not limited to, low energy availability, micronutrient deficiencies, reduced physical activity, increased levels of glucocorticoids and other stress hormones, and reductions in gonadal hormones. Understanding the independent and combined effects of multiple stressors on multiple physiological systems, and how resultant changes influence health, safety, and performance, should be viewed as an obligatory step for the development of effective countermeasures. For example, intensive exercise may effectively mitigate microgravity-related effects of reduced loading on muscle and bone loss but exacerbate the adverse effects of low energy availability and gonadal hormone suppression on the musculoskeletal system. Because of the small number of potential study subjects, it will probably not be possible in the foreseeable future to carry out human studies in space that effectively evaluate the independent and combined effects of multiple stressors. However, a comprehensive characterization of both the stressors and the responses of multiple biologic systems will generate important preliminary data for hypothesis-driven research on multiple stressors (e.g., ground-based human studies).

Finally, this chapter emphasizes the need for effective coupling of biological and engineering problem-solving strategies. It is difficult, if not impossible, to replicate the multiple stressors of the space environment in a ground-based analog. However, creation of an effective exercise countermeasure for the preservation of bone, muscle, and cardiovascular function in a ground-based experiment is productive only if the countermeasure can be implemented in the space environment. This important translational step is heavily dependent on approaching the problem from a multidisciplinary perspective.

SOLVING INTEGRATIVE BIOMEDICAL PROBLEMS THROUGH TRANSLATIONAL RESEARCH

Stress—Physical and Physiological Considerations

There are numerous known biomedical stressors associated with spaceflight and re-adaptation to gravity that may benefit from a translational approach.

Decompression Sickness

Human spaceflights in low Earth orbit or on exploration missions to the Moon, asteroids, or Mars all require many thousands of hours of extravehicular activity (EVA) and inherently carry a higher risk of decompression sickness.1 Suits are necessarily designed to operate at as low a pressure as practicable (e.g., Apollo, 3.8 psi; space shuttle/International Space Station (ISS), 4.3 psi; Russian Orlan, 5.7 psi) so as to maximize suit joint and glove flexibility while maintaining physiologically adequate oxygen and CO2 partial pressures. During the airlock decompression from spacecraft to hypobaric suit pressure, nitrogen dissolved in blood and tissues comes out of solution, creating tiny bubbles (evolved nitrogen), which potentially can cause symptoms of decompression sickness (DCS), colloquially called “the bends.” DCS at 5 psia was not a problem on Apollo, because the spacecraft operated with a 100 percent O2 environment. Primarily for scientific reasons, the space shuttle and the ISS use an Earth-like 14.7 psia, 20.8 percent O2 atmosphere, although the space shuttle can be depressurized to 10.2 psia to shorten EVA prebreathing of pure oxygen. DCS during EVAs is avoided by prebreathing 100 percent O2 to reduce evolved nitrogen. Exercise during prebreathing greatly accelerates denitrogenation. Staged decompression (e.g., to 10.2 psi) followed by a shorter prebreathe interval is sometimes used. Astronauts are also routinely exposed to hyperbaric environments during underwater “neutral buoyancy” EVA training. DCS upon ascent is avoided by limiting the depth and duration of underwater training and by the use of oxygen-enriched breathing gas.

Known Effects

No cases of hypobaric DCS have been reported on Apollo flights, the space shuttle, or the ISS. Decompression using conventional staged protocols normally creates venous gas emboli (VGE or “silent bubbles”).2,3 Small numbers of bubbles produce no symptoms, but in 1-g testing, large numbers of VGE are usually correlated with joint and muscle pain (Type I DCS). Exercise increases the number of venous bubble micronuclei and incidence of symptoms. Most VGE are believed trapped in the lungs. However intrapulmonary (pulmonary arterial to venous) connections exist4 that shunt blood to the systemic arterial side, particularly during exercise. VGE can be easily



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