term, counteracted by increased energy intake [28]. Substrate utilization has been
studied in obese subjects in relationship with physical training (fig.1). Exercise
training program has been shown to prevent the reduction of basal fat oxidation
that is associated with diet-induced weight loss [29]. The impact of high-intensity
exercise on energy expenditure, lipid oxidation and body fatness was also studied
by Yoshioka et al. [30]: in his series it is shown that high intensity exercise
produced a greater postexercise, postprandial oxygen consumption as well as
fat oxidation than the resting session, suggesting that high-intensity exercise
favors a lower body fat deposition which might be related to an increase in postexercise
energy metabolism, that is mediated by beta-adrenergic stimulation.
Insulin resistance, associated to obesity [31] seems also be reduced by
physical training: in a study on obese adult and young rats, it has been showed
that exercise and food restriction can provide protection against development of
insulin resistance in fat cells by slowing development of fat cell hypertrophy
[32]. In this study physical training is shown to be more effective than caloric
restriction, since exercise-trained rats have much smaller and more insulin
responsive fat cells than sedentary controls of the same body weight. Ferguson
et al. [33] have studied the effects of physical training and its cessation on
insulin resistance in obese children: some components (plasma TG, insulin, %
fat) of the insulin resistance syndrome are improved as a result of 4 months of
physical training in obese children, however, these benefits are lost when obese
children become less active. Fasting insulin concentration in relationship to cardiovascular
reactivity to exercise in obese children was studied by Gutin et al.
[34] demonstrating a significant relationship between fasting insulin concentration
and cardiovascular reactivity to exercise, supporting the hypothesis that
the relationship between hyperinsulinemia and hypertension is mediated by
sympathetic nervous tone and that this process begins in childhood. Physical
training seems to have an effect also on plasma leptin concentration in obese
children [35]: it has been demonstrated that leptin decreased during a 4-month
period of physical training, and increased in the 4 months after cessation of PT;
decreasing leptin values were greater in children with higher pretraining leptin
concentrations, in those whose total mass increased least and in those whose
insulin concentrations decreased most.
Leptin levels seem also to be correlated with RMR: a negative correlation
between RMR and leptin levels, independent of body composition has been
0
20
40
60
80
100
Plasma
FA
Plasma
FA
Nonplasma
FA
Nonplasma
FA
CHO
CHO p 0.01
p 0.01
p 0.05
Before After
Fig. 1. Effect of endurance training on plasma free fatty acid turnover and oxidation
during exercise (with permission from Martin et al. [67]).
demonstrated [36]. In this study, differences were also shown in substrate oxidation
rates among DNA sequence variations in the leptin gene (LEPR polymorfism):
Lys656Lys showed a trend to oxidize more carbohydrates and less fat
than Asn656 carrier.
All these data from the literature stress the beneficial role of physical exercise
in obese children, not only for weight loss but also for a significant
improvement of the main metabolic parameters (very often altered in these subjects)
in fact, if we take into account that long term prognosis of obesity could
be severe due to the microvascular complications associated to the disease, the
reversibility of metabolic abnormalities is a crucial aspect for the quality of life
of these children. If the obese child and his family are well informed and educated
about this crucial aspect probably his compliance will be good with a consequent
significant improvement of his health.
Genetic Factors, Development of Obesity and Response to
Physical Training
The contribution of genetic factors to the development of obesity is estimated
to range between 25 and 40% [37]. In most cases obesity susceptibility
is a polygenic trait [38]. The number of genes, markers, and chromosomal
regions that have been associated or linked with human obesity phenotypes is
now above 250 [39].
There is increasing evidence that the major affectors of body fat content,
energy intake and energy expenditure are also influenced by genetic factors, as
well as responsiveness to dietary intervention [40].
Also predisposition to physical fitness has been evaluated in several studies.
The genes and markers with evidence of association or linkage with a performance
or fitness phenotype in sedentary or active people, in response to acute
exercise or for training induced changes, are positioned on the genetic map of all
autosomes and the X chromosome: the 2001 map includes 71 loci on the autosomes
and two on the X chromosome [41]. When the genotype is not available,
inferences of the genetic influences was made from the phenotype, which is
mostly based on the statistical analysis of the distribution in physical activity
measures in related individuals and family. These studies express the risk for a
relative of a very active or non-active person to be very active, or not, compared
to the overall population [42]. If there is a significant association of an allele with
a more active or less active phenotype, almost all carriers of this allele will have
a high daily physical activity level, and only few of the carriers will show a low
daily physical activity level. Maes et al. [43] studied inheritance of physical fitness
in 10-year-old twins and their parents: the significance and contribution of
genetic and environmental factors to variation in physical fitness were tested with
model fitting. Performance-related fitness characteristics were moderately to
highly heritable. Genomic scan on genes affecting body composition before and
after training was studied in 364 sib-pairs from 99 Caucasian families [44]. A significant
linkage for changes in fat-free mass and the IGF1 genes and suggestive
evidence was found for changes in fat-mass and fat-percentage at 1q31 and
18q21–q23, in fat-percentage with the uncoupling protein 2 and 3 genes, and in
BMI at 8q23–q24, 10p15 and 14q11, for fat-mass at 14q11, and finally for
plasma leptin levels with the low-density lipoprotein receptor gene. This interesting
study provides the first genomic scan on genes involved in exercise-traininginduced
changes in body composition. One of the most important genes involved
in the regulation of metabolic response to exercise is the uncoupling protein gene:
the uncoupling protein 3 (UCP 3) is a mitochondrial membrane transporter
mainly expressed in skeletal muscle that is shown to be associated with obesity,
and is also associated in body composition changes after regular exercise [45].
Finally, we could assume that there are many factors (genetic, social,
environmental) affecting the predisposition of children (and adults) to practice
sports and physical activity, and also affecting the metabolic and cardiovascular
effects of PT on MR, RMR, percent fat-free fat mass.
It is obviously assumed that the effect of physical training on obesity in
children is dependent by almost all these factors.
The explanation of these different results on the effects of sport activity
on childhood obesity it is probably due also to genetic characteristics of the
children studied.
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