Effect of Intrauterine Growth Restriction on Respiratory Muscle Function and Exercise Tolerance in Childhood

Introduction

Epidemiological evidence supports the existence of a link between intrauterine growth restriction (IUGR) and reduced exercise capacity in young adulthood. Prolonged intrauterine hypoxia results in redistribution of fetal cardiac output towards the vital organs at the expense of skeletal muscles, and experimental data show that the muscles of animals exposed to IUGR may suffer permanent structural and functional changes. Prematurity, which often accompanies IUGR, is also associated with reduced exercise capacity later in life, supposedly due to airflow limitation, air trapping and/or reduced gas-exchange capacity.

The respiratory muscles (RM) play a central role in the development (and perception) of locomotor muscle fatigue, which represents the major determinant of exercise limitation in otherwise healthy subjects. Heavy and/or sustained respiratory work leads to accumulation of metabolites in RM and triggers reflexes that increase the sympathetic vasoconstrictor outflow to the skeletal muscles, thus promoting fatigue. In support of the above concept, targeted RM training has been shown to increase the fatigability threshold and improve exercise performance.

RM function can be assessed by means of strength and endurance, which can be estimated non-invasively by the maximum inspiratory and expiratory pressure (Pimax and Pemax), and the tension-time index (TTImus), respectively. TTImus is a composite parameter that reflects the balance between the capacity of RM and the load imposed upon them; high TTImus values indicate low endurance and increased risk of respiratory fatigue. In adults, impaired exercise tolerance is associated with reduced RM strength and endurance, both in normal and pathological conditions. However, similar data are not available in children.

Hypothesis and objectives