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Cardiopulmonary exercise performance in prematurely born children
1Department of Pediatrics and Child Health, University of Manitoba, Children's Hospital of Winnipeg, Canada.
Insights
Children born prematurely have lower peak oxygen uptake (VO2) due to lean body mass, not cardiopulmonary limitations. Their exercise ventilation differs from term-born peers, impacting breathing regulation.
Area of Science:
- Pediatric Pulmonology
- Exercise Physiology
- Neonatology
Background:
- Children born prematurely often exhibit reduced peak oxygen uptake (VO2) compared to term-born peers.
- This deficit is frequently attributed to ventilatory limitations during exercise.
Purpose of the Study:
- To compare exercise ventilation and cardiac output in childhood survivors of prematurity-related lung disease with controls.
- To identify the underlying reasons for diminished peak VO2 in this population.
- To describe and compare the ventilatory response to incremental exercise.
Main Methods:
- Pulmonary function tests and progressive exercise tests were conducted on 32 children (8-9 years old).
- Cardiac output and physiologic dead space were measured during submaximal exercise in 15 participants.
- Results were compared to age- and sex-matched, term-born control children.
Main Results:
- Prematurely born children showed lower peak VO2, correlated with lean body mass.
- Heart rate-VO2 relationship and stroke volume were comparable to controls.
- Children with a history of bronchopulmonary dysplasia or hyaline membrane disease exhibited increased exercise hyperpnea (higher breathing frequency) and lower end-tidal PCO2.
Conclusions:
- Reduced peak VO2 in prematurely born children is primarily predicted by lean body mass, not cardiopulmonary factors.
- Ventilation does not appear to limit exercise performance in this group.
- Breathing regulation during exercise seems to differ between prematurely born and term-born children.
Abstract:
Prematurely born children have reduced peak VO2 compared with their peers, inferentially attributed to ventilatory limitation. The primary purpose of this study was to compare exercise ventilation and cardiac output in a sample of childhood survivors of lung disease of prematurity with those of a control group to elucidate reasons for lower peak VO2. A secondary aim was to describe and compare the ventilatory response to incremental exercise. Thirty-two children, aged 8-9 y, were recalled for lung function and progressive exercise tests. Fifteen of them also performed submaximal exercise with measurement of cardiac output (indirect [CO2] Fick) and physiologic dead space. Results were compared with those of term-born, age- and sex-matched, control children. Pulmonary function tests showed mild airflow limitation. Peak VO2 was lower in prematurely born children compared with control children, and was correlated with lean body mass. Their heart rate-VO2 relationship and stroke volume were similar to that of term-born control children. Children with a history of bronchopulmonary dysplasia and hyaline membrane disease as infants exhibited greater exercise hyperpnea than did healthy control children, because of higher breathing frequency, and maintained lower end-tidal PCO2 during submaximal exercise. Physiologic dead space normalized for body weight was similar in preterm and term-born children. Lower peak VO2 in this population is not caused by cardiopulmonary factors, but is best predicted by lean body mass. Ventilation did not limit exercise performance, although it appears that breathing during exercise is regulated differently in prematurely born children than in term-born children.
