Abstract Objective

To investigate the mechanism of gastric motility suppression by exposure to whole-body vibration (WBV). Methods: The gastric motility was evaluated by electrogastrography (EGG) under food intake and autonomic nerve blocking agents in ten

healthy volunteers. Sinusoidal vertical vibration with a frequency of 4 Hz (1.0 ms A2rms) was given to the sub-

ject for 10 min. Results: The amplitude of EGG wave

and the power spectrum corresponding to the slow wave

component was remarkably decreased by vibration exposure. Food intake enhanced the gastric motility about

2.5-fold in the power spectral density. During and after

vibration exposure, the response mode was similar to

those at fasting states. Under the influence of anticholinergic (scopolamine) and alphaadrenergic blocking agents (prazosin), the power spectra were decreased. A further decrease was observed during vibration exposure. A betadrenergic blocking agent (propranolol) led to a marked increase in the amplitude of EGG and its power spectrum. With pretreatment by a beta-adrenergic blocking agent, however, vibration exposure reduced both of them. Conclusions: These results suggest that short-term exposure to WBV can suppress the gastric myoelectric activity, the responses on which may be mediating by neurohumoral e€ects as well as the mechanical e€ect of WBV. Key words Electrogastrography (EGG) á Food intake á Gastric motility á Whole-body vibration

Introduction

An increased prevalence of gastrointestinal symptoms in

workers with whole-body vibration (WBV) exposure has

been reported in some epidemiological studies (Seidel and Heide 1986; Miyashita et al. 1992). It is an interesting problem whether exposure to WBV is a speci(r)c

risk factor for gastric disorders such as gastric neurosis

and nonulcerative dyspepsia. These are functional disorders associated with abnormalities of gastric motility (Talley et al. 1994). Although there are a few experimental studies on acute exposure to WBV concerning the human gastric motility in healthy subjects, the (r)ndings have been inconsistent (Kjellberg and WikstroÈm 1987; Ishitake et al. 1998). The responses of the gastric motility to WBV exposure remain unclear. The gastric slow motion, namely peristalsis, originates from the corpus of the stomach and propagates

through the longitudinal muscle (r)bers to the pylorus. Cutaneous electrogastrography (EGG) measures the

electric activity of gastric smooth muscles and also is a

potentially useful and noninvasive technique for evaluating the gastric motility. Physiologically, the gastric electric activity consists of the pacemaker potential (electric control activity) and the spike potential (electric response activity) (Guyton 1991). The spike potentials by the contraction of muscles of the antrum are superimposed on the pacemaker potential in a cutaneous EGG measurement. The indices of the frequency components and their power spectra provide reliable information about the gastric motility. The human gastric signals are divided into three components: bradygastri (0.5±2.0 cpm), slow wave (2.0±5.0 cpm), and tachygastria (5.0±9.0 cpm) (Chen and McCallum 1993).

In particular, the change of the power density in the slow

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.

Int Arch Occup Environ Health (1999) 72: 469±474

Ã" Springer-Verlag 1999, T. Ishitake (8) á Y. Miyazaki á H. Ando á T. Matoba Department of Environmental Medicine,

Kurume University School of Medicine, 67 Asahi-machi, Kurume 830-0011, Japan e-mail: tishitak@med.kurume-u.ac.jp Fax: +81-942-314370

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