Int Arch Occup Environ Health (1999) 72: 469±474
T. Ishitake á Y. Miyazaki á H. Ando á T. MatobaSuppressive mechanism of gastric motility by whole-body vibration
Received: 7 September 1998 / Accepted: 9 May 1999
Abstract Objective: To investigate the mechanism of
gastric motility suppression by exposure to whole-body Introduction
vibration (WBV). Methods: The gastric motility was
evaluated by electrogastrography (EGG) under food An increased prevalence of gastrointestinal symptoms in
intake and autonomic nerve blocking agents in ten workers with whole-body vibration (WBV) exposure has
healthy volunteers. Sinusoidal vertical vibration with a been reported in some epidemiological studies (Seidel
frequency of 4 Hz (1.0 msA2 rms) was given to the sub- and Heide 1986; Miyashita et al. 1992). It is an inter-
ject for 10 min. Results: The amplitude of EGG wave esting problem whether exposure to WBV is a speci®c
and the power spectrum corresponding to the slow wave risk factor for gastric disorders such as gastric neurosis
component was remarkably decreased by vibration ex- and nonulcerative dyspepsia. These are functional dis-
posure. Food intake enhanced the gastric motility about orders associated with abnormalities of gastric motility
2.5-fold in the power spectral density. During and after (Talley et al. 1994). Although there are a few experi-
vibration exposure, the response mode was similar to mental studies on acute exposure to WBV concerning
those at fasting states. Under the in¯uence of anticho- the human gastric motility in healthy subjects, the
linergic (scopolamine) and alpha-adrenergic blocking ®ndings have been inconsistent (Kjellberg and WikstroÈm
agents (prazosin), the power spectra were decreased. A 1987; Ishitake et al. 1998). The responses of the gastric
further decrease was observed during vibration expo- motility to WBV exposure remain unclear.
sure. A beta-adrenergic blocking agent (propranolol) led
The gastric slow motion, namely peristalsis, origi-
to a marked increase in the amplitude of EGG and its nates from the corpus of the stomach and propagates
power spectrum. With pretreatment by a beta-adrener- through the longitudinal muscle ®bers to the pylorus.
gic blocking agent, however, vibration exposure reduced Cutaneous electrogastrography (EGG) measures the
both of them. Conclusions: These results suggest that electric activity of gastric smooth muscles and also is a
short-term exposure to WBV can suppress the gastric potentially useful and noninvasive technique for evalu-
myoelectric activity, the responses on which may be ating the gastric motility. Physiologically, the gastric
mediating by neurohumoral eects as well as the me- electric activity consists of the pacemaker potential
(electric control activity) and the spike potential (electric
response activity) (Guyton 1991). The spike potentials
Key words Electrogastrography (EGG) á Food intake á
by the contraction of muscles of the antrum are super-
imposed on the pacemaker potential in a cutaneous
EGG measurement. The indices of the frequency com-
ponents and their power spectra provide reliable infor-
mation about the gastric motility. The human gastric
signals are divided into three components: bradygastria
(0.5±2.0 cpm), slow wave (2.0±5.0 cpm), and tachyga-
stria (5.0±9.0 cpm) (Chen and McCallum 1993). In
particular, the change of the power density in the slow
T. Ishitake (8) á Y. Miyazaki á H. Ando á T. Matoba
wave component may re¯ect the contractile activity of
the stomach (Smout et al. 1980; Chen et al. 1994). The
EGG has been widely used as a diagnostic method for
functional disorders associated with abnormalities of the
gastric motility (Geldof et al. 1987; Cucchiara et al.
1992; Jebbink et al. 1995; Parkman et al. 1997). In our Statistics
recent experiments, brief exposure to WBV suppressed
the slow wave component (Ishitake et al. 1998). The aim Data are expressed as medians (25%, 75%) because of the lack of
normality in the distribution. The data of dierent recording pe-
of this study was to clarify the possible mechanism of the riods for vibration exposure in the same subject were statistically
gastric motility suppressed by short-term exposure to compared using the Wilcoxon signed-rank test. Dierences were
considered to be signi®cant at P < 0.05.
Figure 1 shows a representative example of EGG
Ten male healthy volunteers participated in this study. They had no
waveform and its power spectrum at fasting state at the
history of relevant disorders of the gastrointestinal tract, including
dierent recording periods before, during, and after
problems of digestion. The mean age was 22.4 1.7 (SD) years
vibration exposure. Before vibration, two peaks in the
(range 21±26 years) and the mean body mass index was 24.0 2.6
(SD) (range 20.5±28.7). Prior to the study, the experimental pro-
power spectral density were observed. The major com-
cedures were carefully explained to all the subjects, and informed
ponent was around 3 cpm in frequency, the so-called
written consent was obtained from them. The subjects were asked
slow wave component. The small and fast wave com-
not to eat and drink after a regular lunch. The mean fasting time
ponent was the frequency of 5±9 cpm, so-called
was 4 h. The EGG was continuously recorded before, during and
after vibration exposure for 10 min in each subject. Each subject
tachygastria. All subjects showed a dominant slow wave
was tested in two stomach conditions: in fasting state and ®lled
component with the frequency of 2±5 cpm. During
with a regular solid meal (80 g, 135 cm3).
vibration exposure, the amplitude of EGG waveform
These experimental procedures were carried out on dierent
of both components was associated with a remarkable
days for each subject. Three agents for autonomic nerve blocking
(scopolamine butylbromide 10 mg; prazosin hydrochloride 1 mg;
decrease of power spectrum. When vibration exposure
propranolol hydrochloride 20 mg) were administered orally to two
ceased, the amplitudes of EGG and its power spectrum
subjects each on dierent experimental days. Sixty minutes after the
around the slow wave markedly increased.
administration, exposure to WBV was commenced.
A modi®cation of the gastric motility under the in-
During the experiments, the noise level induced by the elec-
¯uence of food intake and vibration exposure was ob-
tromagnetic shaker was 64±66 dB(A). The ambient temperature
served (Fig. 2). Food intake enhanced the gastric
motility, showing a dominant increase of the amplitude
in EGG waveform and the slow wave of its power
spectral density. During and after vibration exposure,
The subjects were asked to sit on a hard ¯at seat without a back-
the response modes were similar to those at fasting state.
rest. Each individual subject chose a comfortable posture. The vi-
However, the responses due to vibration exposure were
bration stimulus was produced by using an electromagnetic shaker
larger than those at fasting state. Table 1 summarized
(ASE-385; Akashi, Japan). A sinusoidal vibration with a frequency
the eect of WBV on EGG at the conditions of fasting
of 4 Hz and an acceleration magnitude of 1.0 msA2 (rms) was ap-
and food intake. At both conditions, the relative powers
(%) of the controls were almost same. Food intake
produced a signi®cant increase in the relative power of
the slow wave and a signi®cant decrease of the
After gentle abrasion of the skin to enhance the electrical con-
tachygastria component. The total power of EGG in-
duction, two disposable Ag/AgCl electrodes (Vitrode, Nihon Ko-
creased about 2.5 times (median). After food intake, the
hden, Japan), 6 cm apart horizontally, were placed half way
eects of vibration exposure were almost the same as in
between the xiphoid and the umbilicus. A reference electrode was
the fasting state. During vibration exposure, the relative
axed to the right upper quadrant of the abdomen. The EGG
signals were ampli®ed with a pre-ampli®er (AB621-G, Nihon Ko-
power of tachygastria in the fasting state was signi®-
hden, Japan). The time constant was 5 s. The high-frequency cuto
cantly greater than in the food intake condition. In
was set at 0.2 Hz to minimize interference from nongastric signals.
contrast, the relative power of the slow wave at fasting
The EGG signals were simultaneously digitized at 2 Hz by an
state was signi®cantly smaller as compared to that at
analog-to-digital converter and ®ltered to remove noises of fre-
quency more than 9 cycles/min (cpm) and less than 0.9 cpm.
Figure 3 shows typical responses to WBV exposure
under the in¯uence of various drugs. Pretreatment with
an anticholinergic (scopolamine) and with an alpha-
adrenergic blocking agent (prazosin) resulted in a decrease
The frequency analysis of EGG was done using fast Fourier
transform (FFT). Power spectrum was calculated every 10 min at
in the power spectra. In contrast, a remarkable increase in
dierent recording periods. Two EGG parameters were used for
the power spectrum was observed after the administration
evaluation: (1) the dominant frequency of the EGG, which may
of a beta-adrenergic blocking agent (propranolol). Under
indicate a peak frequency; (2) the relative powers (%) of the slow
the in¯uence of these drugs, the exposure to WBV caused
wave component (2±5 cpm) and tachygastria component (5±9 cpm)
were divided by the sum of the powers from 0.9 to 9 cpm. Com-
a decrease in both components of the power spectrum
ponents of slow wave and tachygastria were expressed as a per-
following food intake. After exposure, the responses were
almost the same in the three drug conditions.
(Smout et al. 1980). Even a higher WBV frequency with
short-term exposure (10 Hz, 5 min) reduced the power
density of the slow wave component (Ishitake et al.
Brief exposure to WBV (4 Hz, 10 min) can reduce the 1998). Kjellberg and WikstroÈm (1987), however, ob-
power spectral density of the slow wave component of served a biphasic phenomenon with an initial increase
EGG, suggesting suppression of the gastric motility and thereafter a gradual decrease in the power density
with the frequencies of 3, 5.4 and 7.8 cpm by WBV of
Fig. 2 The changes of EGG (A) and their power spectra (B) under
the in¯uence of food intake and acute exposure to whole-body
3 Hz. They suggested that the gastric motility was af-
fected by WBV. The dierence between our ®ndings and
Table 1 Eect of whole-body vibration on EGG in fasting state and following food intake. Relative power indicates the proportion of
total power comprised by each component. Total power is calculated as a percentage of the control. The values are medians (25%, 75%)
73.2 (64.0, 78.7) ± Ã Ð 85.1 (70.8, 86.9)
19.0 (15.1, 27.1) ± Ã Ð 10.3 (5.8, 18.0)
100.0 Ð Ã ÐÐÐÐÐ 255.6 (130.5, 363.0) ± Ã Ð192.0 (105.0, 332.0) ± ÃÐ 253.6 (137.0, 354.0)
theirs may depend on the experimental conditions of the agent can suppress the activity of muscle contraction.
stomach contents, with or without food intake. An in- An alpha-adrenergic blocking agent may suppress the
crease in the amplitude of EGG after eating has been contraction of pylorus ring, and also a beta-adrenergic
observed by many investigators (Chen and McCallum blocking agent would increase the muscle tone (Good-
1991; Levanon et al. 1998). Although they carried out man Gilman et al. 1990). These pharmacological actions
their experiments with no control of food intake or resulted in the suppression of the amplitude of EGG and
fasting time, these two factors were strictly controlled in its power spectra by the anticholinergic (Imai et al. 1998)
our experiment. There is a possibility of misinterpreta- and alpha-blocking agents, and the beta-blocking agent
tion because of confused data at dierent conditions of induced increases in the same parameters in the present
food intake. Possible artifacts such as body movements study.
and startle re¯ex should also be considered because there
Exposure to WBV produced a further reduction in
were no raw EGG waveform data in Kjellberg's report. the activity of the slow wave component following pre-
According to our preliminary study, some artifacts due treatment with these drugs. The reduction of slow wave
to body movement can actually produce an increase in component by vibration may be due to not only the
the power spectrum of the slow wave component.
autonomic nervous system but also humoral and me-
Food intake is, of course, a very important in¯uence chanical factors. As for the humoral factors, the control
on gastric motility. It is widely recognized that a good of the secretion of gastric juice is stimulated by gastrin
correlation is noted among increased amplitude, fre- and the parasympathetic nervous system. Gastrin re-
quency of slow wave and gastric contraction, resulting leased from the pyloric glands can enhance gastric
from the increase of the contractile activity due to eating motility and stimulate hydrochloric acid secretion.
(Sun et al. 1995). Similar responses modes were ob- Parasympathetic stimulation increases the secretion of
served during exposure to vibration under the conditions acid, mucus and pepsinogen by the action of acetyl-
of fasting state and food intake. The changes in relative choline. Tactile stimulation of the surface of the stomach
power of slow wave at the condition of food intake were mucosa can also in¯uence the gastric secretion. Expo-
greater than in the fasting state. It is suggested that a sure to WBV may have a mechanical eect on the
suppressive eect of vibration exposure on gastric mo- stomach wall, leading to increased gastric secretion
tility may be enhanced under the condition of food in- while gastric motility is not aected (Dupuis and Christ
1966). Suppression of the secretion of gastric acid by an
With respect to a mechanism suppressing gastric H2 receptor antagonist is associated with inhibition of
motility, we should consider the neurohumoral and gastric motility (Parkman et al. 1998). As there are few
mechanical factors which mainly regulate gastric motil- convincing data about a relationship between exposure
ity (Guyton 1991). The neural control is provided by the to WBV and gastric secretion, further investigations
autonomic nervous system, which includes both choli- should be carried out.
nergic and adrenergic nerve ®bers. Stimulation of the
The movement of organs are increased by WBV with
parasympathetic nerves leads to an increase in the ac- frequencies of 3±5 Hz and 7±10 Hz (Dupuis and Zerlett
tivity of the gastric motility. On the other hand, stimu- 1986). This suggests that passive gastric movement by
lation of the sympathetic nerves inhibits gastric motility.
The slow wave component may totally re¯ect the gastric
electrical activity, including the muscle tone and con-
tractile activities (Smout et al. 1980; Chen et al. 1994). Fig. 3 The changes of EGG (A) and their power spectra (B) under
drug intervention (1 anticholinergic agent, 2 alpha-blocking agent,
From the pharmacological viewpoint, an anticholinergic 3 beta-blocking agent) and exposure to whole-body vibration
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What Medicine Means To Me, Mens Sana Monographs, Vol. III:6, Vol. IV:1-4. CITATION: Malhotra S., Shafiq N. (2006), What Clinical Pharmacology Means To Us. In: What Medicine Means To Me (Ajai R. Singh, Shakuntala A. Singh Eds.), III:6, IV:1-4, p184-206. What Clinical Pharmacology Means To Us S. Malhotra* N. Shafiq** ABSTRACT Clinical Pharmacology is a specialty with many