Extremely preterm infants, born before 28 weeks of gestation, are a vulnerable population due to immature organ systems and underdeveloped antioxidant defenses. Despite advancements in neonatal care, these infants remain at high risk for various long-term health and developmental complications. Mitochondria, often referred to as the powerhouses of the cell, are essential for cellular energy production, and support high energy demanding processes such as fetal development and postnatal adaptation. Although mitochondrial dysfunction has previously been linked to various disorders common among preterm infants, little is known about their function in extremely preterm neonates, particularly during the critical first month of life. The aim of this study was to evaluate mitochondrial function in platelets and placental tissue from extremely preterm neonates compared to full-term neonates using high-resolution respirometry. Time-dependent changes in mitochondrial function in the extremely preterm cohort were also evaluated over the first postnatal month. Consistently lower mitochondrial respiration was observed in platelets and placental tissue from the extremely preterm group across all measured respiratory parameters. Additionally, the study revealed significant correlations between most respiratory parameters and both gestational age and birth weight, indicating possible mitochondrial immaturity or dysfunction in extremely preterm neonates. Longitudinal assessment of mitochondrial function also revealed dynamic, time-dependent changes in mitochondrial respiration, with an increase at postnatal day 1, followed by a gradual decrease up to two weeks of age. These findings may reflect an overcompensatory mitochondrial response to the oxygen-rich extrauterine environment. This study provides new insights into mitochondrial function in extremely preterm neonates during a critical window of postnatal development.