Hypoxia (hx) in embryos causes a drop in oxygen consumption ( [Formula: see text] ) that rapidly recovers upon return to normoxia. We asked whether or not this pattern varies with the embryo's hypoxic history. The [Formula: see text] of chicken embryos in the middle (E12) or at end-incubation (E19) was measured by an open-flow methodology during 15-min epochs of moderate (15% O2) or severe hx (10% O2). Each hx-epoch was repeated or alternated with air by various modalities (air-hx-air-hx-air-hx-air, air-2·hx-air-2·hx-air, air-5·hx-air), in randomized sequences. The hx drop in [Formula: see text] was larger with severe than with moderate hx; however, in either case, its magnitude was essentially independent of the preceding hx history. E19 embryos had hx drops in [Formula: see text] of the same magnitude whether their incubation was in air or in moderate hx from E4 to E19. A different protocol (air-12·hx-air) gave variable results; with moderate hx, the [Formula: see text] response was similar to that of the other hx regimes. Differently, with severe hx most embryos progressively decreased [Formula: see text] and eventually died. We interpret these data on the basis of what is known on the 'compensatory partitioning' between costs of growth and maintenance. With moderate hx presumably each episode caused an energy shortfall absorbed entirely by the blunted growth. Hypoxic events of this type, therefore, should have no long-term functional effects other than those related to the small birth weight. Differently, the aerobic energy shortfall with severe hypoxia probably impinged on some maintenance functions and became incompatible with survival.
Keywords: Development; Embryonic growth; Hypometabolism; Intermittent hypoxia; Oxygen consumption; Prenatal.
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