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Adult survivors of preterm birth. What spirometry conceals, exercise tests reveal.

On a global scale, the number of preterm births has steadily increased during the past several decades (1). Preterm births (,37 wk gestation) currently account for 11% of all births worldwide (1). Longterm respiratory impairment and reduced exercise capacity are well-documented complications of extreme preterm birth (2–5). Bronchopulmonary dysplasia (BPD), a chronic respiratory condition mainly affecting infants born at less than 28 weeks gestational age, can develop in up to 40% of infants born prematurely with very low birthweight (6). Preterm infants with BPD are at higher risk for subsequent development of chronic obstructive pulmonary disease (COPD), and possibly a more rapid decline of lung function, than preterm infants without BPD (7, 8). Despite considerable advances in the management of BPD in preterm infants (prenatal steroids, surfactant, avoidance of oxygen toxicity and barotrauma), the incidence of BDP has not changed in recent years (9). Moreover, symptomatic adult survivors of BPD are increasingly encountered in clinical practice by pulmonologists. Optimal management of such patients is challenging and awaits a greater understanding of the pathophysiology and natural history of this condition. A recent study confirmed that young adults (mean age, 24 years) who have survived BPD were significantly more likely to have persisting mild spirometric abnormalities, symptoms of wheeze and breathlessness, a diagnosis of asthma, and perceived poor quality of life compared with full-term control subjects (2). In extremely preterm infants (,28 wk gestation), there is interruption of the normal development and maturation of the alveoli and surrounding microvasculature. These factors are thought to be pivotal pathogenic mechanisms of BPD (10). However, it is clear that pathophysiologic abnormalities of BPD are heterogeneous and depend on the nature and extent of the inflammatory injury to the developing lung because of the effects of hyperoxia and infection, together with effects of barotrauma, during prolonged mechanical ventilation. Birth weight, nutrition, sex, history of maternal smoking, and genetic susceptibility are additional factors that shape the expression of the disease. Common physiologic abnormalities described in small studies of adult survivors of BPD include increased large and small airway resistance, increased airway hyperreactivity, pulmonary gas trapping, lung hyperinflation, increased pulmonary vascular resistance, and reduced diffusing capacity for carbon monoxide (2). Computed tomography has revealed emphysema, regional gas trapping, and lung scarring in highly variable combinations (2, 11). Cardiopulmonary exercise testing has confirmed that young adult subpopulations with a history of BPD have reduced peak oxygen consumption compared with healthy control subjects, but the mechanisms of exercise limitation remain unclear and deserve closer attention (4). In this month’s issue of AnnalsATS, Lovering and colleagues (pp. 1528–1537) have carefully explored the possible role of dynamic respiratory mechanical abnormalities in contributing to exercise limitation in a group of adults born prematurely and now in their early twenties (12). The authors compared expiratory flow limitation, breathing pattern, operating lung volumes, dyspnea, and leg discomfort ratings during incremental cycle exercise in three well-characterized groups: adults born preterm either without BPD (PRE) (n = 15) or with BPD (n = 20), and healthy full-term control subjects (n = 20). The PRE and BPD groups both had only minor airway obstruction but had significantly reduced peak work rates, earlier respiratory mechanical constraints on tidal volume expansion (at lower submaximal ventilation), and greater leg discomfort during exercise than control subjects. Compared with PRE and control subjects, those with BPD had greater estimated expiratory flow limitation but, surprisingly, only a minority (5/20) showed minor dynamic lung hyperinflation. A limitation of the study is that comparisons across groups were made at different absolute oxygen consumption, rather than at standardized work rates and ventilation. What is missing, therefore, is a demonstration that increased dyspnea intensity ratings at comparable work rates in both preterm groups reflect higher ventilation and lower inspiratory reserve volume at those comparison points. The physiologic differences between PRE and BPD would be unlikely to have significant sensory consequences in the setting of a preserved resting inspiratory capacity. Notably, the reductions in dynamic inspiratory reserve volume and concomitant increases in dyspnea ratings as ventilation increased throughout exercise were similar in PRE and BPD. The