The evolution of the human cardiovascular system has taken place under Earth’s gravitational conditions, leading to an optimal configuration which results highly sensitive to deviations from this environment. As a matter of fact, alterations in gravitational acceleration (ranging from microgravity to hypergravity) induce a cas cade of physiological responses affecting both cardiac and vascular functions. The mechanism of fluid shift toward the cranial or caudal body compartments, triggered by microgravity and hypergravity respectively, has been identified as the driver of critical cardiovascular alterations, such as cardiac atrophy, hypovolemia, orthostatic intolerance, and diminished venous return. It is widely known that, under increasing gravitational loads, the cardiovascular system experiences pronounced orthostatic stress, resulting in marked changes in several central hemodynamic parameters (such as stroke volume reduction and heart rate elevation), as well as influencing the dynamics of pressure and flow wave propagation, which are inherently delayed due to vessel wall viscoelasticity.