Manferdelli Giorgio, Barton Gregory P, Babb Tony G, Millet Grégoire P, Nelson Michael D, Levine Benjamin D, Goss Kara N
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, Dallas, Texas, USA.
Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Compr Physiol. 2025 Oct;15(5):e70049. doi: 10.1002/cph4.70049.
Premature birth (< 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.
10 preterm born (6F, age: 30 ± 5 years, body mass index [BMI]: 27.0 ± 6.3 kg/m, gestational age: 30 ± 3 weeks) and 8 term born (3F, age: 29 ± 5 years, BMI: 25.4 ± 4.6 kg/m, 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-vOdiff, Fick equation).
Oxygen uptake (V̇O) 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), V̇O (1.58 ± 0.29 vs. 2.52 ± 0.85 L/min, p = 0.017), Q̇c (7.5 ± 1.0 vs. 8.9 ± 1.6 L/min/m, p = 0.057), while a-vOdiff (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/m, p = 0.032).
Preterm born adults present with lower exercise capacity compared to age-matched peers born at term. Central mechanisms, primarily stroke volume, underlie exercise limitation in this population.
早产(妊娠<37周)与运动能力降低有关。然而,具体的潜在机制仍不清楚。本研究调查了静息心肺功能正常但运动时呼吸困难的早产成年人在氧运输链中运动受限的机制。
10名早产成年人(6名女性,年龄:30±5岁,体重指数[BMI]:27.0±6.3kg/m²,胎龄:30±3周)和8名足月出生的成年人(3名女性,年龄:29±5岁,BMI:25.4±4.6kg/m²,胎龄:40±0周)进行静息肺量计检查和心肺运动试验,包括两次5分钟的次最大强度骑行运动(30和60W),随后进行递增运动至疲劳。我们逐次测量气体交换(定制系统)、心率(HR,12导联心电图)、心输出量(Q̇c,乙炔再呼吸法),并计算动静脉氧差(a-vOdiff,Fick方程)。
两组在静息、30W和60W时的摄氧量(V̇O₂)相似。在运动峰值时,与足月出生的同龄人相比,早产成年人的功率输出较低(108±18 vs. 208±69W,p<0.001)、V̇O₂较低(1.58±0.29 vs. 2.52±0.85L/min,p=0.017)、Q̇c较低(7.5±1.0 vs. 8.9±1.6L/min/m²,p=0.057),而动静脉氧差(12.6±1.7 vs. 14.1±1.6mL/dL,p=0.096)和心率在两组间相似(175±16 vs. 185±8bpm,p=0.104)。与足月出生的成年人相比,早产成年人从静息到运动峰值时每搏量指数的增加减弱(8±7 vs. 15±6mL/m²,p=0.032)。
与年龄匹配的足月出生同龄人相比,早产成年人的运动能力较低。该人群运动受限的主要中枢机制是每搏量。