Dose-dependent relationship between severity of pediatric obesity and blunting of the growth hormone response to exercise

In children, exercise modulates systemic anabolism, muscle growth, and overall physiological development through the growth hormone (GH)-insulin-like growth factor I (IGF-I) axis. GH secretion, at rest and during exercise, changes with age and maturational status and can be blunted by hyperlipidemia and obesity, with possible negative effects on physiological growth. However, little is known about the effect of progressively more severe pediatric obesity on the GH response to exercise and its relationship to pubertal status. We therefore studied 48 early- or late-pubertal obese children [body mass index (BMI) >95th percentile, separated in tertiles with progressively greater BMI] and 42 matched controls (BMI <85th percentile), who performed ten 2-min cycling bouts at ∼80% of maximal O2 consumption, separated by 1-min rest intervals. Plasma GH and IGF-I were measured at baseline and end exercise. GH responses were systematically blunted in obese children, with more pronounced blunting paralleling increasing BMI. Although overall the GH response to exercise was greater in late-pubertal than in younger children, this blunting pattern was observed in early- and late-pubertal children. Our results reveal insight into the interaction between pediatric obesity and key modulators of physiological growth and development and underscore the necessity of optimizing physical activity strategies for specific pediatric dysmetabolic conditions

Prenatal and nutritional influences on skeletal development: lessons from animal studies

It is now well established that the onset of adult diseases such as heart disease, stroke, type 2 diabetes and hypertension are linked to an adverse uterine growth environment, in particular through maternal nutrition, during development of the individual. The geographical distribution of the incidence rate of heart disease is similar to that of osteoporosis. This may indicate a link between maternal nutrition during pregnancy and the subsequent risk of developing osteoporosis in the offspring. This review summarises what we know to date, from animal models, about maternal nutrition and the subsequent alterations in the offspring’s skeletal structure