Progressive improvements in perinatal care and respiratory management of preterm infants has resulted in increased survival of extremely low gestational age newborns over the past few decades. However, the incidence of bronchopulmonary dysplasia (BPD), the chronic lung disease after preterm birth, has not changed. Studies of the long-term follow-up of adults born preterm have shown persistent abnormalities of respiratory, cardiovascular, and cardiopulmonary function possibly leading to a lesser exercise capacity. The underlying causes of these abnormalities are incompletely known, but we hypothesize that dysanapsis, i.e., discordant growth and development, in the respiratory and cardiovascular systems is a central structural feature that leads to the lesser exercise capacity in young adults born preterm compared to those born at term. We discuss how the hypothesized system dysanapsis underscores the observed respiratory, cardiovascular, and cardiopulmonary limitations. Specifically, adults born preterm have 1) normal lung volumes but smaller airways that causes expiratory airflow limitation and abnormal respiratory mechanics but without impacts on pulmonary gas exchange efficiency; 2) normal total cardiac size but smaller cardiac chambers, and 3) in some cases, evidence of pulmonary hypertension particularly during exercise, suggesting a reduced pulmonary vascular capacity despite reduced cardiac output. We speculate that these underlying developmental abnormalities may accelerate the normal age-associated decline in exercise capacity, via an accelerated decline in respiratory, cardiovascular, and cardiopulmonary function. Finally, we suggest areas of future research, especially the need for longitudinal and interventional studies from infancy into adulthood to better understand how preterm birth alters exercise capacity across the lifespan.

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