The entire cardiovascular system, not just the heart, form vortexes. Optimize these vortices via exercising in gravity.
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Fluid dynamics of vortex patterns involves the study of rotational flow structures where fluid particles move in helical or circular paths around an axis, creating coherent, energetic structures. These localized regions of rotational motion, characterized by high vorticity—the curl of the velocity field—are essential to understanding turbulence, shear flow, and transport processes in both engineering applications and natural phenomena.
Vortex Formation in the Cardiovascular System
https://www.researchgate.net/publication/229068637_Vortex_Formation_in_the_Cardiovascular_System
Full PDF: https://users.encs.concordia.ca/~kadem/MECH691X/VortexFormationInTheCardiovasc.pdfThe shape of the healthy heart is optimized for vortex ring formation
https://pmc.ncbi.nlm.nih.gov/articles/PMC5032082/Cardiovascular Research by Leonardo da Vinci (1452–1519)
https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.118.314253Viktor Schauberger (1885–1958) was an Austrian naturalist who developed "implosion technology," focusing on natural, spiraling water vortices to generate energy, purify water, and create lift.
https://en.wikipedia.org/wiki/Viktor_SchaubergerStudy Finds Astronauts’ Hearts Become More Spherical in Space
"heart becomes more spherical when exposed to long periods of microgravity in space, a change that could lead to cardiac problems"
The astronauts’ more spherical heart shape appears to be temporary, with the heart returning to its normal elongated shape shortly after the return to Earth. The more spherical shape experienced in space may mean the heart is performing less efficiently, although the long-term health effects of the shape change are not known.
https://www.acc.org/about-acc/press-releases/2014/03/29/09/09/may-hearts-in-spaceWall shear stress and its role in atherosclerosis
The onset of plaque usually occurs in the low WSS area, and the plaque development alters the local WSS topography. low WSS promotes atherosclerosis, while high WSS prevents atherosclerosis. Upon further progression of plaques, high WSS is associated with the formation of vulnerable plaque phenotype.
https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2023.1083547/fullCardiovascular Effects of Exercise: Role of Endothelial Shear Stress
The notion that regular aerobic exercise reduces cardiovascular morbidity and mortality in the general population as well as in patients with coronary artery disease is strongly supported by evidence derived from epidemiologic studies (1., 2., 3.). Physically active people also experience fewer clinical manifestations of coronary artery disease than do less active men and women (4). By contrast, sedentary life-style has been identified as a risk factor for development of coronary artery disease, and there is a strong correlation between physical inactivity and cardiovascular mortality (3,5). Although vigorous physical exertion is a precipitating factor for myocardial infarction, this adverse outcome is usually incurred by persons who otherwise lead a sedentary existence (6,7). Consequently, daily physical aerobic activity is considered an effective component of both primary and secondary prevention of cardiovascular events (8,9).
https://www.sciencedirect.com/science/article/pii/S0735109796003932Sitting and endothelial dysfunction: The role of shear stress
Sedentary activity results in low SS in the lower extremities which may result in increased oxidative stress and impaired endothelial function. This review furthers the use of sitting as model to study the effects of inactivity, discusses possible physiological mechanisms and suggests future directions.
https://pmc.ncbi.nlm.nih.gov/articles/PMC3560806Arterial stiffness and hypertension
Arterial stiffness and hypertension are closely related in pathophysiology. Chronic high blood pressure (BP) can lead to arterial wall damage by mechanical stress, endothelial dysfunction, increased inflammation, oxidative stress, and renin–angiotensin–aldosterone system (RAAS) activation. Hypertension also increases collagen fiber production and accelerates elastin fiber degradation. Stiffened arteries struggle with BP changes, raising systolic BP and pulse pressure. The resulting increased systolic pressure further hardens arteries, creating a harmful cycle of inflammation and calcification. Arterial stiffness data can predict target organ damage and future cardiovascular events in hypertensive patients. Thus, early detection of arterial stiffness aids in initiating preventive measures and treatment plans to protect against progression of vascular damage. While various methods exist for measuring arterial stiffness, pulse wave velocity is a non-invasive, simple measurement method that maximizes effectiveness. Healthy lifestyle changes, RAAS blockers, and statins are known to reduce arterial stiffness. Further research is needed to ascertain if improving arterial stiffness will enhance prognosis in hypertensive patients.
https://pmc.ncbi.nlm.nih.gov/articles/PMC10691097/Exercise and Dietary Influences on Arterial Stiffness in Cardiometabolic Disease
https://www.ahajournals.org/doi/10.1161/hypertensionaha.113.02277The Acute Effect of Exercise on Arterial Stiffness in Healthy Subjects: A Meta-Analysis
Our results show that, although there is a significant reduction in pulse wave velocity 30 min after exercise, the levels of arterial stiffness return to their basal levels after 24 h. These findings could imply that, in order to achieve improvements in pulse wave velocity, exercise should be performed on a daily basis.
https://pmc.ncbi.nlm.nih.gov/articles/PMC7831005/
