The relationship between fetal arterial oxygen saturation and heart and skeletal muscle myoglobin concentrations in the ovine fetus.

Myoglobin, a hemoprotein found in abundance in the muscle of postnatal animals, increases in concentration in response to hypoxia, thereby protecting tissue from damage. Fetuses exposed to intrauterine hypoxemia are also susceptible to organ damage, but the response of fetal muscle myoglobin to hypoxemia is unknown. To study whether fetal muscle myoglobin concentrations are elevated following intrauterine hypoxemia, we exposed eight chronically catheterized late gestation sheep to a wide range of fetal oxygen levels over 15 to 30 days and correlated the level of fetal oxygenation with heart and skeletal muscle myoglobin concentrations measured at sacrifice. A lower level of fetal oxygenation, expressed as the integrated area under the arterial saturation (SaO2)-time curve, was associated with greater myocardial myoglobin concentration (r = 0.90; P < 0.01). This relationship was not observed for skeletal muscle (r = 0.43; P = ns). A lower level of fetal oxygenation was associated with lower myoglobin:iron (w/w) ratio in skeletal muscle (r = 0.71; P < 0.03), implying less incorporation of iron into myoglobin. A similar relationship was not apparent for cardiac tissue. The higher myocardial myoglobin concentrations found in the more hypoxic fetuses were consistent with previous observations in postnatal animals. This likely represents an intracellular compensatory mechanism for sustaining short-term mitochondrial oxygen delivery in a critical organ with a high rate of oxygen consumption. The lack of myoglobin responsiveness to hypoxia in fetal skeletal muscle may be due to its much lower oxygen consumption rate and activity level.