During childhood, varying exercise modalities are recommended to stimulate normal growth, development, and health. This project investigated hormonal and metabolic responses triggered by a resistance exercise protocol in lean children (age: 9.3 ± 1.4 y, body fat: 18.3 ± 4.9%), obese children (age: 9.6 ± 1.3 y, body fat: 40.3 ± 5.2%) and lean adults (age: 23.3 ± 2.4 y, body fat: 12.7 ± 2.9%). The protocol consisted of stepping onto a raised platform (height = 20% of stature) while wearing a weighted vest (resistance = 50% of lean body mass). Participants completed 6 sets of 10 repetitions per leg with a 1-min rest period between sets. Blood samples were obtained at rest preexercise, immediately postexercise and 2 times throughout the 1-hr recovery to analyze possible changes in hormones and metabolites. Children-adult differences included a larger exercise-induced norepinephrine increase in adults vs. children and a decrease in glucagon in children but not adults. Similarities between adults and children were observed for GH-IGF-1 axis responses. Metabolically, children presented with lower glycolytic and increased fat metabolism after exercise than adults did. Obesity in childhood negatively influenced GH, insulin, and glucose concentrations. While adults occasionally differed from children, amount of activated lean mass, not maturation, likely drove these dissimilarities.

These findings suggest that excess adiposity does not appear to negatively affect the immediate GH and T responses to RE in active males; but possibly negatively affects IGF-1. However, the baseline and integrated concentrations during recovery appear negatively affected by excess adiposity.

Background: Following resistance exercise of sufficient intensity, adult males display an acute increase in testosterone (T); such increase appears diminished in obesity. While the predominant source of T production in men is the testes, adrenocortical production of T makes up a greater relative proportion of boys' T. Adrenocortical production of both T and cortisol respond to stress such as exercise. Although obesity diminishes testicular T production, obesity increases activity of the hypothalamic-pituitaryadrenal (HPA) axis. Methods: Subjects consisted of eight obese boys (age 9±1yr, height 142±7cm, mass 48±9kg, lean mass 27±4kg, body fat 40.5±5.0%) and six lean boys (age 9±1yr, height 143±8cm, mass 32±5kg, lean mass 26±4kg, body fat 15.0±3.1%). Participants first warmed up for five minutes on a cycle ergometer, and then performed six sets of ten repetitions per leg of step-ups while wearing a weighted vest; subjects rested 1 minute between sets. Step height was adjusted to 20% of each subject's height, and the vest was weighted with 50% of each subject's lean body mass as measured by DEXA. Blood samples for serum concentrations of T and cortisol were obtained from an indwelling catheter pre-exercise (PRE) and immediately post-exercise (IP). Results: T concentrations increased from PRE to IP in obese boys (+14%; p=0.018) however T concentrations did not change over time in lean boys (-8%; p=0.173). Obese boys displayed a greater percent change in T compared to lean boys (p=0.014). The percent change in concentration of T was correlated to the percent change in concentration of cortisol for all boys (ρ=0.604, p=0.022). Conclusion: T concentrations were increased following exercise in obese boys and changes in T correlated to changes in cortisol in all boys. Increases in T following exercise in obese boys may be the result of greater activity of the HPA axis.