Diaphragm muscle: neonate vs adult

Respiratory distress is the most frequent cause of neonatal ICU admission in the US.¹ One reason neonates poorly tolerate increased work of breathing is the immature development of their ventilatory musculature. The diaphragm is the main muscle of inspiration and undertakes the majority of the work of breathing. Structurally and functionally, the diaphragm of a newborn is prone to early fatigue and failure with increased respiratory load.²

Infants have a lower percentage of fatigue-resistance Type I muscle fibers relative to adults. Skeletal muscle fibers are classified as type I or type II. Muscle fiber typing is determined by histochemical staining of myosin ATPase concentration. Type I fibers have a low percentage of myosin ATPase, leading to a high oxidative, low glycolytic capacity. These fibers are also referred to as slow-twitch, or endurance fibers, due to their resistance to fatigue. Type II fibers have a much higher percentage of myosin ATPase activity, creating a high glycolytic, low oxidative capacity. Type II fibers are also known as fast-twitch fibers. They have a robust metabolic demand and thus fatigue much quicker than Type I fibers.³

Structurally, the neonatal diaphragm is also not as efficient as adults. Unlike the dome-shaped diaphragm of adults, neonatal diaphragms are morphologically flattened. The diaphragm connects to the rib cage only anterolaterally, with the distance between the ribs and insertion site increasing posteriorly. This creates a large angle of insertion with a small area of apposition, requiring more force to pull the diaphragm caudally and increase the intrathoracic pressure required for inspiration.^_2,4