Abstract
Purpose
Premature birth (<Ab 37 weeks gestation) is associated with lower exercise capacity. However, the specific underlying mechanisms remain poorly defined. This study investigated the mechanisms of exercise limitation across the oxygen transport chain in preterm-born adults with normal resting cardiopulmonary function but exertional dyspnea.
Methods
10 preterm born (6F, age: 30 ± 5 years, body mass index [BMI]: 27.0 ± 6.3 kg/m2, gestational age: 30 ± 3 weeks) and 8 term born (3F, age: 29 ± 5 years, BMI: 25.4 ± 4.6 kg/m2, gestational age: 40 ± 0 weeks) adults performed resting spirometry and a cardiopulmonary exercise test, consisting of two 5-min submaximal cycling exercises (30 and 60 W), followed by an incremental protocol to exhaustion. We measured breath-by-breath gas exchange (custom designed system), heart rate (HR, 12-lead ECG), cardiac output (Q̇c, acetylene rebreathe), and calculated arterial–venous oxygen difference (a-
vO2diff, Fick equation).
Results
Oxygen uptake (V̇O2) was similar between groups at rest, 30 and 60 W. At peak, compared to term-born peers, preterm adults showed lower power output (108 ± 18 vs. 208 ± 69 W,
p < 0.001), V̇O2 (1.58 ± 0.29 vs. 2.52 ± 0.85 L/min,
p = 0.017), Q̇cindex (7.5 ± 1.0 vs. 8.9 ± 1.6 L/min/m2,
p = 0.057), while a-
vO2diff (12.6 ± 1.7 vs. 14.1 ± 1.6 mL/dL,
p = 0.096) and HR were similar between groups (175 ± 16 vs. 185 ± 8 bpm,
p = 0.104). The increase in stroke volume index from rest to peak exercise was blunted in preterm compared to term-born adults (8 ± 7 vs. 15 ± 6 mL/m2,
p = 0.032).
Conclusion
Preterm born adults present with lower exercise capacity comparted to age-matched peers born at term. Central mechanisms, primarily stroke volume, underlie exercise limitation in this population.
