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J Nutr Sci Vitaminol, 46, 309-315, 2000
Effects of Capsaicin-containing Yellow Curry Sauce on Sympathetic
Nervous System Activity and Diet-induced Thermogenesis
in Lean and Obese Young Women
Tamaki MATSUMOTO,1,2 Chiemi MIYAWAKI,1 Hidetoshi UE,1 Toshiaki YUASA,3
Aya MIYATSUJI4 and Toshio MORITANI1,*
1 Laboratory of Applied Physiology, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto 606-8501, Japan
2 International Buddhist University, Osaka 583-8501, Japan3 Life Science Laboratory, Omron Corporation, Kyoto 600-8530, Japan
4 Comfort Laboratory, Products Development, Apparel Division Group, Gunze Limited, Kyoto 626-0043, Japan
(Received August 28, 2000)
Summary The present study was designed to investigate the effect of capsaicin, a pun
gent component of red pepper, on the sympathetic nervous system (SNS) activity and en
ergy metabolism in 16 age- and height-matched lean and obese young women. The sympa
tho-vagal activities were assessed by means of spectral analysis of heart rate variability
(HRV) during the resting condition and after the meal (2,016kJ) with capsaicin (3mg).
Energy expenditure was also measured under the two conditions. There was no significant
difference in any of the parameters of the HRV between the obese and control groups at rest.
After the capsaicin diet, however, the very low frequency component (0.007-0.035Hz) as
sociated with thermogenesis (315.8•}78.0vs. 814.8•}211.7ms2 Hz-1, p<0.05) as well as
its responsiveness (delta changes: 14.6•}104.4vs. 369.2•}121.7ms2 Hz-1, p<0.05) were
significantly lower in the obese than the control group. Energy expenditure was signifi
cantly increased in the control group after the meal (5, 574.7•}221.2 to 6,114.7•}239.0 kJ
day-1; p<0.01), but no such significant thermogenic response was detected in the obese
group despite nearly identical lean body mass of the control group. Our data indicate that
regardless of the resting level of sympatho-vagal activities, the reduced sympathetic respon
siveness to physiological perturbation such as a capsaicin diet, which may cause impaired
diet-induced thermogenesis and further weight gain, could be an important etiological fac
tor leading to obesity in young women.
Key Words capsaicin, sympathetic nervous system activity, heart rate variability, diet-in
duced thermogenesis, obesity
Capsaicin is the major pungent principle in various species of Capsicum fruits such as hot chilli peppers and has long been globally used as an ingredient of spices,
preservatives and medicines (1).The physiological effects of capsaicin have been ex
tensively reviewed in previous animal studies. It has been shown that dietary supplementation of capsaicin in high fat diets lowered the perirenal adipose tissue weight and serum triglyceride concentration in rats due to enhancement of energy metabolism (2, 3). Watanabe et al. (4, 5) have investigated neurophysiological functions of capsaicin and have demonstrated that capsaicin increases energy metabolism by catecholamine secretion from the adrenal medulla through sympathetic activation via the central nervous system. The sympathothermogenic effect of capsaicin has also been demonstrated in humans. According to the recent study of Yoshioka et al. (6), energy expenditure increased immediately after the meal containing red pepper; whereas
this enhancement of energy metabolism by a red-pep
per diet was inhibited after the administration of ƒÀ
- adrenergic blocker, propranolol.
The sympathetic nervous system (SNS) and adrenal
medulla combine to form the sympathoadrenal system,
which is one of the important regulators of a number of
physiological processes. Since the coordination of en
ergy homeostasis is particularly dependent on the nor
mal functioning of the sympathoadrenal system, alter
ations in the SNS activity are widely believed to con
tribute to the pathophysiology of obesity (7, 8).
Whereas, no consensus has been made among investi
gators as to the predominant sympathetic abnormality
(an increase or decrease) (9, 10), which may be partly
attributable to the difficulties in adequately assessing
the sympathetic function modulating energy metabo
lism in humans.
The electrocardiogram (ECG) R-R interval, or inter
beat interval of heart rate is determined by the net effect
of sympathetic and parasympathetic input. Heart rate
variability (HRV) power spectral analysis has been
proved as a reliable non-invasive method and has pro-
* To whom correspondence should be addressed . E-mail: [email protected]
309
310 MATSUMOTO T et al.
vided a comprehensive quantitative and qualitative evaluation of neuroautonomic function under various
physiological conditions (11-15). In general, the highfrequencies (>0.15 Hz) of HRV are associated with almost entirely vagal nerve activity and low-frequencies
(<0.15 Hz) of HRV might be mediated by both vagal and SNS activities (16-18). The frequencies much lower than 0.1Hz have been thought to reflect thermoregulatory fluctuations in vasomotor tone (19, 20). We have recently demonstrated that very low (VLO) fre
quency components (0.007-0.035Hz) were selectively increased against thermogenic perturbation such as acute cold exposure and mixed-food ingestion (21, 22). This finding suggests the possibility of evaluating the SNS activities associated with energy metabolic regulation by means of HRV spectral analysis in humans.
Although disagreement still exists regarding the resting level of the SNS activity, reduced sympathetic response to external physiological stimulation such as
glucose ingestion has been found in the obese population (23-25). Because of its strong sympatho-thermo
genic effect, investigating capsaicin-induced SNS activity and metabolic change may provide further information as to the sympathetic abnormality in human obesity. To the best of our knowledge, however, no data re
garding the physiological effects of capsaicin in obese individuals are currently available.
Therefore, the aim of the present study was to evaluate thermogenic sympathetic function in response to capsaicin-containing spicy food by means of HRV power spectral analysis, as well as to investigate the magnitude of diet-induced thermogenesis in age and heightmatched lean and obese young women.
METHODS
Subjects. Eight lean and eight obese young women volunteered to participate in this study. The two groups were matched in age and height. The percentage of body fat and lean body mass was determined by means of dual-energy X-ray absorptiometry (Hologic ODR=1000). Descriptive characteristics of the subjects are presented in Table 1.
The study protocol was approved by the Committee on Ethics of Kyoto University Graduate School. All subjects were carefully instructed about the study and all gave their written informed consent to participate in the study. The subjects completed a standardized health
questionnaire for past medical history, medication, lifestyle, diet, smoking habits, alcohol consumption, and physical activity. The subjects were non-smokers in
good health and had no personal or family history of diabetes mellitus, cardiovascular disease, or other metabolic diseases. All subjects were weight stable at the time of the study with no more than a two-kg weight loss or gain over the six months before the study. Each subject was instructed to avoid any food or beverages containing alcohol or caffeine after 9:00 p. m. of the day preceding the study.
Experimental procedure. Subjects came to the laboratory at 9:00 a. m., and all experiments were per
Table 1. Physical characteristics of subjects
Values are means•}SE.
Controlvs. Obese: ** p<0.01.
formed in the morning. The room was temperature
controlled (23-24•Ž) and quiet with minimization of
arousal stimuli. The subjects were instrumented with
ECG electrodes and then rested for at least 30min be
fore the beginning of the experiment.
After the resting period, CM5 lead ECG and gas ex
change parameters using an Aero-monitor AE 280
(Minato Medical Science) were continuously recorded
while the subject remained seated in a comfortable
chair for 10min. The subject then ingested rice with
spicy yellow curry sauce containing 3mg capsaicin
over a ten-minute period. The amount of capsaicin used
in this study was about 10 times greater than one in
volved in a retort pouch of regular curry sauce on the
market. The experimental meal composition was as fol
lows: 60% carbohydrate, 30% fat and 10% protein as
energy, respectively. The energy content of the meal was
2,016 kJ. It should be noted that based on the results of
our preliminary research including capsaicin dose re
sponse experiments and previous studies (6, 26-28),
the amount of capsaicin and energy content of the ex
perimental meal were decided. Thus, the same absolute
caloric load rather than a relative one was provided to
both lean and obese subjects as a thermogenic pertur
bation although there was a significant difference in
body weight between the two groups.
Immediately after the meal was ingested, the ECG
and gas exchange measurements were performed con
tinuously for 30min. During resting and postprandial
conditions, all subjects breathed in synchrony with a
metronome at 15times . min-1(0.25Hz) to ensure that
respiratory-linked variations in heart rate did not over
lap with low-frequency heart rate fluctuations (below
0.15Hz) from other sources.
R-R spectral analysis. Our R-R interval power spec
tral analysis procedures have been fully described else
where (12-14, 21). Briefly, analog output of the ECG
monitor (Life Scope, Nihon Kohden) was digitized via a
13-bit analog-to-digital converter (Trans Era HTB 410)
at a sampling rate of 1,000Hz. The digitized ECG signal
was differentiated, and the resultant ORS spikes and the
intervals of the impulses (R-R intervals) were stored se
quentially on a hard disk for later analyses (12, 13).
Before R-R spectral analysis was performed, the
stored R-R interval data were displayed and aligned se-
Effects of Capsaicin on Autonomic Nervous System and Thermogenesis in women 311
quentially to obtain equally-spaced samples with an effective sampling frequency of 2Hz (29) and displayed on a computer screen for visual inspection. Then, the DC component and trend were completely eliminated by digital filtering for the band-pass between 0.007 and 0.5Hz. The high-pass filtering at 0.007Hz was chosen to include the frequency components associated with thermogenic functions of the autonomic nervous system (ANS) (21, 22). The root mean square value of R-R interval was calculated as representing the average am
plitude. After passing through the Hamming-type data window, power spectral analysis by means of a fast Fourier transform was then performed on consecutive 512-s time series of R-R interval data obtained during the test. To evaluate ANS activity in each subject of the
present study, we analyzed very low frequency (0.007- 0.035Hz, VLO), low frequency (0.035-0.15Hz, LO), high vagal component (0.15-0.5Hz, HI) and total
power (0.007-0.5Hz, TOTAL) by integrating the spectrum for the respective band width. Since our previous studies (21, 22) have shown that VLO frequency component reflects the SNS activity related to energy metabolic regulation, we defined VLO and VLO divided by TOTAL (VLO/TOTAL) as the absolute and relative thermogenic SNS activities, respectively (21). The mean heart rate of each 512-s segment was also calculated together with standard deviation.
It has been shown that physiological factors such as age might influence HRV (30). No significant difference was, however, found in physical characteristics or clinical features between the lean and obese groups, except for body weight and body fat content, which are associated with an obese state. Thus, the components of HRV spectral analysis were not normalized with any of the physiological parameters in the present study.
Calculation of energy expenditure. Energy expendi
ture (EE) was determined from the oxygen (02) con
sumption and respiratory quotient (RO) calculated as
the ratio of carbon dioxide (CO2) produced to 02 con
sumed by using the formula: EE (kcal. min-1)=
{ 4.686+[(RQ-0.707)•€0.293]•~0.361}XVO2, where
4.686 kcal•EL-1 is the energy value of 1 liter 02 at a
nonprotein RO of 0.70 7; RQ is the measured respiratory
quotient; 0.707 is the RQ when only fat is oxidized;
0.293 is the difference between the RO for carbohydrate
and fat oxidation; 0.361 is the difference in energy
value of a liter of oxygen between an RO of 1 and that of
0.707; and VO2 (L•Emin-1) is the rate of oxygen con
sumption at STPD conditions (31). Energy expenditure
expressed as kcal•Emin-1 was then converted to that as
kJ•Eday-1(1 kcal=4.2kJ).
Statistical analyses. All statistical analyses were per
formed using a commercial software package (SPSS ver
sion 7.5 for Windows, SPSS inc., Illinois). Statistical dif
ferences between groups were assessed using Student's
unpaired t-test. A paired t-test was performed to com
pare before and after food ingestion within a respective
group. p values <0.05 were considered to be statisti
cally significant. Data are expressed as mean•}SE.
RESULTS
Figure 1 represents typical sets of raw R-R interval
and the corresponding power spectral data obtained
from the control and obese subjects, respectively, during
the resting and postprandial conditions. R-R variability
and frequency components in the power spectra did not
seem to differ in the obese and the control subjects dur
ing the resting condition. After the ingestion of the cap
saicin diet, the VLO frequency component related to the
thermogenic SNS activity predominantly increased in
Fig. 1. Examples of ECG R-R interval changes and the corresponding power spectra for a control subject and an obese subject'during the resting and after the capsaicin diet.
312 MATSUMOTO T et al.
Fig. 2. Comparison of TOTAL power, very low (VLO) and low (LO) frequency components, and VLO/TOTAL between
preprandial and postprandial conditions, in the control and the obese groups, respectively. Results are expressed as
mean•}SE for each group. * p<0.05, ** p<0.01.
the control group; whereas, this VLO frequency compo
nent remained unchanged in the obese subjects.
Figure 2 represents group data with respect to the
R-R spectral parameters (TOTAL, VLO, LO, and VLO/
TOTAL) obtained from 8 control and 8 obese subjects
during the resting and postprandial conditions. TOTAL,
VLO and LO tended to be lower in the obese group com
pared to the control group during the resting condition;
however, no significant difference was found in any of
the parameters of HR variability (TOTAL, VLO, LO, HI
and VLO/TOTAL) between the control and obese
groups.
After the capsaicin diet, heart rate increased signifi
cantly both in the control (57•}3.3 to 62•}3.5 bpm,
p<0.01) and the obese groups (67•}2.8 to 72•}2.8
bpm, p<0.01). HI frequency component related to PNS
activity did not show any significant change in either
group. As Fig. 2 shows, the control group demonstrated
a significant increase in TOTAL (2,896.8•}8 51.7 to
3,547.4•}988.1 ms2, p<0.05), VLO (445.6•}188.0 to
814.8•}211.7 ms2, p<0.01), LO (611.1•}149.1 to
894.0•}174.8 ms2, p<0.01) and VLO/TOTAL (0.17•}
0.05 vs. 0.26•}0.03, p<0.05) after the diet. These find
ings suggest that capsaicin enhances the global ANS
activity, which may be predominantly attributable to
the significant increase in the thermogenic sympathetic
nerve activities. In the obese group, however, these four
parameters did not significantly increase in response to
the capsaicin diet. Moreover, during the postprandial
condition, the obese group demonstrated significantly
lower TOTAL (1,563.4•}269.6 vs. 3,547.4•}988.1
ms2, p<0.05), VLO (315.8•}78.0 vs. 814.8•}211.7
ms2, p<0.05) and LO (419.7•}61.5vs. 894.0•}174.8
ms2, p<0.05) frequency components as well as
markedly reduced responsiveness in the VLO frequency
component (delta changes from resting to postprandial
conditions: 14.6•}104.4vs. 3 69.2•}121.7ms2, p<
0.05) as compared to the control group.
Energy expenditure was significantly increased in the
control group after the capsaicin diet (5,574.7•}221.2
to 6,114.7•}239.0 kJ•Eday-1; p<0.01); however, no
such significant thermogenic change was found in
the obese group during the postprandial condition
(6,191.8•}274.3 to 6,531.8•}337.3kJ day-l; NS). RO
tended to increase in the control group after the cap
saicin diet; however no significant difference was de
tected in RO between the resting and postprandial con
ditions in the two groups.
DISCUSSION
The present study provides new information regard
ing physiological effects of capsaicin on the SNS activity
and diet-induced thermogenesis in lean and obese
young women. Our data demonstrate that despite the
nearly identical resting sympatho-vagal activities, obese
young women possess much reduced sympathetic re
sponsiveness to capsaicin-containing spicy food, as well
as a lower capacity to enhance energy metabolism after
food ingestion.
It has been shown that the thermogenic action of
capsaicin on energy metabolism is neurophysiologically
modulated. Briefly, capsaicin stimulates primary affer
ent neurons (32), which are transmitted to the spinal
cord. Adrenal sympathetic efferent nerve activity is
Effects of Capsaicin on Autonomic Nervous System and Thermogenesis in Women 313
then enhanced through the excitation of the central
nervous system, which causes marked catecholamine
secretion from the adrenal medulla (5, 33). Pharma
cological blockade experiments have suggested that cat
echolamines secreted into the blood react with ƒÀ-adren
ergic receptors in peripheral organs, which enhance en
ergy metabolism and consequently increase body heat
production (3, 6, 33).
In the present study, we used HRV power spectral
analysis in order to investigate the enhancing effect of
capsaicin on the SNS activity in lean and obese young
women. In contrast with other techniques such as cate
cholamine assay and microneurography, measurement
of the HRV integrates pre-synaptic and post-synaptic
end-organ response, thus providing a more comprehen
sive quantitative and qualitative evaluation of neuro
autonomic function. Concerning the thermogenic com
ponent of the SNS activity, Landsberg and Young (34)
demonsssssrated that catecholamine turnover within car
diac tissue fluctuated with thermogenic stimulation
such as cold exposure, fasting and overfeeding. This
finding indicates that the cardiac SNS activity could
precisely reflect autonomic events that affect energy
metabolism elsewhere in the body. A recent study has
shown that metabolic changes after glucose ingestion
are associated with a predominant sympathetic activity
in cardiac sympatho-vagal balance evaluated by HRV
spectral analysis (24). In their study, the validity of HRV
spectral analysis was confirmed by the measurement of
plasma catecholamine concentration: a strong positive
correlation was found between changes of HRV and
plasma norepinephrine concentration in response to
glucose ingestion. We have recently conducted a phar
macological experiment to explore further the relation
ship between HRV and thermoregulation and have
found that complete autonomic blockade causes the
abolishment of heart rate fluctuations and significant
reduction of energy expenditure (11, 21, 22). Further
more, we have identified the VLO frequency component
and have demonstrated that this frequency component
of HRV selectively increased against external thermo
genic perturbation such as acute cold exposure and
food intake in non-obese healthy volunteers (21, 22).
With all these facts taken into account, the VLO fre
quency component is thought to reflect more precisely
the SNS activity modulating energy metabolism and
possibly the sympatho-thermogenic effect of capsaicin
in humans.
By applying this analysis procedure in the present
study, we provide evidence of significant differences in
thermogenic sympathetic response to a capsaicin diet
and energy metabolism after the meal among lean and
obese young women. In lean women, the ANS, espe
cially the thermogenic component of the SNS activity,
significantly increased immediately after the capsaicin
diet. Energy expenditure was also significantly en
hanced 30min after the meal in this group. These re
sults are consistent with the findings of previous animal
and human studies. Watanabe et al. (5) reported that
intravenous administration of capsaicin in rats caused a
rapid and marked increase in adrenal sympathetic nerve activity followed by the significant increase in adrenal epinephrine secretion. Oxygen consumption began to increase almost immediately after the rats had been injected with capsaicin and reached the maximal level within 20-30 min (3). In humans, Henry and Emery (35) reported that spiced food containing chilli and mustard sauces caused a 44% increase in the energy expenditure 15min after the meal. According to a recent study of Lim et al. (28), both catecholamine concentration and energy expenditure increased 30min after non-obese healthy young males had taken a meal with 10g of hot red pepper. Thus, these findings including our data confirm that capsaicin has a strong acute sympatho-thermogenic effect on non-obese individuals.
In contrast, this effect of capsaicin was not detected in the obese young women in the present study: thermogenic SNS activity as well as its responsiveness after the capsaicin diet was markedly reduced in the obese subjects despite the similar level of ANS activity of the lean subjects at rest. Concerning energy expenditure after the meal, no significant increase was found in the obese group although lean body mass was almost identical to that in the control group.
It has been shown that neonatal (5) and adult (33) capsaicin pretreatment inhibited capsaicin-induced adrenal catecholamine secretion in anesthetized rats. According to the results of the health questionnaire, however, our subjects did not have a long-term dietary history of eating spices such as chilli or hot red peppers. Prior to participation in this study, some of them re
ported a strong distaste for extremely spicy foods, preferring instead, mildly spicy food. Thus, we assume that daily dietary habit or taste sensitivity to capsaicin did not affect the data obtained in the present investigation. Reduced sympathetic response to food ingestion has
been reported in previous studies. Bazelmans et al. (23) reported a decreased stimulation of norepinephrine ap
pearance in obese subjects in response to overfeeding. Spraul et al. (25) have also found a negative correlation between the percentage of body fat and the increase in the muscle sympathetic nerve activity (MSNA) in response to glucose ingestion while fasting; MSNA correlated positively with body fat. A previous study of Paolisso et al. (24) using HRV spectral analysis has shown that the rise in the sympathetic nerve activity after glucose ingestion negatively correlated with body fat content, whereas it positively correlated with glucose-induced thermogenesis and glucose uptake. Recent research in our laboratory (22) has demonstrated that the VLO frequency component of HRV was markedly reduced in obese young women after mixedfood ingestion. The methodology such as experimental designs, selection of subjects and measurements for ANS are not always the same as that used in the present study; however, our findings support these previous investigations and reinforce the finding that the altered specific sympathetic function related to thermogenic capacity may be a significant sign reflecting the autonomic state in human obesity.
314 MATSUMOTO T et al.
In conclusion, we examined the effect of capsaicin on
the SNS activity and energy metabolism in age and
height-matched lean and obese young women. The un
derlying physiological mechanism of SNS activity mod
ulating energy metabolism and its association with obe
sity remains elusive in humans. Results found in the
present study, however, indicate that regardless of the
resting level of the ANS activity, the reduced sympa
thetic responsiveness to thermogenic perturbation such
as that found in the capsaicin diet, which may cause
impaired diet-induced thermogenesis and further
weight gain, could be an important etiological factor
leading to obesity in young women.
REFERENCES
1) Suzuki T, Iwai K. 1984. Constituents of red pepper
spices: Chemistry, biochemistry, pharmacology, and
food science of the pungent principle of Capsicum
species. In: The Alkaloids (Brossi A, ed), Academic
Press, New York, Vol 23, p 227-229.
2) Kawada T, Hagihara K, Iwai K. 1986. Effects of cap
saicin on lipid metabolism in rats fed a high fat diet. J
Nutr 116: 1272-1278.
3) Kawada T, Watanabe T, Takaishi T, Tanaka T, Iwai K.
1986. Capsaicin-induced ƒÀ-adrenergic action on en
ergy metabolism in rats: Influence of capsaicin on oxy
gen consumption, the respiratory quotient, and sub
strate utilization. Proc Soc Exp Biol Med 183: 250-256.
4) Watanabe T, Kawada T, Iwai K.1987. Enhancement by
capsaicin of energy metabolism in rats through secre
tion of catecholamine from adrenal medulla. Agric Biol
Chem 51: 75-79.
5) Watanabe T, Kawada T, Kurosawa M, Sato A, Iwai K.
1988. Adrenal sympathetic efferent nerve and cate
cholamine secretion excitation caused by capsaicin in
rats. Am J Physiol 255: E23-E27.
6) Yoshioka M, Lim K, Kikuzato S, Kiyonaga A, Tanaka H,
Shindo M, Suzuki M. 1995. Effects of red-pepper diet on
the energy metabolism in men. J Nutr Sci Vitaminol 41:
647-656.
7) Bray GA. 1986. Autonomic and endocrine factors in
the regulation of energy balance. Fed Proc 45:
1404-1410.
8) Bray GA. 1991. Obesity, a disorder of nutrient parti
tioning: The MONA LISA Hypothesis. J Nutr 121:
1146-1162.
9) Macdonald IA. 199 5. Advances in our understanding
of the role of the sympathetic nervous system in obesity.
Int J Obes 19 (Supple 7): S2-S7.
10) Young JB, Macdonald IA. 1992. Sympathoadrenal ac
tivity in human obesity: heterogeneity of findings since
1980. Int J Obes 16: 959-967.
11) Hayashi T, Masuda I, Shinohara M, Moritani T, Nakao
K. 1994. Autonomic nerve activity during physical ex
ercise and postural change: investigations by power
spectral analysis of heart rate variability. Jpn J Biochem
Exerc 6: 30-37.
12) Moritani T, Hayashi T, Shinohara M, Mimasa F, Shibata
M. 1993. Comparison of sympatho-vagal function
among diabetic patients, normal controls and en
durance athletes by heart rate spectral analysis. J Sports
Med Sei 7: 31-39.
13) Moritani T, Hayashi T, Shinohara M, Mimasa F, Masuda
I, Nakao K. 1995. Sympatho-vagal activities of NIDDM
patients during exercise as determined by heart rate spectral analysis. In: Glucose Fluxes, Exercise and Diabetes (Kawamori R, Vranic M, Horton ES, Kubota M, eds), Smith-Gordon, London, p 91-96.
14) Oida E, Moritani T, Yamori Y. 1997. Tone-entropy analysis on cardiac recovery after dynamic exercise. I Appl Phsiol 82: 1794-1801.
15) Yamamoto Y, Hughson RL, Peterson JC. 1991. Autonomic control of heart rate during exercise studied by heart rate variability spectral analysis. J Appl Phsiol
71: 1136-1142.16) Akselrod S, Gordon D, Ubel FA, Shannon DC, Barger
AC, Cohen RJ.1981. Power spectrum analysis of heart rate fluctuation: a quantitative probe of beat-to-beat cardiovascular control. Science 213: 220-222.
17) Akselrod S, Gordon D, Madwed JB, Snidman NC, Shannon DC, Cohen RJ. 1985. Hemodynamic regula tion: investigation by spectral analysis. Am J Physiol 249: H867-H875.
18) Pagani M, Lombardi F, Guzzetti S, Rimoldi O, Furlan R, Pizzinelli P, Sandrone G, Malfatto G, Dell'Orto S, Piccaluga E, Turiel M, Baselli G, Cerutti S, Malliani A. 1986. Power spectral analysis of heart rate and arterial
pressure variabilities as a marker of sympatho-vagal in teraction in man and conscious dog. Circ Res 59: 178-193.
19) Hyndman BW, Kitney RI, Sayers BM. 1971. Spontaneous rhythms in physiological control systems. Nature 233: 339-341.
20) Kitney RI. 1975. Entrainment of the human RR inter val by thermal stimuli. J Physiol Lond 252: 37P-38P.
21) Matsumoto T, Miyawaki T, Ue H, Kanda T, Zenji C, Moritani T. 1999. Autonomic responsiveness to acute cold exposure in obese and non-obese young women. Int J Obes 23: 793-800.
22) Moritani T, Matsumoto T. 1998. Comparison of auto nomic responsiveness, plasma leptin concentration,
and energy metabolism in obese and non-obese young women. In: Proceedings of the third annual congress of the European college of sports science (Sargeant AJ, Siddons H, eds), Health Care Development: Liverpool,
p158.23) Bazelmans J, Nestel PT, O'Dea K, Esler MD. 1985.
Blunted norepinephrine responsiveness to changing energy states in obese subjects. Metabolism 34: 154-159.
24) Paolisso G, Manzella D, Ferrara N, Gambardella A, Abete P, Tagliamonte MR, DeLucia D, Furgi G, Picone C, Gentile S, Rengo F, Varricchio M. 1997. Glucose inges
tion affects cardiac ANS in healthy subjects with different amounts of body fat. Am J Physiol 273: E471-E478.
25) Spraul M, Anderson EA, Bogardus C, Ravussin E. 1994. Muscle sympathetic nerve activity in response to glucose ingestion: Impact of plasma insulin and body fat. Diabetes 43: 191-196.
26) Segal KR, Edano A, Blando L, Pi-Sunyer FX. 1990. Comparison of thermic effects of constant and relative caloric loads in lean and obese men. Am J Clin Nutr 51: 14-21.
27) Yoshioka M, St-Pierre S, Suzuki M, Tremblay A. 1998. Effects of red pepper added to high-fat and high-carbo
hydrate meals on energy metabolism and substrate utilization in Japanese women. Br J Nutr 80; 503-510.
28) Lim K, Yoshioka M, Kikuzato S, Kiyonaga A, Tanaka H,
Effects of Capsaicin on Autonomic Nervous System and Thermogenesis in Women 315
Shindo M. Suzuki M. 1997. Dietary red pepper inges tion increases carbohydrate oxidation at rest and dur ing exercise in runners. Med Sci Sports Exerc 29: 355-361.
29) Rompeleman O, Coenen AJR, Kitney RI 1977. Measurement of heart-rate variability: part 1-com
parative study of heart-rate variability analysis methods. Med Biol Eng Comput 15: 233-239.
30) Conny MA, Louis AA, Jeroen CW, Gerard BA, Herman P. 1993. Heart rate variability. Ann Intern Med 118: 436-447.
31) Ravussin E, Schutz Y, Acheson KJ, Dusmet M, Bourquin L, Jequier E. 1985. Short-term, mixed-diet overfeeding in man: no evidence for "luxuskonsumption". Am J
Physiol 249: E470-E477.32) Longhurst JC, Kaufman MP, Ordway GA, Musch TI.
1984. Effects of bradykinin and capsaicin on endings of afferent fibers from abdominal visceral organs. Am J Physiol 247: R552-R559.
33) Watanabe T, Kawada T, Kurosawa M, Sato A, Iwai K. 1991. Thermogenic action of capsaicin and its analogs. In: Obesity: Factors and Controls (Romsos DR, Himms
Hagen J, Suzuki M, eds), Karger AG, Basel, p6 7-77.34) Landsberg L, Young JB. 1978. Fasting, feeding and reg
ulation of the sympathetic nervous system. N Engl J Med 298: 1295-1301.
35) Henry CJK, Emery B. 1986. Effect of spiced food on metabolic rate. Hum Nutr Clin Nutr 40C: 165-168.