Abstract

Newborns are equipped with a number of natural adaptation mechanisms preventing them from impaired energy supply, despite their elevated (size-related) metabolic rate. These include the diving response known from aquatic mammals, which - being composed of apnea, bradycardia, and vasoconstriction - ensures an economical use of O2 reserves and results in a subsequent influx of lactate out of peripheral tissues. From a metabolic point of view, mammalian fetuses behave "like an organ of the mother" and thus exhibit a hibernation-like deviation from the overall metabolic size relationship that adapts them to the limited intrauterine O2/substrate availability. In case of lacking supply, they can reduce their energy demands even further by foregoing growth, with the placenta acting as a gatekeeper. Postnatal hypoxia does not only result in the suppression of non-shivering thermogenesis, but also in a hypoxic hypometabolism that otherwise has only been known from poikilothermic animals. After prolonged apnea, gasps do occur that maintain a rudimentary heart action through short elevations in pO2 (autoresuscitation). Overall, these mechanisms postpone a critical O2 deficit and thereby provide a "resistance" rather than a "tolerance" to hypoxia. As they are based on an (active) reduction in energy demand, they are not easy to distinguish from the (passive) breakdown of metabolism resulting from hypoxia.

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