of
[6,6,-2H2]glucose
(30) and the Tris-trimethylsilyl derivative of
[2H5]glycerol
(31), via gas chromatography-mass spectrophotometry (GC-MS). An
additional 2-ml amount of each blood sample was placed in test tubes
containing 0.2 ml of an aprotinin (0.5 TiU/ml) and EDTA (82 mM)
solution and later were analyzed for plasma insulin concentration
(radioimmunoassay; ICN Biomedicals, Costa Mesa, CA). The final 3 ml of
each blood sample were placed into a test tube containing 0.15 ml of
EDTA (82 mM) for later determination of plasma glycerol (fluorometric
assay; Ref. 9), glucose (glucose oxidase autoanalyzer; Yellow Springs
Instruments, Yellow Springs, OH), and FFAs (colorimetric assay; Ref.
22). In each tube, plasma was separated by centrifugation (3,000 rpm
for 20 min at 4°C), immediately frozen, and stored at
70°C until analysis.
Isotope enrichment sample preparation. Plasma samples (1 ml) were deproteinized by adding 1 ml 0.3 N Ba(OH)2 and 1 ml 0.3 N Zn(SO)4. Each tube was then vortexed and incubated in an ice bath for 20 min. After centrifugation (3,000 rpm for 15 min at 4°C), the supernatant was placed into separate tubes for glucose (0.5 ml) and glycerol (1.5 ml) analysis and the water was removed from the tubes via vacuum centrifugation (Savant Instruments, Farmingdale, NY). The aldonitrile acetate derivative of glucose was prepared by adding 100 µl of hydroxolamine-hydrochloride solution (20 mg/ml in pyridine) to the dried sample. After a 30-min incubation at 100°C, 75 µl of acetic anhydride (Supelco, Bellefonte, PA) were then added and the samples remained incubating for an additional hour. Finally, the samples were evaporated under N2. Before injection into the GC-MS, the samples were reconstituted with ethyl acetate. The Tris-trimethylsilyl derivative of glycerol was prepared by reconstituting the dried sample with 30 µl of a trimethylsilyl solution (Tri-Sil; Pierce, Rockford, IL).
Preliminary testing and diet.
O2 peak was
determined while subjects were cycling an ergometer (Monark, model 819;
Varberg, Sweden) with a continuous protocol that lasted 7-10 min.
Blood lactate threshold was determined on a separate occasion as
previously described (6). Subjects consumed the same meals during the day before each experimental trial (~500 g carbohydrate). In the evening before each day of testing (12 h before planned arrival at the
laboratory), a standardized meal was consumed, containing ~200 g of
carbohydrate. Subjects performed a standardized exercise-training bout
2 days before each experiment, and they did not exercise again until
the experimental trial.
Measurement of gas exchange. Inspired
air volume was measured with a Parkinson-Cowan CD4 dry gas meter
(Rayfield Equipment, Waitsfield, VT), as subjects inhaled through a
two-way Daniel's valve. The expired gases were continuously sampled
from a mixing chamber and analyzed for oxygen (model SA3, Applied
Electrochemistry; Ametek, Pittsburgh, PA) and carbon dioxide (Beckman,
model LB-2; Schiller Park, IL). These instruments were interfaced to a
computer for calculations of the rate of oxygen consumption
(O2) and respiratory
exchange ratio.
Calculations. The Ra glycerol was measured to quantify whole body lipolysis. The accuracy of this calculation requires that one mole of glycerol appears in blood after the hydrolysis of every triglyceride. It has recently been suggested that Ra glycerol may underestimate whole body lipolysis because of phosphorylation of glycerol within the muscle by glycerol kinase and by incomplete triglyceride hydrolysis, forming di- and monoglycerides (18). Both of these possibilities would prevent glycerol from appearing in the systemic circulation after lipolysis. To the contrary, others have indicated that neither of these phenomena occur in skeletal muscle or in adipose tissue (21, 31) and that glycerol enters the circulation (19), providing an accurate index of lipolysis.
Ra glycerol, as well as the rate of appearance of glucose (Ra Glc) and the Rd Glc, was calculated with the non-steady-state equation of Steele (29) modified for use with stable isotopes
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Statistical analysis. A two-way ANOVA (treatment by time) for repeated measures with Tukey's post hoc analysis was used to determine significant differences among trials. Planned comparisons for mean values of insulin and glucose were evaluated with paired Student's t-test with a Bonferroni correction factor (P < 0.05).
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RESULTS |
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Low-intensity exercise. During
Low-Fast, plasma glucose and insulin concentrations remained near basal
levels throughout exercise (4.6-5.1 mM and 6-8 µU/ml,
respectively; Fig. 1). Thirty minutes after
the first carbohydrate ingestion during Low-Fed (60 min of exercise),
plasma glucose concentration increased >30% and plasma insulin
concentration increased nearly threefold (9.1 ± 1.3 vs. 26 ± 4.9 µU/ml for 30 and 60 min, respectively;
P < 0.05). Both plasma glucose and
insulin concentrations remained significantly elevated
(P < 0.05) during the second hour of
Low-Fed vs. Low-Fast (Fig. 1).
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Ra glycerol (i.e., index of
whole body lipolysis) increased ~80% above preexercise levels during
the first 30 min of exercise (Fig.
2A).
During Low-Fast, Ra glycerol
increased an additional 50% during the 30- to 120-min period.
Conversely, carbohydrate ingestion attenuated any further rise in
Ra glycerol during the 30- to 120-min period of exercise. However, the absolute rate of
lipolysis did not decline below the 30-min value when
subjects were fed carbohydrate, and it remained >5
µmol · kg1 · min
1
throughout exercise (Fig. 2A).
Similar to
Ra glycerol, plasma FFA
concentration increased twofold above basal levels by the end
of exercise when subjects were fasted and carbohydrate ingestion attenuated this increase (Fig. 2B).
As a result, during the second hour of exercise,
Ra glycerol and plasma FFA
concentrations were lower (P < 0.05)
during Low-Fed vs. Low-Fast. Despite a >20% suppression in
Ra glycerol and plasma FFA
concentration during the 50- to 60-min period of Low-Fed vs. Low-Fast,
fat oxidation was identical when subjects were fed and fasted at this
time (5.3 ± 0.7 vs. 5.3 ± 0.8 µmol · kg
1 · min
1,
respectively). Fat oxidation was not different among trials until the
80- to 90-min period of exercise (Fig. 3),
and lipolysis was >25% in excess of fat oxidation at this time (5.1 ± 0.7 vs. 4.0 ± 0.4 µmol · kg
1 · min
1,
respectively; P < 0.05).
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Similar to plasma glucose and insulin concentrations,
Ra Glc and
Rd Glc remained relatively
unchanged from resting levels throughout exercise when subjects were
fasted (Fig. 4). During Low-Fed,
Ra Glc doubled during the 30 min after the first carbohydrate ingestion (from 12.8 ± 0.7 to 24.9 ± 2.8 µmol · kg1 · min
1
at 25 and 55 min, respectively; P < 0.05) and remained about twofold greater
(P < 0.05) than Low-Fast throughout
the second hour of exercise (Fig.
4A). Furthermore, plasma glucose
concentration increased during the 30- to 60-min period of Low-Fed
(Fig. 1). However, Rd Glc
did not increase until 70 min (nonsignificant) and was not
significantly (P < 0.05) elevated
above Low-Fast until the 80- to 90-min period of exercise (Fig.
4B), the same time that fat
oxidation was first significantly reduced (Fig. 3). Figure 5 compares the time course of the increase
in Rd Glc during Low-Fed vs.
Low-Fast with the reduction in fat oxidation during exercise (both
converted to
cal · kg
1 · min
1).
It is evident that both the time course and the magnitude of the
increase in Rd Glc were
closely matched to the reduction in fat oxidation.
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After carbohydrate ingestion, carbohydrate oxidation increased, and
thus fat oxidation decreased, in parallel with the increase in
Rd Glc (Table
1). As a result, the calculated rate of
muscle glycogen oxidation was not different between Low-Fed and
Low-Fast at any time (Table 1).
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Moderate-intensity exercise. During
Mod-Fast, plasma glucose concentration decreased ~25% during the
second hour of exercise (Fig. 6).
Similarly, plasma insulin concentration decreased progressively and was
very low by the end of exercise when subjects fasted (1.1 ± 0.2 µU/ml at 120 min). Carbohydrate ingestion during Mod-Fed prevented
these reductions in plasma glucose and insulin concentrations (Fig. 6).
The small but significantly greater (P < 0.05) mean plasma insulin concentration during the second hour of
Mod-Fed vs. Mod-Fast (5.4 ± 1.3 vs. 2.0 ± 0.4 µU/ml) was
associated with a slight yet significant suppression
(P < 0.05) in
Ra glycerol during the
final 20 min of exercise and in plasma FFA concentration during the
final 30 min of exercise (Fig. 7). However,
this elevation in plasma insulin concentration was apparently not
sufficient to significantly affect
Ra Glc or
Rd Glc during Mod-Fed vs.
Mod-Fast (Fig. 8) nor did it affect
glycogen oxidation (Table 1). Consequently, fat oxidation was not
different whether subjects were fasted or fed during moderate-intensity
exercise (Fig. 3).
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DISCUSSION |
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The principal finding of the present study was that despite a >50% lower lipolytic rate and plasma FFA concentration throughout the final 1 h of exercise when subjects were fed carbohydrate during low-intensity exercise compared with when they were fasted, fat oxidation was not reduced below Low-Fast levels until 80-90 min of exercise. At this time, lipolysis was 25% greater (P < 0.05) than fat oxidation and thus was not a limiting factor. Similarly, when subjects were fed carbohydrate during moderate-intensity exercise, lipolysis and plasma FFA concentration were reduced 20-25% during the final 1 h of exercise. However, lipolysis remained in excess of fat oxidation, and fat oxidation was not reduced below Mod-Fast levels at any time.
Clearly, when whole body lipolysis is suppressed below the ability of
the muscle to oxidize fatty acids, fat oxidation is limited by a low
lipolytic rate. For example, we have recently reported that elevating
plasma insulin concentration to 10-30 µU/ml before exercise
prevented lipolysis from increasing above 4 µmol · kg1 · min
1
during exercise at 45%
O2 peak and that this
low rate of lipolysis limited fat oxidation during exercise (13). In
the present study, however, despite a suppression of both lipolysis and
fat oxidation when subjects were fed carbohydrate during low-intensity
exercise, lipolysis was maintained above 5 µmol · kg
1 · min
1.
Therefore, after carbohydrate ingestion during low-intensity exercise,
lipolysis was not suppressed to the low levels we observed during
exercise after a preexercise meal (13) and lipolysis remained in excess
of fat oxidation. It is unlikely that a high rate of intracellular
reesterification limited FFA availability sufficiently to reduce fat
oxidation in the present study, because the rate of intracellular
reesterification is very low during exercise (32) and has been shown to
be unaffected by an elevation in plasma insulin concentration in vivo
(3). Our findings imply that more fatty acids were liberated via
lipolysis than were oxidized, and thus the suppression of lipolysis
after carbohydrate ingestion during exercise apparently did not limit
fat oxidation. Maintenance of a relatively high lipolytic rate in the
present study was likely due to the fact that exercise was initiated
while subjects were fasted and was maintained for 30 min before
ingestion of carbohydrate. Lipolysis increased dramatically with the
onset of exercise when subjects were fasted (25). In the present study,
lipolysis increased ~80% during the first 30 min of low-intensity
exercise, before carbohydrate ingestion. Thereafter, when the subjects
were fed, lipolysis remained stable, whereas it increased when they
were fasted.
Interestingly, as shown presently, as well as by others (5, 6), fat oxidation does not decline after carbohydrate ingestion during moderate-intensity exercise, when plasma insulin concentration was only slightly elevated (~3 µU/ml), despite a 40-50% lower plasma FFA concentration. A decline in plasma FFA concentration is indicative of a reduction in adipose tissue lipolysis. The present observation that an ~25% lower lipolytic rate when subjects were fed carbohydrate resulted in a 30-40% lower plasma FFA concentration without reducing total fat oxidation suggests that the suppression of lipolysis occurred predominantly in the adipocyte. Although the use of intramuscular triglycerides (IMTG) during exercise is controversial (16, 28), several studies have reported that IMTG provide the majority of total fat oxidized in endurance-trained individuals during moderate-intensity cycling (8, 14, 25). It has recently been demonstrated that elevating plasma insulin concentration to 42 µU/ml before exercise lowered IMTG oxidation during exercise in trained subjects (8). However, the relative reduction in plasma FFA oxidation after carbohydrate ingestion was >60% greater than the reduction in IMTG oxidation (8). These observations imply that IMTG may be less sensitive to the antilipolytic effect of insulin compared with triglycerides in adipose tissue. It seems that this relative insensitivity of IMTG to the very small increase in plasma insulin concentration observed after carbohydrate ingestion during moderate-intensity exercise (~3 µU/ml) may have prevented the reduction in lipolysis from limiting fat oxidation during exercise by allowing whole body lipolysis to exceed fat oxidation.
It has been demonstrated that when lipolysis was suppressed
sufficiently to reduce fat oxidation, muscle glycogen oxidation was
increased to maintain energy production during exercise (11, 13).
However, it is well-known that carbohydrate ingestion during continuous
exercise at moderate to high intensities (>65%
O2 peak) does
not affect the change in muscle glycogen concentration during exercise
(5, 12). Our findings confirm that the calculated rate of muscle
glycogen oxidation is not altered by carbohydrate ingestion during
exercise. Because the reduction in lipolysis from carbohydrate
ingestion does not impair fat oxidation or increase muscle
glycogenolysis during moderate- to high-intensity exercise, the
ingested carbohydrate provides extra energy in the form of blood
glucose, leading to maintained carbohydrate oxidation and enhanced performance.
The inability of carbohydrate ingestion to reduce muscle glycogen
oxidation during moderate-intensity exercise may be explained by the
relative insensitivity of IMTG lipolysis to insulin (allowing lipolysis
to exceed fat oxidation) and by the fact that carbohydrate ingestion at
this intensity failed to significantly increase blood glucose uptake
during the 30- to 120-min period. During low-intensity exercise,
however, the hyperglycemia and hyperinsulinemia and elevation in
Rd Glc glucose after
carbohydrate ingestion were compensated by a reduction in fat
oxidation. In a previous study from our laboratory, hyperglycemia and
hyperinsulinemia (>10 mM and ~20 µU/ml, respectively) evoked by
intravenous glucose infusion during moderate-intensity exercise (73%
O2 peak) increased
carbohydrate oxidation (and reduced fat oxidation) without affecting
muscle glycogen utilization, despite very high rates of glucose
disposal (120-200
µmol · kg
1 · min
1;
Ref. 7). These observations indicate that when plasma glucose and
insulin concentrations are increased sufficiently to increase Rd Glc, regardless of
intensity (i.e., low or moderate), blood glucose oxidation increases
with a compensatory reduction in fat oxidation, rather than a decline
in muscle glycogen oxidation.
Presently, we found that the reduction in fat oxidation during low-intensity exercise elicited by hyperglycemia and hyperinsulinemia coincided in time with the increase in Rd Glc (Fig. 4). Rd Glc provides a reasonable representation of blood glucose uptake and oxidation in exercising muscle (4). Although this association between an increase in Rd Glc and a decline in fat oxidation does not directly imply a causal relationship, an increase in blood glucose uptake and oxidation during exercise may have a direct effect on muscle, reducing its ability to oxidize fat. This supports the notion that carbohydrate metabolism in general, and increased glycolytic flux from blood glucose in this case, may regulate the relative contribution of fat and carbohydrate to total energy production during exercise.
It has recently been reported that acute hyperglycemia and hyperinsulinemia and a subsequent increase in glycolytic flux directly reduced muscle fatty acid oxidation by impairing long-chain fatty acid entry into the mitochondria (8, 27). The proposed mechanism for this impairment is that an increase in glycolytic flux increases the concentration of malonyl-CoA concentration in muscle (10), which, in turn, inhibits the enzyme that regulates the entry of long-chain fatty acids into the mitochondria (i.e., carnitine palmitoyltransferase I). Thus malonyl-CoA "senses" the availability of carbohydrate (26) and modifies the ability of the muscle to oxidize fat (i.e., via carnitine palmitoyltransferase I inhibition). This indicates that carbohydrate metabolism in muscle, as reflected by glycolytic flux, is the primary factor regulating fat oxidation under conditions where both FFA and carbohydrate are available to muscle for oxidation. This mechanism has been documented in rat heart and skeletal muscle, whereas evidence of this mechanism in human muscle remains less clear (23).
In summary, carbohydrate ingestion and the resultant insulin response during exercise suppressed lipolysis. However, the lipolytic rate remained in excess of fat oxidation after carbohydrate ingestion during both low- and moderate-intensity exercise, indicating that this suppression in lipolysis was not responsible for reducing fat oxidation. A reduction in fat oxidation occurred at the time of an increase in Rd Glc and glycolytic flux. Therefore, carbohydrate ingestion during both low- and moderate-intensity exercise did not suppress lipolysis sufficiently to reduce fat oxidation. However, under conditions where lipolysis is in excess of fat oxidation, carbohydrate ingestion and the resultant insulin response may regulate carbohydrate oxidation by increasing blood glucose uptake and, by doing so, fat oxidation may be reduced by a phenomenon specific to the exercising muscle.
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ACKNOWLEDGEMENTS |
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We greatly appreciate the technical support of Dr. Andrew Coggan and Michael Sullivan. We additionally appreciate the assistance from Paul Below, Melissa Domenick, Pete Flatten, Ricardo Fritzsche, Wes Earwood, Matt Oseto, Tom Switzer, Trace Adams, and the participants of this study.
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FOOTNOTES |
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This study was supported by National Institute of Diabetes and Digestive and Kidney Diseases Grant DK-46017 (R. R. Wolfe and E. F. Coyle), Mars Inc., and the Gatorade Sports Science Institute.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: E. F. Coyle, The Univ. of Texas at Austin, Rm 222 Bellmont Hall, Austin, TX (E-mail: coyle{at}mail.utexas.edu).
Received 30 April 1998; accepted in final form 5 January 1999.
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