Methods

Subjects

Thirty pubescent boys (13 lean and 17 obese) were included in the study.

Anthropometry and evaluation of pubertal stage

The body mass index (BMI) was calculated from weight and height (kg/m²). Z-scores of BMI were calculated according to the Rolland-Cachera model.6 Fat mass (FM) and fat-free mass (FFM) were determined using dual x ray absorptiometry (Hologic QDR-4500 A, Beaune, Saint-Etienne, France). Prepubertal development was verified by a trained paediatrician according to the method of Tanner.7

Experimental design

No dietary restriction was imposed for the day before exercise testing. Children received a standard breakfast on entering the hospital for the day (07.00 h). Two hours later they performed a graded exercise on a cycle ergometer (Ergoline 500, Bosch, Berlin, Germany) linked to a gas analyser (Ergocard Schiller, Baar, Switzerland) to determine V.o₂peak). The subjects warmed up for 5 min at 0 W. The first step was fixed at 30 W with a rectangular progression of 20 W every 3.5 min.7 The speed rate was constant for the whole test (50–60 rpm).

Indirect calorimetry and energy substrate oxidation

The fat oxidation rate was calculated by measuring the respiratory exchange ratio (RER = V.co₂/V.o₂). V.o₂ and V.co₂ (ml/min) were determined as the means of measurement during the last 30 s of each step as previously described.8 The following formula was used:

Fat (mg/min)  =  −1.7012 V.co₂ + 1.6946 V.o₂

The fat oxidation rate obtained at the end of each step of the test permitted us to construct a curve of fat oxidation vs exercise intensity for each individual. The curve was used in determining energy fat oxidation levels at 0%, 20%, 30%, 40%, 50% and 60% of V.o₂peak.

The maximal fat oxidation rate point is the power at which the increase in lipid oxidation induced by increasing workload reaches a maximum (Fat max).

Statistical analysis

Data were analysed using SAS/STATS software. Values are given as mean (SE). Unpaired Student t tests were used to compare anthropometric characteristics. Significant differences between fat oxidation rates were determined using factorial ANOVA. Post hoc comparisons were made using the Sheffe test for significant differences. The level of significance was set at p<0.05.

Results

Subjects

The characteristics of the study subjects are shown in table 1. Mean V.o₂peak values were significantly different between obese and lean boys (29.5 (5.34) ml/kg/min and 44.3 (2.31) ml/kg/min, respectively; p<0.05).

Fat oxidation rate during exercise

Figure 1 shows the fat oxidation rates expressed according to FFM (mg/min/FFM). In this instance, lean subjects used more fat than obese subjects during exercise at 40%, 50% and 60% of V.o₂peak.

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Figure 1

Fat oxidation rate (mg/min/FFM) in lean boys (closed circles) and obese boys (open circles) with the exercise intensity expressed as relative peak oxygen consumption (V.o₂peak). *p<0.05. L, lean; Ob, obese; FFM, fat-free mass.

Fat max

Fat max occurred at a lower level of V.o₂peak in obese subjects than in lean subjects (47.4% (1.26%) vs 54.8% (1.03%), p<0.05). Fat max was also lower in obese subjects than in lean subjects (6.53 mg/min/FFM vs 8.23 mg/min/FFM, p<0.05).

Discussion

The main result of this study suggests that pubertal obese boys have lower fat oxidation rates at 40%, 50% and 60% of V.o₂peak than lean boys when FFM is considered. No significant differences were found at 20% and 30% of V.o₂peak.

Fat max occurs at a significantly higher percentage of V.o₂peak in lean pubertal boys than in obese pubertal boys. The results of this study agree with those of Riddell et al4 and Brandou et al.5 Riddell et al showed that, in healthy boys aged 11–12 years, Fat max occurs at 56% of V.o₂peak and the fat oxidation rate is 8.18 mg/min/FFM. Brandou et al5 found that Fat max occurred at 50% of maximal aerobic power in prepubertal obese boys (6.94 mg/min/FFM) and at 47% of theoretical maximal aerobic power in postpubertal obese boys (5.43 mg/min/FFM).

During exercise the fat oxidation rate in mg/min increases with FFM. However, in relative values which better express the effectiveness of FFM (qualitative aspect) to oxidise fat, a decrease in fat oxidation was observed in obese subjects.

Muscular modifications induced by obesity and being sedentary may partially explain the differences in fuel oxidation mechanisms. Muscle fibre type distribution is modified with obesity. Compared with lean subjects, obese subjects have a higher percentage of type II fibres (fast twitch fibres where carbohydrate oxidation predominates) and a lower percentage of type I fibres (oxidative slow twitch fibres where fat oxidation predominates).9 Changes observed in muscle fibre type distribution in relation to obesity could explain the decrease in fat oxidation rates in obese children. Others factors which may have a significant effect on the differences in fat oxidation rates in obese and lean subjects include hormonal changes during exercise, differences in fatty acid mobilisation and differences in activation of α₂-adrenergic receptors.10

Conclusion

This study shows that obesity significantly alters muscle metabolic capacities to oxidise fat during moderate exercise (40–60% V.o₂peak). Exercise intensity should be adapted to the metabolic capacities of children during weight management programmes and physical education classes. However, an increase in daily activity levels such as walking or cycling at low intensity exercise (20–30% V.o₂peak) will have the same effect in obese and healthy boys.