# Effect of Controlled Expiratory Pressures on Cerebrovascular Changes During Valsalva Maneuver
## 1 Introduction  
Valsalva maneuver (VM) is a common phenomenon that occurs during straining in daily life, such as lifting heavy objects, defecating, or coughing. In this phenomenon, increased intrathoracic pressure suddenly and rapidly increases the blood pressure, triggering changes in the cardiovascular and autonomic nervous systems. This same movement can also be achieved by performing a voluntary forced expiratory effort against a closed airway (e.g., closed mouth and nose). This technique is simple to perform, has a short performance time (generally 15 s), and is also non-invasive and highly reproducible; therefore, it is currently used in various clinical fields. In particular, it can cause immediate changes in the cardiovascular and autonomic nervous systems; therefore, it has been usedas a method to test heart disease (heart failure, heart murmus, or atrial septal defects) and cardiac autonomic function or to evaluate cerebral autoregulation [1; 2; 3; 4; 5; 6].  
The VM can physiologically affect not only cardiac function but also vascular function. Vascular elasticity is its major function that provides a passive mechanism for smoothing the pulsatile blood flow from the heart to peripheral sites [7], and that is influenced by the constriction and relaxation of vascular smooth muscle cells. Therefore, dysfunction has been shown to contribute to arterial stiffness [8]. Accordingly, the balance of constriction and relaxation of arteries can improve vascular elasticity.  
The VM directly provides pressure stimulation to the arteries and stimulates vascular smooth muscle cells, potentially changing vascular tone [9]. In particular, increased blood pressure and autonomic nerve activity during VM can change the vascular tone. Blood vessels undergo autoregulation of the myogenic response to prevent damage from increased blood pressure and blood vessel tension [9]. In addition, the parasympathetic nerve, which is activated to restore blood pressure in the final phase of the VM, can relax blood vessels [10]. Such changes in the constriction and relaxation of blood vessels can improve blood vessel function.  
In addition, the VM also affects cerebral blood flow, and some studies have reported the risk of changes in cerebral blood flow. A previous study reported that when expiratory pressure increased to 40 mmHg, arterial pressure and cerebral blood flow increased, leading to the risk of aneurysm rupture and tissue damage [11]. In addition, low blood pressure caused by VM can reduce cerebral blood flow and cause syncope [12]. Therefore, to improve cerebrovascular function, it is necessary to perform the VM that can safely induce hemodynamic changes in the brain and improve vascular function.  
Generally, 40 mmHg is the most representative standard for VM pressure. However, to date, VM research has been conducted at various intensities, generally of around 20-40 mmHg, to reduce potential side effects at 40 mmHg and allow easier application of the technique [11; 13; 14; 15]. However, to date, the changes in cerebral hemodynamic changes in response to various VM strengths remain largely unknown. Therefore, it is necessary to determine which VM strength is more suitable for cerebrovascular response with low risk by comparing various pressure levels.  
Given this context, in the present study, we aimed to investigate changes in common carotid artery (CCA) blood velocity and vascular function, as well as hemodynamic changes in the brain during VM performed at pressure intensities of 30 mmHg and 40 mmHg, in order to ascertain the more suitable intensity for vascular stiffness. The hypotheses of this study were as follows: First, both 30 mmHg and 40 mmHg VM would cause changes in the hemodynamic response of the CCA and the prefrontal region. Second, graded (30 mmHg and 40 mmHg) VM would have different effects on vascular function.