Andean Man & the Astronaut

In 1958, Bruno Balke, a former German Luftwaffe doctor working for the United States Air Force (USAF), led a team of airmen up Colorado’s Mount Evans. Could acclimatization to the thin mountain air boost the oxygen efficiency of future astronauts living in artificial low-pressure spacecraft environments? To judge their improvement, Balke, an expert in the nascent field of space medicine, compared their performance not with military test-pilots, but with high-altitude Indigenous people he had studied in the Peruvian Andes. This article expands discussions of race in space history beyond Black scientists, mathematicians, and pilots in the Civil Rights era to this earlier case of the permanent residents of Morococha, Peru, who participated in efforts to define an ideal spacefaring body. More than recovering the story of a nearly forgotten group of astronaut-adjacent test-subjects, this article shows how racial discrimination in space medicine functioned by inclusion. Balke studied and even celebrated the bodies of Morocochans, but never considered them potential astronauts. This article begins with Balke’s participation in the 1938 Nazi-funded expedition to summit Nanga Parbat in the Himalayas, and his follow-on work acclimatizing Luftwaffe pilots during World War Two. Then it focuses on his USAF work in the 1950s studying miners living and working in Morococha, Peru, and his attempt to replicate their altitude tolerance in American airmen on Mount Evans. Recovering Balke’s work places the high-altitude Indigenous person and the mountaineer alongside the familiar figure of the pilot in the genealogy of the early American astronaut.

Remote ischemic preconditioning for prevention of high-altitude diseases: fact or fiction?

Preconditioning refers to exposure to brief episodes of potentially adverse stimuli and protects against injury during subsequent exposures. This was first described in the heart, where episodes of ischemia/reperfusion render the myocardium resistant to subsequent ischemic injury, which is likely caused by reactive oxygen species (ROS) and proinflammatory processes. Protection of the heart was also found when preconditioning was performed in an organ different from the target, which is called remote ischemic preconditioning (RIPC). The mechanisms causing protection seem to include stimulation of nitric oxide (NO) synthase, increase in antioxidant enzymes, and downregulation of proinflammatory cytokines. These pathways are also thought to play a role in high-altitude diseases: high-altitude pulmonary edema (HAPE) is associated with decreased bioavailability of NO and increased generation of ROS, whereas mechanisms causing acute mountain sickness (AMS) and high-altitude cerebral edema (HACE) seem to involve cytotoxic effects by ROS and inflammation. Based on these apparent similarities between ischemic damage and AMS, HACE, and HAPE, it is reasonable to assume that RIPC might be protective and improve altitude tolerance. In studies addressing high-altitude/hypoxia tolerance, RIPC has been shown to decrease pulmonary arterial systolic pressure in normobaric hypoxia (13% O2) and at high altitude (4,342 m). Our own results indicate that RIPC transiently decreases the severity of AMS at 12% O2. Thus preliminary studies show some benefit, but clearly, further experiments to establish the efficacy and potential mechanism of RIPC are needed.

Age and altitude tolerance in rats: temperature, plasma enzymes, and corticosterone

Tolerance to a 4-h altitude exposure (6,096-8,230 m) was determined in immature, young, and old male rats. The critical survival thresholds were 8,230 m for immature rats and 7,620 m for young and old rats. Hypothermia in immature rats was directly related to hypoxic severity. Body weight loss, elevated plasma corticosterone concentration, and a mean body temperature of 32.5 degrees C were characteristics of immature rats that survived at the critical threshold. Body temperature, weight change, and plasma corticosterone concentration were similar at all altitudes in young adult and old rats. Plasma enzyme activities were relatively unchanged in immature rats, but aspartate aminotransferase (EC 2.6.1.1) and lactate dehydrogenase (EC 1.1.1.27) activities in old rats, in addition to fructose-diphosphate aldolase (EC 4.1.2.13) activity in young adults, were initially elevated (P less than 0.05) at the critical survival threshold (7,620 m). Body temperature and plasma corticosterone (but not plasma enzyme activities) are important criteria for determining altitude tolerance of immature rats. However, plasma asparatate aminotransferase and lactate dehydrogenase activities are more suitable criteria for assessing tolerance in young adult and old rats.

Avian cerebral blood flow: influence of the Bohr effect on oxygen supply

To clarify the problems of altitude tolerance in birds, we studied the combined effect of hypocapnia and hypoxia on cerebral blood flow (CBF) in ducks. CBF was measured by the xenon clearance method. Normocapnic hypoxia causes CBF to increase when the arterial O2 tension (PaO2) falls below 60--70 mmHg. Hypocapnic hypoxia significantly shifts the blood flow curve so that blood flow does not increase until a lower PaO2 (50--60 mmHg) is reached. This gives the appearance that hypocapnia suppresses the hypoxia-induced increase in CBF. However, due to the Bohr effect, the hypocapnic blood contains significantly more O2 than does the normocapnic blood at the same PaO2. Therefore, when CBF is expressed as a function of O2 content, rather than PO2, CBF in the hypocapnic group does not differ significantly from the CBF in the normocapnic group. We interpret this to mean that because of the significantly greater oxygen content of the hypocapnic blood at a given PaO2, the degree of hypoxia experienced by these brains is not as severe as that experienced by the normocapnic brains.