Abstract
This study aimed to measure hemolysis before, during and after 60 days of the ground-based spaceflight analog bed rest and the effect of a nutritional intervention through a prospective randomized clinical trial. Twenty male participants were hospitalized for 88 days comprised of 14 days of ambulatory baseline, 60 days of 6° head-down tilt bed rest and 14 days of reambulation. Ten participants each received a control diet or daily polyphenol associated with omega-3, vitamin E, and selenium supplements. The primary outcome was endogenous carbon monoxide (CO) elimination measured by gas chromatography. Hemolysis was also measured with serial bilirubin, iron, transferrin saturation blood levels and serial 3-day stool collections were used to measure urobilinoid excretion using photometry. Total hemoglobin mass (tHb) was measured using CO-rebreathing. CO elimination increased after 5, 11, 30, and 57 days of bed rest: +289 ppb (95% CI 101–477 ppb; p = 0.004), +253 ppb (78–427 ppb; p = 0.007), +193 ppb (89–298 ppb; p = 0.001) and +858 ppb (670–1046 ppb; p < 0.000), respectively, compared to baseline. Bilirubin increased after 20 and 49 days of bed rest +0.8 mg/l (p = 0.013) and +1.1 mg/l (p = 0.012), respectively; and iron increased after 20 days of bed rest +10.5 µg/dl (p = 0.032). The nutritional intervention did not change CO elimination. THb was lower after 60 days of bed rest −0.9 g/kg (p = 0.001). Bed rest enhanced hemolysis as measured through all three by-products of heme oxygenase. Ongoing enhanced hemolysis over 60 days contributed to a 10% decrease in tHb mass. Modulation of red blood cell control towards increased hemolysis may be an important mechanism causing anemia in astronauts.
Highlights
Space anemia after exposure to microgravity was first observed in six astronauts from Gemini missions[1]
carbon monoxide (CO) elimination was higher after 5, 11, 30, and 57 days of bed rest compared to baseline: +289 ppb (101–477 ppb), +253 ppb (78–427 ppb), +193 ppb (89–298 ppb) and +858 ppb (670–1046 ppb), respectively; (Fig. 2a)
CO elimination increased on average 23%
Summary
Space anemia after exposure to microgravity was first observed in six astronauts from Gemini missions[1]. Later studies correcting for environmental oxygen concentrations failed to resolve the anemia in 4 returning astronauts from the Spacelab 1 mission[2]. Epidemiological data from over 5 decades of American and Canadian presence in space confirmed and characterized space anemia[6]. The search for mechanisms to explain space anemia has generated multiple hypotheses and experiments over the past decades such as: ineffective erythrocyte production and/or egress from the bone marrow[3,7,8], low erythropoietin levels or sensitivity[3,4], and production of abnormally-shaped erythrocytes[9]. In situations of hemoconcentration the excess erythrocytes can be sequestered in the spleen[7], remain in circulation until timedetermined senescence[3], or their lifespan can be shortened preferentially affecting young erythrocytes[4] or affecting erythrocytes of all ages[10]
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