During childhood, heart growth is closely associated with somatic growth including increases in body weight, fat-free body mass (FFM), and height. However, with age, greater variability in heart size in relationship to body size is observed, presumably attributable to the increased effect of cardiac workload. At this time, little is known as to what functional attributes (eg, aerobic fitness) contribute to cardiac workload and the relative contribution of these attributes to heart growth during childhood and adolescence. In this article, we report cross-sectional and longitudinal relationships among aerobic fitness, body size, blood pressure (BP), and left ventricular mass (LVM) through puberty including the predictors of heart growth during puberty and the tracking of LVM from pre-puberty to late and post-puberty. Describing the predictors of heart size and heart growth and establishing the likelihood that a large heart, relative to peers, may (or may not) remain a large heart should aid pediatricians in discerning between normal developmental increases in LVM and increases in LVM suggestive of excessive heart growth (left ventricular hypertrophy).


Using a repeated-measures design, we assessed aerobic fitness, FFM, fatness, weight, height, sexual maturation, resting BP, peak exercise BP, and LVM in 125 healthy children (mean baseline age: 10.5 years) for a period of 5 years. All subjects were either in prepuberty or early puberty at the beginning of the study. At follow-up, 110 subjects attempted all research procedures (87% of the initial cohort). Using anthropometry and bioelectrical impedance, we measured FFM, fatness, weight, and height quarterly (once every 3 months) for a total of 20 examinations. Resting BP and LVM (2-dimensional echocardiography) were also assessed quarterly. Aerobic fitness, peak exercise BP, and sexual maturation (staging of secondary sex characteristics and, for boys, serum testosterone) were measured annually (5 examinations). The same field staff conducted all examinations.

Statistical methods included Spearman rank correlation coefficients (rs) calculated to estimate how well the year 5 LVM was predicted by LVM at earlier years. We also categorized the LVM data into tertiles and reported the percentage who remained in the extreme tertiles in year 5, given they began in that tertile in year 1. Gender-specific stepwise multivariate analysis was used to evaluate predictors of follow-up LVM and predictors of changes in LVM. The latter model examined whether the variability in the changes in LVM, as quantified by subject-specific slopes, could be explained by changes in predictor variables, also quantified by subject-specific slopes.


At baseline and at follow-up, boys tended to be taller, leaner, more aerobically fit, and had greater LVM than girls. Rate of change for these variables was also greater in boys than girls. For example, LVM increased 62% in boys and 48% in girls. At year 5, subjects had advanced at least 1 stage in genital or breast development and over 80% of the subjects were in late- or post-puberty. Significant and strong tracking of heart size (rs = .65–.87) was observed. The likelihood that a subject would be in an extreme tertile for heart size at follow-up was approximately doubled if he or she started there at baseline.

In boys, baseline FFM explained 54% of the variability in follow-up LVM. Change in aerobic fitness and change in FFM explained 55% of the variability in change in LVM. In girls, baseline aerobic fitness and fatness explained 45% of the variability in follow-up LVM. Because FFM did not enter in this model, we constructed an alternative model in which baseline aerobic fitness adjusted for FFM was entered. Using this approach, 43% of the variability in follow-up LVM was explained by baseline FFM, fatness, and adjusted aerobic fitness. Change in FFM explained 58% of the variability in change in LVM. For both boys and girls, all statistically significant variables entered as positive regression coefficients.


Our tracking results suggest predictability in LVM, most likely attributable to normal growth and regulated by the genetic and hormonal influences that affect FFM as well as LVM. Our multiple regression results indicate that during adolescence FFM is an important determinant of heart size and heart growth for both boys and girls but changes in aerobic fitness, presumably attributable to improvements in cardiac function, also affect heart growth in boys. This latter finding indicates that the known age-related decrease in the ability of body size to fully predict heart size begins sooner in males than females. It also suggests that changes in cardiac functioning as well as morphologic increases in lean tissue cause the “athletic heart syndrome.”

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