ABC | Volume 112, Nº1, January 2019

Original Article Shekarforoush & Naghii Cardioprotection by whole-body vibration Arq Bras Cardiol. 2019; 112(1):32-37 Table2 – Incidence and duration of ventricular arrhythmias during 30 min of ischemia Groups PVC (n) VT VF Episodes Duration Episodes Duration Cont 283 ± 50 31 ± 4 70 ± 14 2.0 ± 0.9 32.3 ± 19.4 WBV1 271 ± 32 17 ± 1 * 54 ± 19 2.3 ± 0.8 33.2 ± 17.9 WBV3 229 ± 55 13 ± 3 ** 12 ± 4 * 1.0 ± 0.6 13.7 ± 10.3 p-value 0.702 0.002 0.018 0.559 0.475 PVC: premature ventricular complexes; VT: ventricular tachycardia; VF: ventricular fibrillation; WBV1: whole body vibration training for one week; WBV3: whole body vibration training for 3 weeks The ischemia reperfusion model in the experimental animals provides an option to evaluate the occurrence of ischemia‑induced arrhythmias and infarct size after an intervention. Posa et al. demonstrated that 6 weeks of voluntary exercise was protective against IR injury by reducing the myocardial infarct size. 23 An important finding is that one‑to‑several days of exercise can also reduce myocardial damage due to IR injury. 24 Studies have demonstrated that regular exercise increases antioxidant capacity in the heart, which can minimize oxidative stress following IR. 25 During all sporting activities, externally-applied forces induce vibrations within the body tissues. 10 WBV has been proposed as an efficient alternative to moderate intensity exercise. 26 Although recent studies have suggested that WBV leads to improvements in numerous health outcomes, including bone mineral density, 27 muscle strength, or cardiovascular fitness, 28 no research has been performed so far to evaluate the effects on IR injury. The present study demonstrated that WBV is able to reduce myocardial infarct size and ischemia-induced arrhythmia during IR injury in rats. In the course of myocardial infarction, ventricular arrhythmias such as VT and VF are the most important cause of mortality. 29 Therewas nodifference in the ratioof AAR/LVbetween the control andvibrationanimals, indicating thatall animals suffered a comparable degree of ischemic area. Therefore, the reductionof infarct size and arrhythmia in vibration-treatedanimals was due to the effect of the training. There are two types of VF: a sustained VF (SVF) that never terminates spontaneously and requires electrical defibrillation and a transient VF (TVF) that terminates by itself and spontaneously reverts into a sinus rhythm. Although it was believed for many years that TVF appears only in small mammals (rats, guinea pigs and rabbits), no differences were found in cardiac muscle mass, heart rate and action potential duration between animals with TVF and those with SVF. Intercellular uncoupling during ischemia most likely due to an increase in the intracellular Ca 2+ and H + ions or a decrease in the intracellular cAMP may lead to SVF. Therefore, any defibrillating intervention should prevent intercellular uncoupling, most probably by increasing the intracellular concentration of cAMP, decreasing elevated [Ca 2+ ] i or preventing Ca 2+ overload. 30 The results of the present study suggested that all VF episodes were self‑limited in the vibration groups. Thus, vibration training could reduce the risk of sudden death during ischemia, through both attenuation of the ischemia‑induced arrhythmia and facilitation of spontaneous defibrillation. The exact mechanism of action by which vibration reduces the incidence of fatal VF episodes cannot be directly assessed by our study. However, the increased ventricular fibrillation threshold in trained hearts during acute regional ischemia was shown in previous studies. 31 Additionally, exercise training has been reported to increase the levels of cAMP 32 and to improve cardiomyocyte function and diastolic Ca 2+ control in rats with post-infarction heart failure. 33,34 Several studies have also shown a positive correlation between infarct size and the occurrence of severe ventricular arrhythmias. 35,36 Currently, exercise training has been introduced as the only practical method of providing cardioprotection against IR injury. If vibration-induced protection is nearly as effective as the exercise, it could be an alternative to exercise training, especially for those who are unable to perform traditional exercises. Delineating the mechanisms mediating vibration‑induced protection against IR injury is important and could lead to the development of pharmacological or molecular approaches against cardiovascular diseases. Limitations of the study One of the limitations of the present study is that it was carried out on rats. Even though the large number of animal studies have conducted and contributed much to our understanding of disease mechanisms, their findings for predicting the effectiveness of strategies in humans has remained controversial. 37,38 Therefore, the results need to be confirmed by clinical trials in the future. The frequency, amplitude, and the time of exposure of the subjects to vibration are important variations in clinical and experimental trials. However, due to lack of knowledge regarding optimum training protocols, the method was based on the methodology available in our laboratory. The proposed method has shown that is effective in improving health status by influencing cardiovascular disease (CVD) risk factors. 18,39 We recommend evaluating the various vibration regimes on the IR injury in future studies. Conclusions The present experimental data provide new evidence that vibration training can enhance cardiac tolerance to IR injury in an in vivo rat infarct model. It reduces infarct size and ischemia‑induced arrhythmias and improves arrhythmia-related mortality by reducing fatal VF episodes and by facilitating spontaneous defibrillation. The finding that vibration training increases myocardial resistance to VF in this model offers experimental support for the epidemiological data associating exercise training with decreased sudden cardiac death. However, more evidence is needed in this regard. 35