The study was conducted in Neurophysiology Laboratory of Department of Basic and Clinical Physiology, BP Koirala Institute of Health Sciences (BPKIHS), Dharan (during 2011–2012). The study population included 30 healthy tailors (study group) and 30 healthy volunteers (control group). Average duration of occupation in the study group was more than 12 years. Subjects ranged in age from 18 to 60 years with average of 35 years. None of the subjects were suffering from any known neuromuscular or musculoskeletal diseases, cardiovascular diseases, and respiratory diseases and were not taking any drugs which affect nerve conduction study. Subjects from both study and control groups were not indulging in smoking or drinking. All the participants provided written informed consent that had been previously approved by the institutional ethical committee. The ethical approval for the study was obtained from the institutional ethical committee. Subjects who passed the initial screening based on clinical history or physical examination were selected for motor nerve conduction studies (MNCSs).

Prior to the study, all subjects were informed of the study procedure, purposes, and known risks and thereby obtained their informed consent. This study was conducted according to the guidelines of the Declaration of Helsinki and approved by the institutional ethical committee, BPKIHS, Dharan, Nepal. The sites of stimulation and recording of common peroneal nerve are shown in the (Table 1). The nerve tested was common peroneal nerve (both right and left). Digital Nihon Kohden Machine (NM-420S, H636, Japan) with its accessories was used for nerve conduction studies. The temperature of the recording room was kept around 26 ± 2 °C_. Anthropometric and cardio-respiratory parameters of the subjects were recorded as shown in the (Tables 2 and 3).

For motor nerve conduction study, the stimulator using adhesive tape was used for surface stimulation. It was placed on the skin overlying the nerve at two or more sites along the course of the nerve after cleaning the site with skin purifier. Before applying a brief pulse of current, ground electrode was placed between the stimulating and recording electrodes. The recording and reference electrode were placed using belly tendon montage with the recording electrode placed over the mid belly of the respective muscle, as close to the estimated end plate site as possible and the reference to the tendon at a minimum distance of 3 cm. The sites of stimulation and recording electrodes for common peroneal nerve are shown in (Table 1) and (Fig. 1) [16].

Stimulation of the nerve being studied was accomplished using a brief burst of direct electric current. The gain was set at 5 mv per division. Stimulation duration was in the range of 0.2 ms and the amount of current never exceeded more than 50 mA because it was the upper limit available in the machine. The current of the stimulator was initially set to zero, then gradually increased with successive stimuli. A compound muscle action potential (CMAP) appeared that grew larger with the increasing stimulus strength (Fig. 2). Current was increased to the point that CMAP no longer increased in size, from that point the current was increased by another 20% to ensure supra-maximal stimulation.

The SPSS package (Statistical Package for Social Sciences, Version-20, and Chicago, Illinois, USA) for personal computer was used for the statistical analysis. Shapiro-Wilk’s W test was applied to examine normality in the distribution of data. Results are presented as mean ± standard deviation (SD). The differences in variables between the groups were tested using Student’s t-test. A p ≤0.05 was considered significant.

Right and left common peroneal CMAP proximal and distal latencies were significantly high in study group in comparison to control group. Our results are quite in agreement with the result of Feinberg et al.[17]. According to their studies, there was increase in CMAP latency due to peripheral nerve injuries in some of hockey players, but in contrast with the study conducted by Budaket al. [18]. They found that there was decrease in CMAP latency in their studies of lower extremities in long distance runners. Also, our findings are in contrast with the studies conducted by several researchers [19, 20]. According to their studies there was positive effect of physical training on nerve conduction parameters. In another study, there was also decreased nerve conduction in the workers occupationally exposed to mechanical vibration [21]. Murata K et al. showed that there was effect of vibration in peripheral nervous system and found negative impact of vibration on nerve conduction in workers of vibrating tool industry [22]. Latency is a reflection of the activation pattern of individual neurons comprising the peripheral nerve. In the compound action potential produced in a nerve conduction test, the fastest arriving fibers (the most myelinated) determine the onset latency and hence the velocity of that nerve. Prolonged latencies reflect the dropout of faster myelinated fibers and result in slower nerve velocities [23, 24].

Our results showed that right and left common peroneal CMAP-Amplitude (proximal and distal) were found significantly low in the study group in comparison to control group. Our results are similar to the results of the study conducted by Chatterjee et al. [25]. They found that there was reduced CMAP-Amplitude in rock-drillers and reduced muscle mass as well. Although our findings are in contrast with the study ofRoss et al. [26]. They found positive effect of hypertrophied muscles on CMAP-Amplitude of peroneal nerves in long distance runners. Reduced nerve conduction amplitude in the presence of a normal nerve conduction velocity would indicate a dropout of smaller-diameter axons in the nerve, accounting for the decreased amplitude of the compound muscle action potential (CMAP) while maintaining a normal nerve conduction velocity. The lack of change of the nerve conduction velocity would indicate that the axonal injury has not affected the faster (most myelinated) fibers contained in the nerve bundle [27].

Selective injury of fiber types can be observed in various hereditary neuropathies. By contrast, nerve compression injuries cause damage at the point of compression and can involve a mixed population of large- and small-diameter axons resulting in a decrease in both the amplitude and the latency of the evoked nerve response (representing an axonal, demyelinating polyneuropathy) [28].

The earlier portion of the evoked peak represents the larger-diameter fibers and the latter portion of the response, progressively smaller-diameter fibers. Collectively, the height of the nerve conduction amplitude is a representation of all the axon bundles comprising the nerve [29]. Injury to axons within the nerve bundle will result in a dropout in the total number of axons actually stimulated in the nerve bundle and hence a reduction in the amplitude of the evoked compound motor action potential [30]. Therefore, reduction of the nerve conduction amplitude indicates the degree of axonal injury in the nerve bundle [5, 31].

Our results showed that right and left common peroneal MNCV were found significantly reduced in study group when compared to control group. There are reports in the literature that strength and muscle power athletes present higher motor nervous conduction velocity (MNCV) than endurance athletes, despite not having significant difference between these modalities, as well as that the MNCV of trained individuals is greater than in untrained and injured individuals. It has also been reported that the MNCV is greater in the dominant limb (D_L) when compared with the non-dominant limb (N_DL) in trained subjects [32, 33] On the other hand, it has been mentioned that hypertrophy of muscles adjacent to the nervous tract of the dominant limb of trained individuals may lead to compression of the nerve and consequent reduction of MNCV [34].

According to Untunen et al. there was polyneuropathy and muscle weakness in operators with vibration syndrome who had been working on vibrating tools for a long time [35].

The pathophysiology of vibration-induced neuropathy is complex, but includes morphological changes, such as degeneration of nerve fibres and fibrosis [36, 37]. Stromberg et al. reported pathological changes in biopsies from the posterior interosseus nerve in patients exposed to vibration, and concluded that demyelination might be the primary lesion in neuropathy following vibration exposure [38].

Studies performed on rats simulating vibration from hand-held power tools, reported axonal damage and myelin fragmentation in nerves that had been exposed to vibration, explaining the observed increased stress response in the vibration exposed rat nerves [39–42].

Most studies show a reduction in conduction velocity, indicating demyelination, of the fastestlarge myelinated fibres and in later stages, when the patients have more pronounced symptoms, a lower amplitude, indicating a loss of nerve fibers [43].

Vibration of mechanical sewing machine could have overshadowed the effect of regular exercise of lower limbs by chronic paddling in tailors. Poor nerve conduction study (NCS) parameters (L-CMAP, Amp-CMAP and MNCV) of peroneal nerves of both right and left legs in study group as compared to control group could be due to vibration effect of mechanical sewing machine. Most probably the effect of exercise (regular paddling) has not been able to counter the detrimental effect of vibration on lower limbs [22].