Department of Biological Sciences, Northern Arizona University, Flagstaff, Arizona, USA.
Oxford Cardiovascular Clinical Research Facility, Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK.
J Physiol. 2022 Feb;600(3):463-482. doi: 10.1113/JP281848. Epub 2022 Jan 12.
Progressive improvements in perinatal care and respiratory management of preterm infants have resulted in increased survival of newborns of extremely low gestational age over the past few decades. However, the incidence of bronchopulmonary dysplasia, 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 lower 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 a lower exercise capacity in young adults born preterm than 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, which 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.
在过去的几十年中，围产期护理和早产儿呼吸管理的不断进步导致极低出生体重儿的存活率提高。然而，支气管肺发育不良（早产儿出生后慢性肺部疾病）的发病率并未改变。对早产儿出生后成年人的长期随访研究表明，呼吸、心血管和心肺功能存在持续异常，可能导致运动能力降低。这些异常的根本原因尚不完全清楚，但我们假设，呼吸和心血管系统的发育不同步（即生长发育不协调）是导致早产儿出生后运动能力低于足月出生者的核心结构特征。我们讨论了假设的系统发育不同步如何强调观察到的呼吸、心血管和心肺局限性。具体来说，早产儿出生的成年人有：（1）正常的肺容量但较小的气道，这导致呼气气流受限和异常的呼吸力学，但对肺气体交换效率没有影响；（2）正常的总心脏大小但较小的心脏腔室；（3）在某些情况下，存在肺动脉高压的证据，特别是在运动期间，尽管心输出量减少，但提示肺血管容量减少。我们推测，这些潜在的发育异常可能通过加速呼吸、心血管和心肺功能的正常年龄相关下降，加速运动能力的正常年龄相关下降。最后，我们提出了未来研究的领域，特别是需要从婴儿期到成年期进行纵向和干预性研究，以更好地了解早产如何改变整个生命周期的运动能力。
