The study by Zhai et al. [6] showed that positive acceleration exposure significantly affects heart rate, respiratory rate, and heart rate variability. The results suggest that the exposure leads to increased tone in human sympathetic nerve and significant increment in HRV. The study by Wang et al. [7] showed that the reduction of Connexin 43 may be involved in the mechanism of myocardial ischemia arrhythmia induced by acceleration. The study by Duanmu et al. [8] showed that the monophonic action potential (MAP) of ventricu1ar muse1e cells decrease and the transmural dispersion of repolarization (TDR) increase, maybe the electrophysiological mechanisms of arrhythmia induced by +Gz, and propafenone can antagonize this effect. The study by Zhou et al. [9] showed that the results demonstrated that the expression decrease and distribution disturbance of Cx43 in the ventricles of rats after repeated +Gz exposures could be recovered. These findings facilitate our understanding of the mechanisms of arrhythmia caused by +Gz and provide new protective measures. The study by Skyttä et al. [10] focused on twenty-four pilots monitored with a Holter monitor during 26 hours including a high-Gz flight in order to evaluate heart rate (HR) and cardiac rhythm. They recorded maximally 27 ventricular and 97 supraventricular ectopic beats, 10 junctional rhythms, 5 gray-out, 1 vestibular symptom, and 1 instance of numbness of the feet during the flight. The study by Zawadzka-Bartczak et al. [11] showed that abrupt onset and offset of acceleration induces hemodynamic changes that activate a number of reflex cardiovascular responses. At high +Gz on a centrifuge, apparently healthy subjects occasionally develop serious cardiac arrhythmia such as supraventricular tachycardia or asystole.

The study by Shao et al. [12] aimed to investigate the harmful effects of repeated positive acceleration (+Gz) in medium intensity on cardiac function of pilots. The centrifuge test of +Gz tolerance was performed in 38 fighter pilots. Repeated +Gz exposure in medium intensity seems not to influence the cardiac systolic function of pilots, but may have a slight and temporary harmful effect on cardiac diastolic function, implying that attention should be paid to protect the cardiac function of pilots after a repeated +Gz exposure. The study by Ji et al. [13] showed that the cardiac arrhythmias under +Gz acceleration could be taken as an index of evaluating cardiovascular compensatory function and warning against acceleration induced loss of consciousness. The study by Tripp et al. [14] reported the use of two-dimensional echocardiography in normal men during +Gz acceleration. The heart’s position in relation to the chest did not change during acceleration up to +7 Gz. End-diastolic volumes (EDV) and stroke volumes (SV) decreased during a +Gz acceleration ramp that increased until the subject experienced peripheral light loss (PLL) (P < 0.05). An inflated G-suit partially counteracted this effect. By 30 seconds of a +3 Gz acceleration plateau, the protective effects of the inflated G-suit to maintain EDV is lost and the EDV of the inflated G-suit was lower than the EDV of the uninflated G-suit (P < 0.05).

The study by Li et al. [15] aimed to study the effect of +Gz on myocardial microstructure of iniature swine with coronary stenosis. The ventricular microstructure does not change significantly in miniature swine with mild coronary stenosis but changes significantly in those with moderate and severe stenosis at the maximum +Gz tolerance. The study by Carter et al. [16] showed that exposure to acceleration forces (+Gz) and anti-G protective manoeuvres causes changes in cardiac preload and afterload. These changes can result in cardiac hypertrophy or enlargement. The study by Öztürk et al. [17] aimed to reveal the negative or positive cardiac responses to this occupational high +Gz exposure. The study design was cross-sectional and observational. They have evaluated 21 echocardiographic parameters of 63 pilots who applied for aircrew periodic medical examination. They conclude that according to the results of their study, long term +Gz exposure has no effects on cardiac morphologic and systolic functions but has effects on right ventricular diastolic functions.

The study by Liu et al. [18] showed that the −Gx exposures has a significant influence on the levels of inflammatory factors in the myocardium of rabbits, which could be involved in the mechanism of myocardium injure induced by −Gx. It may lead to ultrastructural damage of myocardial tissue. The study by Zhang et al. [19] suggested that repeated exposures to high +Gz could increase the expression of ICAM-1 in cardiovascular endothelium of rats, indicating that cell adhesion moleecules (CAMs) induced 1eucocyte diapedesis played a role in producing myocardial injuries due to high +Gz stress. The study by Jamshidi et al. [20] investigated the effect of body acceleration on human cardiac function. Finite element analysis is conducted to simulate geometrical and mechanical properties of human heart. Based on the finite element analysis, ventricular volume change, stress and deformation of heart model are evaluated. It is revealed that when the body is subjected to high accelerations, structural changes in the heart reduce blood supply to body up to 7.2% at +6G.

The study by Guo et al. [21] aimed to investigate the injury degree on heart of pure alternated +8Gz and alternated +8Gz and −8Gz (±Gz) exposures on rats. The changes of plasma levels of myocardium enzymes in rats of ±Gz group were more prominent than that of +Gz group. It is suggested that the harmful effect of alternated ±Gz exposures on heart is more prominent than that excerted by +Gz exposures only. The study by Li et al. [22] aimed to observe the changes of serum myocardial enzymes in rats after acute and chronic +Gz exposures. Two +Gz stress profiles can induce the increase of serum myocadial enzyme in rats, and the injury effect of acute +Gz stress is more remarkable.

The study by Chen et al. [23] showed that Rhodiola crenulata compound preconditioning could regulate the concentration of corticosterone in the serum of the rats exposed +10 Gz, which may be related with its protective effect on high sustained +Gz-induced injury of myocardium. The study by Ye et al. [24] showed that hypobaric hypoxia preconditioning (HHP) can reduce oxidative damage of myocardial tissue caused by acceleration and has myocardial protective effect, the mechanism is related to enhancing the activity of antioxidant enzymes and reducing oxidative stress on the activation of NOS and then inhibiting the release of NO in rats. The study by Sun et al. [25] showed that hyperbaric oxygen preconditioning (HBOP) can improve myocardial function and vascular endothelial function in pilots with poor acceleration tolerance, thereby improving their lower body negative pressure (LBNP) tolerance.