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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 e€ects 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 di€erent 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. Di€erences 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 di€erent 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 di€erent 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 di€erent 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 e€ect 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 e€ects 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 axed 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 di€erent 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 di€erence between our ®ndings and Table 1 E€ect 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) ± à Р85.1 (70.8, 86.9) 19.0 (15.1, 27.1) ± à Р10.3 (5.8, 18.0) 100.0 Ð Ã ÐÐÐÐÐ 255.6 (130.5, 363.0) ± à 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 di€erent 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 e€ect on the suppressive e€ect 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 a€ected (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 WBV reaches a maximum around resonance frequencies Guyton A (1991) Textbook of medical physiology. 8th edn.
and produces some excitatory e€ects on gastric motility and secretion. Although no subject complained of dis- Imai K, Chihara E, Ishimuaru K, Iwa M, Ikeda K, Sakita M (1998) E€ect of atropine sulfate and neostigmine on electrogastro- comfort during WBV exposure in the present study, we grams in normal volunteers (in Japanese). Auton Nerv Syst 35: should consider the e€ect of the resonance frequency on gastric motility, which the biodynamic transmission of Ishitake T, Kano M, Miyazaki Y, Ando H, Tsutsumi A, Matoba T vibrations depends on. In conclusion, acute exposure to (1998) Whole-body vibration suppresses gastric motility in WBV may suppress the activity of contractile smooth Jebbink H, Van Berge-Henegouwen G, Bruijs P, Akkermans L, muscle. The responses may be mediated by neurohu- Smout A (1995) Gastric myoelectrical activity and gastrointes- moral e€ects as well as the mechanical e€ect.
tinal motility in patients with functional dyspepsia. Eur J Clin Kjellberg A, WikstroÈm BO (1987) Acute e€ects of whole-body vi- bration: stabilography and electrogastrography. Scand J Work Levanon D, Zhang M, Orr W, Chen J (1998) E€ects of meal vol- Chen J, McCallum RW (1991) Response of the electric activity in ume and composition on gastric myoelectrical activity. Am J the human stomach to water and a solid meal. Med Biol Eng Miyashita K, Morioka I, Tanabe T, Iwata H, Takeda S (1992) Chen J, McCallum RW (1993) Clinical applications of electrogas- Symptoms of construction workers exposed to whole body vi- trography. Am J Gastroenterol 88: 1324±1336 bration and local vibration. Int Arch Occup Environ Health 64: Chen J, Richards RD, McCallum RW (1994) Identi®cation of gastric contractions from the cutaneous electrogastrogram. Am Parkman H, Miller M, Trate D, Knight L, Urbain JL, Maurer A, Fisher R (1997) Electrogastrography and gastric emptying Cucchiara S, Riezzo G, Minella R, Pezzolla F, Giorgio I, Auricchio scintigraphy are complementary for assessment of dyspepsia.
S (1992) Electrogastrography in non-ulcer dyspepsia. Arch Dis Parkman H, Urbain J, Knight L, Brown K, Trate D, Miller M, Dupuis H, Christ W (1966) UÈber das Schwingungsverhalten des Maurer A, Fisher R (1998) E€ect of gastric acid suppressants Magens unter dem Ein¯uss sinusfoÈrmiger und Stochastischer on human gastric motility. Gut 42: 243±250 schwingungen. Int Z Angew Physiol Einschl Arbeitsphysiol 22: Seidel H, Heide R (1986) Long-term e€ects of whole-body vibra- tion: a critical survey of the literature. Int Arch Occup Environ Dupuis H, Zerlett G (1986) The e€ects of whole-body vibration.
Springer, Berlin Heidelberg New York, pp 39±44 Smout A, Van der Schee EJ, Grashuis JL (1980) What is measured Geldof H, Van der Schee EJ, Van Blankenstein M, Grashuis JL in electrogastrography? Dig Dis Sci 25: 179±187 (1987) Electrogastrographic study of gastric myoelectrical ac- Sun V, Smout A, Malbert C, Edelbroek M, Jones K, Dent J, tivity in patients with unexplained nausea and vomiting. Gut Horowitz M (1995) Relationship between surface electrogas- trography and antropyloric pressures. Am J Physiol 268: G424± Goodman Gilman A, Rall T, Nies A, Taylor P (1990) Goodman and Gilman's The pharmacological basis of therapeutics, 8th Talley N, et al (1994) The functional gastroduodenal disorders.

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