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: moritani@virgo.jinkan.kyoto-u.ac.jp

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.

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