Abstract
The study examined the distinct and synergistic effects of hypoxia and bed rest on the erythropoietin (EPO) concentration and relative changes in plasma volume (PV). Eleven healthy male lowlanders underwent three 21‐day confinement periods, in a counterbalanced order: (1) normoxic bed rest (NBR; PIO 2: 133.1 ± 0.3 mmHg); (2) hypoxic bed rest (HBR; PIO 2: 90.0 ± 0.4 mmHg, ambient simulated altitude of ~4000 m); and (3) hypoxic ambulation (HAMB; PIO 2: 90.0 ± 0.4 mmHg). Blood samples were collected before, during (days 2, 5, 14, and 21) and 2 days after each confinement to determine EPO concentration. Qualitative differences in PV changes were also estimated by changes in hematocrit and hemoglobin concentration along with concomitant changes in plasma renin concentration. NBR caused an initial reduction in EPO by ~39% (P = 0.04). By contrast, HBR enhanced EPO (P = 0.001), but the increase was less than that induced by HAMB (P < 0.01). All three confinements caused a significant reduction in PV (P < 0.05), with a substantially greater drop in HBR than in the other conditions (P < 0.001). Thus, present results suggest that hypoxia prevents the EPO suppression, whereas it seems to exaggerate the PV reduction induced by bed rest.
Highlights
Erythropoietin (EPO), a glycoprotein hormone produced by the adult kidney (Bauer and Kurtz 1989; Lundby et al 2014) whose main function is to regulate the production rate of red blood cell volume, is governed primarily by the relative amount of O2 available to the tissues (Jelkmann 2011)
It is well established that exposure to hypoxia prompts a rather rapid increase in EPO concentration (Eckardt et al 1989; Knaupp et al 1992), which reaches its zenith after 3–4 days, and is thereafter followed by a gradual decline toward the pre-hypoxia levels (Gunga et al 1994; Berglund et al 2002)
Contrary to the hypoxic confinements, normoxic bed rest (NBR) caused an initial reduction in EPO by ~39% (P = 0.04, d = 2.33)
Summary
Erythropoietin (EPO), a glycoprotein hormone produced by the adult kidney (Bauer and Kurtz 1989; Lundby et al 2014) whose main function is to regulate the production rate of red blood cell volume, is governed primarily by the relative amount of O2 available to the tissues (Jelkmann 2011). It is well established that exposure to hypoxia prompts a rather rapid increase in EPO concentration (Eckardt et al 1989; Knaupp et al 1992), which reaches its zenith after 3–4 days, and is thereafter followed by a gradual decline toward the pre-hypoxia levels (Gunga et al 1994; Berglund et al 2002). There is evidence to suggest that the EPO secretion is modulated by changes in blood volume (Berglund et al 1987; Ehmke et al 1995; Breymann et al 2000); albeit the underlying mechanism is not yet clear (cf Kirsch et al 2005). A prolonged period of bed rest suppresses EPO synthesis, presumably due to the central venous pressure increase resulting from the thoraco-cephalad blood volume shift at the initial stage of recumbency (Gunga et al 1996). Whether, and to what extent, a hypoxic stimulus superimposed on bed rest would counteract the bed rest-induced erythropoietic suppression remains unclear
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