Theoretical analysis of the mechanisms of a gender differentiation in the propensity for orthostatic intolerance after spaceflight

• Published in: Theoretical biology and medical modelling Vol. 7; no. 1; p. 8
• Main Authors: Summers, Richard L, Platts, Steven, Myers, Jerry G, Coleman, Thomas G
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 18.03.2010; BioMed Central
• Subjects: Astronauts; Computer simulation; Computer-generated environments; Diagnosis; Dysautonomia; Female; Health aspects; Humans; Male; Methods; Microgravity; Models, Biological; Orthostatic Intolerance - physiopathology; Risk factors; Sex Characteristics; Space Flight - trends; Weightlessness - adverse effects; United States
• ISSN: 1742-4682; 1742-4682
• DOI: 10.1186/1742-4682-7-8

A tendency to develop reentry orthostasis after a prolonged exposure to microgravity is a common problem among astronauts. The problem is 5 times more prevalent in female astronauts as compared to their male counterparts. The mechanisms responsible for this gender differentiation are poorly understood despite many detailed and complex investigations directed toward an analysis of the physiologic control systems involved. In this study, a series of computer simulation studies using a mathematical model of cardiovascular functioning were performed to examine the proposed hypothesis that this phenomenon could be explained by basic physical forces acting through the simple common anatomic differences between men and women. In the computer simulations, the circulatory components and hydrostatic gradients of the model were allowed to adapt to the physical constraints of microgravity. After a simulated period of one month, the model was returned to the conditions of earth's gravity and the standard postflight tilt test protocol was performed while the model output depicting the typical vital signs was monitored. The analysis demonstrated that a 15% lowering of the longitudinal center of gravity in the anatomic structure of the model was all that was necessary to prevent the physiologic compensatory mechanisms from overcoming the propensity for reentry orthostasis leading to syncope.