This paper explored the effect of vibration preconditioning on SBF and Temp responses to a fixed pressure stimulus in plantar soft tissue. The results showed that vibration preconditioning could significantly reduce the increase of SBF during hyperemia and may help to maintain a relatively constant temperature in the recovery stage after the release of compression, as shown in Fig. 3 where there is no significant difference between the temperature at the Baseline and Recovery stages in vibration preconditioning test.
When epidermal pressure exceeds capillary pressure, the microvascular network becomes blocked . This hinders the supply of oxygen and nutrition to the tissues and affects the transportation of metabolic waste and toxic substances in the lymphatic system [19–23]. After the pressure is released, the skin blood flow increases to compensate for the reduced oxygen supply to the ischemic tissue . Excessive pressure can lead to an accumulation of xanthine oxidase in hypoxic-ischemic tissue, which may cause oxidative stress during the hyperemia process, and increase the risk of developing pressure ulcers [8, 11, 25]. In this study, a pressure of 300 mmHg was applied to the plantar soft tissue for three minutes to compress and induce local ischemia. When the compression was removed, a protective reactive hyperemia occurred to compensate for the oxygen depletion and accumulation of waste . Thus, all subjects in both tests (Vibration Preconditioning and No Vibration) displayed reactive hyperemia after the release of compression (Fig. 1).
Normally, the level of reactive hyperemia is related to the degree of tissue ischemia [26, 27]. This study used the hyperemia response to assess the degree of ischemia caused by a pressure stimulus . Previous studies have shown that vibration can improve microcirculation, maintain enzymatic oxidation defenses, reduce oxidative stress in hypoxia-ischemic tissue, and protect cell restorability and tissue viability [29, 10, 12, 11]. In our study, vibration was applied as a preconditioning step prior to compression. The results showed that preconditioning with vibration significantly reduced the peak SBF during hyperemia (Fig. 2). This implies that vibration preconditioning can effectively alleviate ischemia, and the size of the vibration in this study was enough to induce fewer peaks of SBF and Temp during hyperemia in the short time after compression (during Recovery stage) to compensate for oxygen depletion. However, there was no significant difference in the SBF hyperemia between the two tests (Fig. 2). A possible reason for this is the inherent ability of the healthy subjects recruited for this study to regulate their SBF, and the vibration stimulation in the Vibration test was of low enough intensity as to not have a demonstrable effect on the hyperemic response. Therefore, the two tests demonstrated a similar level of hyperemia to compensate for the ischemia [24, 16]. Zhu et al reported that the total hyperemia in a subject’s foot after a walking stimulus was significantly decreased when vibration preconditioning was used . This contrasts with the results of this study, possibly because of the different parameters for the vibration stimulation. In this current study vibration was applied at 30 Hz, whereas Zhu et al. used a stronger vibration of 100 Hz, which may produce a stronger SBF response. In addition, the compression stimulus in Zhu’s study was applied by asking the subjects to walk for a fixed duration and velocity, but individual variations in plantar pressure could not be accounted for. This would directly affect the SBF response in plantar tissue. This current study applied the same compression stimulus to all subjects. The difference methods of applying pressure may be another reason for the different results between the two studies.
The results of this study also revealed a significant increase in plantar skin temperature after the removal of compression during both tests. Moreover, Temp was significantly higher during the first 1 min of the Recovery stage than the basal temperature in the No Vibration test, but not in Vibration Preconditioning test. The results of increase in temperature in the recovery stage were in accordance with the variations of SBF, and the significant increase in Temp may imply a greater reactive hyperemia in the No Vibration test. Skin temperature is mainly regulated by the sympathetic nerve, which also plays a vital role in regulating vasomotion. Thus, skin temperature has been used as an alternative to SBF for characterizing microvascular responses . However, the regulation of temperature related to central and peripheral blood flow is mainly regulated by dry heat exchange [31, 32]. And the mechanisms underlying the regulation of skin temperature and blood flow are distinct [33, 32]. Therefore, the correlation between skin temperature and SBF is nonlinear . As shown in Fig. 1, there was a significant difference in SBF between the two tests during the Recovery stage, but there was no significant difference in Temp. This implies that the Temp response and SBF response to vibration preconditioning are likely governed by distinct mechanisms.
Compression for 3 min at 300 mmHg is commonly used to investigate post-occlusion microvascular responses because it is sufficient to cause tissue ischemia and induce compensative hyperemia [18, 9]. In our study, the same compression stimulation was applied to the plantar tissue in both tests to induce ischemia. It has been reported that low intensity vibration at 30–35 Hz can effectively reduce damage caused by mechanical strain and oxidation [35, 11]. Therefore, this study used a preconditioning vibration step with a frequency of 30 Hz and an amplitude of 2 mm.
This study has some limitations that should be acknowledged. First, the vibration stimulus had fixed parameters (frequency, amplitude and intermittent duration). Variations in these parameters could affect the physiochemistry and microcirculation responses. To determine the optimal parameters, further investigation is required to understand the relationship between the vibration parameters and the protective effect of vibration preconditioning. Similarly, the compression stimulation also had fixed parameters (duration and intensity) in this study. Changing these parameters could induce different levels of ischemic damage and disturb the protective effects of vibration preconditioning. Thirdly, only healthy subjects were enrolled in this preliminary study. These experimental results were also applicable for diabetic people who have the same physiological hyperemic responses. Future studies are warranted to verify the clinical effectiveness of vibration preconditioning in people with diabetes.