|| Checking for direct PDF access through Ovid
Exposure to a microgravity environment decreases the maximal rate of O2 uptake (V˙O2max) in healthy individuals returning to a gravitational environment. The magnitude of this decrease in V˙O2max is, in part, dependent on the duration of microgravity exposure, such that long exposure may result in up to a 38% decrease in V˙O2max. This review identifies the components within the O2 transport pathway that determine the decrease in postmicrogravity V˙O2max and highlights the potential contributing physiological mechanisms. A retrospective analysis revealed that the decline in V˙O2max is initially mediated by a decrease in convective and diffusive O2 transport that occurs as the duration of microgravity exposure is extended. Mechanistically, the attenuation of O2 transport is the combined result of a deconditioning across multiple organ systems including decreases in total blood volume, red blood cell mass, cardiac function and mass, vascular function, skeletal muscle mass, and, potentially, capillary hemodynamics, which become evident during exercise upon re-exposure to the head-to-foot gravitational forces of upright posture on Earth. In summary, V˙O2max is determined by the integration of central and peripheral O2 transport mechanisms, which, if not maintained during microgravity, will have a substantial long-term detrimental impact on space mission performance and astronaut health.