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Laboratory of Nutrition Chemistry, Division of Applied Life Sciences, Graduate School of Agriculture, Kyoto University, Kyoto 606-8502, Japan
1To whom correspondence should be addressed.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSExperimental designRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • (-)-hydroxycitrate • endurance exercise • carbohydrate utilization • lipid oxidation • Std ddY mice
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSExperimental designRESULTSDISCUSSIONREFERENCES |
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). Athletes expect that these dietary supplements
might compensate for a lack of training. These dietary supplements may
enhance the effects of training. A number of studies revealed that the
most important effect of endurance training may be the sparing effect
of glycogen utilization during exercise through an increase in the
ability of skeletal muscle to oxidize lipids (Maughan 1998
, Williams 1998
).
Costill et al. (1978)
and Ivy et al. (1979)
suggested that caffeine has a positive ergogenic effect.
They proposed that the effect is achieved by an elevation in
catecholamines, which enhance fat oxidation either by increasing free
fatty acid
(FFA)2levels or muscle triacylglycerol lipolysis (Graham and Spriet 1991
). Plasma FFA were elevated 1 h after caffeine
ingestion in some studies (Powers et al. 1983
,
Sasaki et al. 1987
). The failure to demonstrate
consistently an increase in FFA may be a result of increased uptake by
the active muscle. A number of supplements such as capsaicin and its
analogs (Kim et al. 1997
, 1998a
, and 1998b
),
medium-chain triglycerides (Matsumoto et al. 1996
)
and Nanpao, a traditional Chinese medicine (Saito et al. 1998
), have been reported to increase endurance performance.
However, caffeine is a substance prohibited by International Olympic
Committee, medium-chain triglycerides increase the serum ketone
body concentration, causing a sense of fatigue (Matsumoto et al. 1996
), and an effective dose of capsaicin (10 mg/kg body) is
too pungent for human use.
Recently, (-)-hydroxycitrate (HCA) has been reported to affect
lipid metabolism (Kriketos et al. 1999
, McCarty 1994
and 1995
). HCA is an active ingredient that is extracted
from the rind of the Indian fruit, Garcinia cambogia
(Lewis and Neelakantan 1965
); it is available as an
herbal supplement and decreases adipose tissue weight after ingestion
for a few weeks (Chee et al. 1977
, Greenwood et al. 1981
, Rao and Sakariah 1988
). HCA is a
competitive inhibitor of ATP:citrate lyase (EC 4.5.3.8), inhibits fatty
acid synthesis and reduces appetite in rodents (Watson et al. 1969
). Whether HCA administration affects lipid oxidation and
endurance exercise performance is unclear. We speculated that HCA may
aid in aerobic performance, but no research exists concerning such an
effect. The purpose of this study was to investigate the possibilities
of HCA as a dietary supplement to increase endurance exercise
performance.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSExperimental designRESULTSDISCUSSIONREFERENCES |
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Seven-week-old male Std ddY mice (Japan SLC, Hamamatsu, Japan)
were used. They were housed in standard cages (33 x 23 x 12
cm; 6 mice/cage) under controlled conditions of temperature (22 ± 0.5°C), humidity (50%) and lighting (lights on from 1800 to
0600 h). They were given free access to water and a nonpurified
commercial diet (type MF; Oriental Yeast, Tokyo, Japan) containing
(g/kg diet): water, 70; protein, 240; fat, 51; fiber, 32;
carbohydrates, 545. All animals received humane care as outlined in the
NIH guidelines (NRC 1985
) and by the Kyoto University Animal Care
Committee. HCA used in this study was in free acid form and was
provided by Nippon Shinyaku (Kyoto, Japan). In all experiments, HCA was
dissolved in distilled water and administered orally as a 0.48 mol/L
solution.
Apparatus.
The gas analyzer used for the assessment of metabolic rate in the mice consisted of six acrylic metabolic chambers, CO2 and O2 analyzers (model RL-600, AlcoSystem, Tokyo, Japan), and a switching system (model ANI6-A-S, AlcoSystem, Tokyo, Japan) to sample gas from each metabolic chamber. Each metabolic chamber had a 125.4 cm2 floor and was 6.5 cm in height. Room air was pumped through the chambers at a rate of 1.0 L/min. Expired air was dried in a cotton thin column and then directed to an O2/CO2 analyzer. Air from each chamber was sampled for 60 s. During the last 1 s, the O2 and CO2 concentrations were measured 100 times and the average was used for the calculation of oxygen consumption and the respiratory exchange ratio (RER). Therefore, the data for each chamber could be obtained every 7 min and the data were stored on a spreadsheet.
The oxygen consumption (VO2), carbon dioxide exhaustion
(VCO2), RER, carbohydrate oxidation and lipid oxidation
were calculated using the following equations:
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where FEN2 is the concentration of nitrogen in the exhaust air, FIN2 is the concentration of nitrogen in the room air, FEO2 is the concentration of oxygen in the exhaust air, FIO2 is the concentration of oxygen in the room air, FECO2 is the concentration of carbon dioxide in the exhaust air, FICO2 is the concentration of carbon dioxide in the room air and VT is the air flow through the chamber corrected to standard temperature pressure dry.
The swimming system used in the experiment for the measurement of the
swimming time of mice to exhaustion was an adjustable-current
swimming apparatus for mice. The details were described previously
(Ishihara et al. 1997
, Matsumoto et al. 1996
). Briefly, an acrylic plastic pool (90 x 45 x 45 cm) was filled with water to a depth of 38 cm; the current was
generated with a pump (type C-P60H; Hitachi, Tokyo, Japan). This
swimming apparatus was used previously to evaluate the effects of food
and nutrients such as capsaicin (Kim et al. 1997,
1998a
and 1998b
), overdose of caffeine (Ishihara et al. 1997
, Matsumoto et al. 1996
), Nanpao
(Saito et al. 1998
) and medium-chain triglycerides
(Fushiki et al. 1995
).
The running system used in the experiment was the treadmill (model
Simplex II, Columbus, OH) for running of mice. The system consisted of
three running lanes of equal dimensions (28.8 x 4.7 x 4 cm)
and each lane was encased within a metabolic chamber with an inside
volume of 
1000 cm3; an electric air fan
provided mixing of the air. The system could therefore monitor
respiratory gases of up to three mice independently.
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Experimental design |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSExperimental designRESULTSDISCUSSIONREFERENCES |
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After a 1-wk preliminary period, 60, 54 and 12 mice were used to measure the effects of a single oral HCA treatment on respiratory gas, serum variables and glycogen accumulation, respectively. Mice (n = 60) were separated into three groups with equal body weights; each mouse was placed into a metabolic chamber designed to measure respiratory gas. Mice were prohibited access to the diet and water from 0930 h. At 1000 h, they were administered orally 100 (10 mg) or 300 µL (30 mg) of a 0.48 mol/L HCA solution or water, and the respiratory gas was analyzed for 2 h after the administration. To measure serum variables, another 54 mice were separated into three groups, prohibited access to the diet and administered HCA orally as described above. They were killed by decapitation either 30 or 100 min after the administration. Blood was rapidly collected from the neck, and the concentrations of serum glucose, FFA and triglyceride were measured. To investigate the effect of HCA on glycogen accumulation, 12 other mice were separated into three groups as described above, given free access to the commercial diet after administration of the agent and killed by decapitation 16 h later. The gastrocnemius muscle and liver were rapidly removed, frozen in liquid N2, weighed and kept at -80°C to analyze the concentration of tissue glycogen.
Experiment 2. HCA treatment and maximum swimming time.
Mice (n = 18) were forced to swim to exhaustion at
a flow rate of 8 L/min twice at 3-d intervals during the preliminary
period of 1 wk and then were divided into three groups. They were
orally administered 100 (10 mg) or 300 (30 mg) µL of a
0.48 mol/L HCA solution or 100 µL of water (control)
at 1700 h and given free access to the commercial diet and water.
Starting the next day, mice swam until fatigue every day at the flow
rate of 8 L/min, and the maximum swimming time was measured. Mice were
administered HCA solutions orally every day after swimming (at 1700
h).
Experiment 3. Chronic HCA treatment and lipid oxidation.
Mice (n = 18) were divided into two groups so that the mean body weights were equal in both groups. They were orally administered 100 µL of 0.48 mol/L HCA (10 mg) or water (control) twice a day (first administration, from 1000 to 1100 h; second administration, from 1700 to 1800 h) for 25 d. Mice had free access to food and water; body weight and food intake were measured every day. After the first administration at d 26, each mouse was placed into a treadmill chamber and allowed to rest for 1 h, followed by a 1-h run at the speed of 15 m/min; respiratory gas was monitored. On d 27, they were killed by decapitation and the gastrocnemius and quadriceps muscles, epididymal and perirenal adipose tissues, liver, spleen, heart and kidneys were removed, and tissues were weighed.
Biochemical analyses.
The muscle glycogen content was measured spectrophotometrically
by a method using enzymatic techniques as described elsewhere
(Passonneau and Lauderale 1974)
. Briefly, after
hydrolysis of the muscle sample in 0.6 mol/L HCl at 100°C for 2 h, the glucose residues were determined with a commercial kit (Glucose
CII Test Wako, Wako Pure Chemical, Osaka, Japan).
Blood was collected from the severed neck veins; serum was obtained by centrifugation (3000 x g for 10 min) and stored at -80°C until analysis. Serum glucose, FFA and triglycerides were measured with commercial kits (Glucose CII, NEFA C, triglyceride G Test Wako, Wako Pure Chemical).
Statistical analysis.
Data are presented as means ± SEM. All of the statistical analyses were performed by StatView version 4.5 (SAS Institute, Cary, NC). Body weight, organ weights, serum variables, glycogen concentrations and maximum swimming time until fatigue were analyzed by ANOVA, and post-hoc comparisons were made using Fisher’s test. In Experiment 1, carbohydrate and lipid oxidation, and the RER were analyzed by two-way repeated-measures ANOVA, and post-hoc comparisons were made using Fisher’s test. In Experiment 3, comparisons between the control and the HCA group were made by two-way repeated-measures ANOVA and were analyzed independently for at rest and during running. Differences were considered significant at P < 0.05.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSExperimental designRESULTSDISCUSSIONREFERENCES |
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The RER was greater than in controls in the group administered 30 mg
HCA, but not in that administered 10 mg, at 20 and 30 min (Fig. 1A
). Oxygen consumption did not differ among the groups (Fig. 1
B). Carbohydrate oxidation (Fig. 2
B) was greater and lipid oxidation (Fig. 2
A) was lower than in
controls at 20 and 30 min after administration in the group
administered 30 mg, but not in that administered 10 mg.
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The concentration of glycogen in the gastrocnemius muscle 16 h after administration was 4.31 ± 0.22, 5.65 ± 0.45 and 4.36 ± 0.30 mg/g wet tissue in mice fed 0 (control), 10 and 30 mg HCA, respectively. There was a significant difference between the control and 10-mg HCA groups. Liver glycogen concentration did not differ among groups (data not shown).
HCA treatment and maximum swimming time (Experiment 2).
In the group administered 10 mg HCA, the increase in maximum swimming
time on d 1 was slightly longer (P = 0.21) than that of
the control group. The increase on d 3 was significantly longer than
that of the control group after 3 d of treatment (Fig. 3
, P < 0.05).
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Administration of 10 mg HCA twice a day for 25 d did not
affect food intake (Fig. 4
, histogram). There were no differences in body weight among the groups
before treatment, but after 3 wk, the HCA group was 1.2 g lighter
than the control group (Fig. 4
, line, P = 0.34).
Epididymal adipose (P = 0.24) and perirenal adipose
(P = 0.18) tissue weights tended to be lower, whereas
relative liver (3.84 ± 0.47 vs. 4.25 ± 0.18%) and spleen
(0.24 ± 0.06 vs. 0.31 ± 0.03%) weights were significantly
greater in HCA-treated mice than in controls.
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). Thirty minutes after administration, the RER began to decrease in
mice administered HCA but not in the control group. The RER in the
control group and HCA group was 0.86 ± 0.01 and 0.82 ± 0.02
at 1 h after administration, respectively (P < 0.05, two-way repeated-measures ANOVA when at rest, Fig. 5
). The
RER increased abruptly by 0.05 in both groups after the start of the
running exercise (at 65 min in Fig. 5
), but decreased gradually after
the belt speed reached the set value of 15 m/min (at 75 min in Fig. 5
).
The RER reached 0.8 at the end of the running period in both groups
and was significantly lower in the HCA-administered group
throughout the running period (P < 0.01, two-way
repeated ANOVA during running). Oxygen consumption of mice in both
groups gradually decreased to 80 mL/kg body during rest in the
metabolic chamber and increased to 100–120 mL/kg body during the
running period (data not shown).
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). Lipid oxidation during the first 20 min of running was higher in the
HCA group than in the control group (P < 0.0001 during
running, two-way repeated-measures ANOVA, Fig. 6A
).
Although there was no difference in carbohydrate oxidation before the
start of the running period, carbohydrate oxidation during the 60-min
running period was lower in the HCA group than in the control group
(P < 0.0001, two-way repeated-measures ANOVA,
Fig. 6B
).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSExperimental designRESULTSDISCUSSIONREFERENCES |
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Because acute administration of 10 mg HCA did not affect the RER but
increased serum FFA concentration 100 min after administration, lipid
metabolism may be promoted and carbohydrate utilization could be
spared. Also, the glycogen concentration of gastrocnemius muscle became
significantly higher in these mice 16 h after administration.
Hellerstein and Xie (1993)
reported that administration
of 0.263 mmol/(kg · d) [1.64 mg/(d · mouse)] increased liver
glycogen accumulation in rats administered HCA and refed glucose
intravenously (Hellerstein and Xie 1993
).
In this study, in mice chronically administered 10 mg HCA twice a day,
the RER was significantly lower during the 60-min running period
(P < 0.01). Lipid oxidation was significantly greater
and carbohydrate oxidation was significantly less in these mice during
the early stages of running (P < 0.05). During the
transition from rest to moderate-intensity exercise, the muscle
shifts from using primarily circulating FFA to using a blend of FFA,
extramusclar glucose and muscle glycogen (Ahlborg et al. 1974
, Bergstrom et al. 1967
, Wahren et al. 1971
). Carbohydrate storage in the body is limited compared
with the energy storage in adipose tissue, and sparing of carbohydrate
during exercise is therefore beneficial for competition. A diet
resulting in greater utilization of lipids may affect carbohydrate
utilization at the early stage of exercise and result in an increased
capacity for endurance exercise. For example, capsaicin or its analog
caused epinephrine secretion and increased lipid oxidation 2 h
after administration; thus, the mice that were given capsaicin or its
analog 2 h before the start of exercise had significantly greater
endurance capacity (Kim et al. 1997
and 1998b
). In this
study, the RER in mice fed HCA gradually began to decrease from 30 min
before the start of exercise, and the differences between the two
groups continued for the first 15 min of running. The enhancement of
lipid oxidation at the early stage of exercise could lead to increased
endurance exercise capacity. For example, in high fat diet–adapted
rats, muscle glycogen was spared during the early stages of prolonged
exercise (Nakamura et al. 1998
), and the running time
until exhaustion was longer than that in rats adapted to a low
carbohydrate diet (Miller et al. 1984
). In subjects
ingesting a caffeine solution before the start of running, glycogen
utilization was spared for the first 15 min of exercise and endurance
exercise time until fatigue was longer than in subjects who ingested
dextrose (Spriet et al. 1992
).
The RER in the HCA group continued to decrease, and there was a
significant difference between the control mice and HCA-treated
mice during the 60-min rest (preexercise) period after administration
(Fig. 5)
. The divergence of the RER of the two groups with time was not
considered to be due to a transition from the fed to the
food-deprived state of mice. HCA was given 60 min before the start
of exercise and mice had free access to food until treatment was given.
Chronic administration did not reduce food intake, and there were no
differences in the RER among the groups 30 min after HCA administration
(at 30 min in Fig. 5
). Hence, we considered that the divergence of the
RER was due to HCA. Chronic HCA administration might have increased
energy expenditure during the 3-wk experimental period in this study.
In studies from the University of South Carolina, subjects receiving
750 mg/(d · person), equivalent to 0.375 mg/(d
· mouse) lost 4–5 kg weight during the 8-wk study period
(Conte 1993
). In another recent study, rats fed a high
(75%) carbohydrate diet and supplemented with HCA (52 mmol HCA/kg 70%
dextrose diet, 65 kJ/g) for 28 d had a 12.6% increase in 24-h
energy expenditure with no change in the RER (Vasseli et al. 1998
).
Numerous studies have shown that endurance exercise performance is
augmented by the promotion of lipid oxidation. There are several
mechanisms by which HCA may promote lipid oxidation. HCA could be
acting through stimulation of the autonomic nervous system, a direct
effect on metabolism in specific tissues or organs, or effects on
energy substrate flux and availability. Promotion of lipid oxidation by
administration of HCA may be attributed to the activity of carnitine
palmitoyltransferase (CPT-I), which plays an important role in
regulating the flux of long-chain fatty acids into mitochondrial
oxidative metabolism in mammalian tissues (Ruderman et al. 1999
). CPT-I activity is completely inhibited by
malonyl-CoA, whose production is suppressed by HCA.
Chronic consumption of a high fat diet has been reported to
increase endurance exercise performance (Lambert et al. 1994
, Starling et al. 1997
). A single or
short-term feeding of a high fat diet elevated the serum FFA
concentration but did not increase endurance exercise performance
(Okano et al. 1996
and 1998
, Whitley et al. 1998
). It is thought that the continuously high serum FFA
concentration during chronic consumption of a high fat diet could
increase lipid oxidation capacity. In this study, the serum FFA
concentration was significantly elevated by single administration of 10
mg HCA, but the RER and endurance exercise performance were unaffected
(our pilot study). Mice chronically administered 10 mg HCA had an
enhanced lipid oxidation capacity during exercise (Fig. 5
, 6)
.
Recently, Kriketos et al. (1999)
did not detect any
effect of HCA administration on lipid oxidation in men during either
rest or moderately intense exercise on a cycle ergometer. However, in
those studies, subjects received a daily dose of 3.0 g per subject
[nearly equal to 1.5 mg/(d · mouse)] for 3 d, which
is a much smaller dose than that used in other studies. Also, their
experimental period of 3 d was quite short compared with the other
studies. Chee et al. (1977)
observed that the rate of
hepatic fatty acid synthesis was depressed by a single intraperitoneal
injection of 0.4 mmol HCA [83.2 mg/(d · mouse)] or a
single meal containing 52.6 mmol/kg diet [32.8 mg/(d ·
mouse)] in rats and chickens. Rao et al. (1988)
reported that rats fed a diet containing 2 g/kg HCA for 15 d had
significantly less epididymal fat. Our present study was based on pilot
studies conducted in our laboratory, in which we used a dose of HCA
that ranged from 5 to 30 mg/(d · mouse), taking into
consideration the results of the studies by Chee et al. (1977)
and Rao et al. (1988)
.
Acute administration of 30 mg HCA increased the RER, in contrast to the decrease due to chronic administration of 10 mg HCA. In addition, because 30 mg HCA reduced food intake by 87% (pilot study), we judged that the dose of 30 mg was not suitable for investigation of the effect of HCA on endurance exercise performance, and did not examine the effect of chronic administration of 30 mg HCA.
Acute administration of 30 mg HCA increased the RER and depressed
lipid oxidation for the first 3 h after administration. The
mechanism responsible for the observed increase in RER is uncertain.
One possible mechanism may be due to a buffering action of serum. For
example, serum lactic acid concentration is high at the end of the
intense exercise. The blood pH is constantly adjusted within a
relatively narrow range, and carbon dioxide is thus liberated from the
carbonate in the blood in order to adjust pH when lactic acid
accumulates in the blood. The liberated carbon dioxide is expired from
the lungs, increasing the RER. Similarly, after administration of 30 mg
HCA, HCA in blood could cause the liberation of carbon dioxide from the
carbonate in the blood in order to adjust pH, and the liberated carbon
dioxide expired from the lungs might result in an increase in the RER.
We contend that the effect is negligible when a smaller dose (10 mg) of
HCA is administered. It should be noted that HCA used in the previous
experiments was not a lactone but a free acid. Another possible
mechanism is the stress-induced release of epinephrine or
norepinephrine. We observed that mice orally administered 30 mg (300
µL of 0.48 mol/L) HCA repeatedly rubbed their faces with
their hands. The endocrinological changes in the mice were not
evaluated here. RER is increased by an infusion of the stress hormones,
cortisol, epinephrine and glucagon, in amounts designed to simulate
plasma levels seen in patients after trauma (Weissman et al. 1986
).
In summary, oral administration of 10 mg HCA elevated serum FFA concentration and increased muscle glycogen concentration in mice at rest. Mice that were chronically (twice daily for 25 d) administered HCA had a significantly reduced RER at rest and during running exercise. Lipid oxidation was increased and carbohydrate utilization was less in the early stage of running exercise. These results indicated that the enhancement of endurance exercise by orally administered HCA in mice might have occurred by the attenuation of glycogen consumption caused by the promotion of lipid oxidation during running exercise.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Manuscript received December 28, 1999. Initial review completed February 15, 2000. Revision accepted August 11, 2000.
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