Journal of Childhood Obesity Open Access

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Physical Activity: Benefits for Prevention and Treatment of Childhood Obesity

Pinto RM1-5*, Silva JVP5,6, Monteiro GMC5,6, de Resende RC5,6, Clemente RD5,6 and de Souza CSB4,5

1Department of Biology, Replicon Research Center, Catholic University of Goiás, Goiânia, Brazil

2Postgraduate Program in Genetics, Catholic University of Goiás, Goiânia, Brazil

3Health Sciences PhD Program, Federal University of Goiás, Goiânia, Brazil

4Professor of Pediatrics, Federal University of Goiás, Goiânia, Brazil

5Academic League of Endocrinology and Nutrology, Federal University of Goiás, Goiânia, Brazil

6Graduate Student of Medicine, Federal University of Goiás, Goiânia, Brazil

*Corresponding Author:

Pinto RM
Department of Biology, Replicon Research Center
Catholic University of Goiás, Goiânia, Brazil
Tel: +55 62 992637102
E-mail: drarenatamachado@gmail.com

Received date: June 11, 2018; Accepted date: July 09, 2018; Published date: July 16, 2018

Citation: Pinto RM, Silva JVP, Monteiro GMC, de Resende RC, Clemente RD, et al. (2018) Physical Activity: Benefits for Prevention and Treatment of Childhood Obesity. J Child Obes S2-003

Copyright: © 2018 Pinto RM et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Abstract

Common obesity, also named exogenous obesity, is a complex disease with multifactorial etiology. In such complex diseases, it is necessary that genetic factors associate with a favorable environment for the phenotype to emerge. After birth, the child´s lifestyle is extremely relevant for determining or preventing the development of obesity.

The practice of Physical Activity (PA) plays a prominent role in the regulation of energy expenditure, since it is the only activity that is totally under conscious control. PA is capable of promoting positive adaptations on childhood obesity and act as aid in its prevention and treatment.

In obese children, the practice of PA leads to: improvement in body composition (reduction of fat mass and increase of lean mass), improvement in cardiorespiratory fitness, strength gain, proprioception, increased caloric expenditure, increased resting metabolic rate, increased tolerance to the use of glucose as an energy substrate, increased insulin sensitivity, improvement in lipid metabolism, and reduction of the inflammatory status.

Keywords:

Obesity; Physical activity; Physical exercise; Childhood obesity

Abbreviations:

%BF: Percentage Body Fat; AC: Abdominal Circumference; BMI: Body Mass Index; BW: Body Weight; CL: Cardiac Load; CFV: Cardiac Frequency Variation; CRP: C Reactive Protein; DS: Dyslipidemia; DM: Diabetes Mellitus; GI: Glucose Intolerance; HDL: High Density Lipoprotein; Il-6: Interleukin 6; IN: Insulin; IR: Insulin Resistance; LDL: Low Density Lipoprotein; LPA: Level of Physical Activity; MM: Muscle Mass; PA: Physical Activity; PAI-1: Plasminogen Activator Inhibitor-1; SBP: Systolic Blood Pressure; SNA: Sympathetic Nervous Activity; TC: Total Cholesterol; TG: Triglycerides; TNF-a: Tumor Necrosis Factor-a; WHO: World Health Organization; VO2max: Maximum Volume of Oxygen.

Introduction

Obesity is a disease of energy homeostasis caused by excess of energy supply in relation to the demands of the body. As a consequence, there is an exaggerated energy accumulation in the form of adipose tissue. In adults, the World Health Organization (WHO) defines obesity as a body mass index (BMI) value upper or equal to 30 kg/m2. In children and adolescents the nutritional status is based on the BMI-for-age 2006 WHO growth standards. Obesity is defined as when the BMI is above 2 standard deviations from the mean for sex and age [1].

BMI has the limitation of not distinguish fat from free-fat mass, which can upper or under estimated obesity. Methods that measure directly the fat mass are more specific and sensible to classify obesity in children, such as densitometry and bioelectrical impedance analysis, as they provide information of body composition [2-4] although they are not routinely used in clinical practice.

Obesity prevalence has increased worldwide, reaching epidemic proportions in many developed and developing countries, being an important cause of morbidity and mortality in the developing world [5]. A report published in 2014 by the Overseas Development Institute of Great Britain [6] shows a general picture of the evolution of obesity around the world in the last 30 years: North America has 70% of the adult population overweight, the largest on the planet; Latin America has a slightly lower index of 63%, which is well above the 30% that was observed in the 1980s.

Specific for childhood obesity a high prevalence is also seen worldwide [7-9]. In the US the obesity prevalence is of 16.9% in 2-19 years-old age group and 8.4% in the 2-5 years-old group [10], with an upward trend of prevalence of children with the severest forms of obesity, with 2% of class 3 obesity prevalence [11].

Determinants of Childhood Obesity: Nature or Nurture?

Common obesity, also named exogenous obesity, is a complex disease with multifactorial etiology. In such complex diseases, it is necessary that genetic factors associate with a favorable environment for the phenotype to emerge [12,13]. Generally, many studies suggest a strong genetic component in human obesity, but pleiotropic genetic syndromes and monogenic diseases account for only 1% of obesity cases [12]. Endocrinological conditions such as Cushing Syndrome and hypothyroidism, are only found in 1 to 3% of obese children [9,14].

Studies with monozygotic twins show that heredity accounts for 40% to 70% of inter-individual variation in cases of common obesity, meaning that 30% to 60% is due to environmental factors [9,12].

The environment can affect human weight since the womb [15,16]. The prenatal factors that interfere with the risk of future obesity include: gestational diabetes mellitus (DM) [16], maternal obesity [17], and smoking during pregnancy [16,18]. Epigenetic changes, like DNA methylation or histone modification in gene regulatory regions are mechanisms that induce these heritable changes in adiposity and explain how these prenatal factors predispose to future obesity [9,19].

After birth, the child´s lifestyle is extremely relevant for determining or preventing the development of obesity. Some habits augment obesity risk, like: formula-feeding instead of breastfeeding, overeating, preference for fast food, omitting breakfast, midnight snacking, playing video games, excess of screen time and lack of exercise [9,20-23].

Physical Activity and Physical Exercise

Physical activity (PA) and physical exercise are terms that describe different concepts. Although they are usually confused with one another, and the terms are sometimes used equivalent [24].

PA is defined as any movement produced by skeletal muscles that result in energy expenditure. Physical activity in daily life can be categorized into occupational, sports, conditioning, household, or other activities. Exercise is a subset of PA that is planned, structured, and repetitive and has a final or an intermediate objective, like the improvement or maintenance of physical fitness. Physical fitness is a set of attributes that are either health or skill related [25].

For children and adolescents, PA include games, sports, transportation, chores, recreation, physical education, or planned exercise, in the context of family, school, and community activities [26].

WHO Recommendations for Physical Activities in Childhood

WHO seeking to improve cardiorespiratory and muscular fitness, bone health, cardiovascular and metabolic health biomarkers recommends that children and youth aged 5-17 should accumulate at least 60 minutes of moderate to vigorous intensity PA daily. Amounts of PA greater than 60 minutes provide additional health benefits and most of the daily PA should be aerobic [27].

Sedentary children should start with small amounts of PA and gradually increase duration, frequency and intensity over time. The concept of accumulation refers to meeting the goal of 60 minutes per day by performing activities in multiple shorter bouts spread throughout the day (e.g. 2 bouts of 30 minutes), then adding together the time spent during each of these [28,29]. Vigorous intensity activities should be incorporated, including those that strengthen muscle and bone, at least 3 times per week [29].

These recommendations are relevant to all healthy children aged 5-17 years, unless specific medical conditions indicate the contrary, irrespective of gender, race, ethnicity, or income level. Whenever possible, children and youth with disabilities should also meet these recommendations. Although, they should work with their health care provider to understand the types and amounts of physical activity appropriate for them considering their disability [30].

Physical Activity and Childhood Obesity

The practice of PA plays a prominent role in the regulation of energy expenditure, since it is the only activity that is totally under conscious control. PA is capable of promoting positive adaptations on childhood obesity and act as aid in its prevention and treatment [9,31].

Obesity promotes a low-grade chronic inflammation state with the release of cytokines such as tumor necrosis factor, Creactive protein and interleukin 6 [31]. The practice of PA reduces the levels of these inflammatory cytokines [32-34] in addition to increasing cytokines with anti- inflammatory action such as interleukin 10 [31,35] and adiponectin [34,36,37] even without concomitant dietary modification or other lifestyle changes [38].

Regular PA is associated with improvements in aerobic capacity [39-45] strength, muscle growth [46,47] bone mass [35] and weight or body composition [35,41,42,44-49]. Metabolic benefits include the reduction of blood pressure [38,39,48] reduction of glycemia [39,48] leptin [36,37,50-52] and insulin resistance [41,48,49] improvement of the lipid profile with reduction of total cholesterol and increase of HDL cholesterol [31,49,52-55].

Dieting alone often fails to achieve long-term weight maintenance in obese patients, probably because the weight loss itself leads to a reduction in leptin levels that result in an increase in hunger [38]. The association of PA to diet modifications emerges as an optimal measure to modify the regulation of adipose tissue activity and the systemic target organs responses to it.

Active muscle tissue produces the hormone “Irisin”, a 112- amino acid peptide whose main function is to modify white adipose tissue cells into “brite”-brown-in-white-adipocytes whose characteristics resemble those of brown adipose tissue. These cells are rich in mitochondria that increase thermogenesis and energy expenditure they also have a secretory profile of adipokines contrary to that found by white adipose tissue, with secretion of cytokines with anti-inflammatory and improver of insulin sensitivity effects [56,57].

There is an inverse association between PA level and emergence of obesity, especially in the early stages of life [29,32,58]. The magnitude of benefits may vary depending on the type and amount of PA [38,59]. Many studies were designed to access multiple effects that different forms of PA have on childhood weight and health. Table 1 summarizes the main results.

Study Country No. (F:M) Nutritional Status Type of exercise Outcome
Araujo et al. [39] Brazil 30 (21:9) Obese Aerobic plus resistance #V02max; $GI
Davis et al. [48] USA 222 (128:94) Overweight and obese Aerobic $GI;$IR;$%BF;$BMI
Fazelifar et al. Iran 24 (0:24) Overweight and obese Aerobic plus resistance; none #Adiponectin
Fazelifar et al. [36] Iran 24 (0:24) Overweight and obese Aerobic plus resistance; none $ Leptin
Karacabey [50] Turkey 40 (0:40) Overweight and obese Aerobic; none $Leptin
Kim et al. [32] Korea 26 (0:26) Overweight and obese Aerobic; none #Adiponectin;$CRP
Laguna et al. [40] Spain 437 (227:210) Overweigt and eutrophic Cycloergometer #CFV;$BMI
Lai et al. [41]2013 China 88 (48:40) Obese Aerobic $CFV;$%BF;$IG;$DS
Lee et al. [42] USA 45 (0:45) Obese Aerobic plus resistance $%BF;$BMI;$BW;#MM
Legantis et al. [43] Greece 48 (23:25) Overweight and eutrophic Isometric grip #SNA;#CL;#SBP
Manki et al. Tunisia 131 (63:68) Obese Walking #V02max; $%BF
Militao et al. Brazil 34 (17:17) Overweight and obese Recreative activities $%BF;$PAS;$TC;$TG
Monteiro et al. [33] Brazil 48 (27:21) Overweight and obese Aerobic plus resistance; aerobic $IL-6;$TNF-a;$PAl-1
Park et al. [45] Korea 29 (15:14) Overweight and obese Aerobic plus resistance #V02max; $AC;$BMI
Plonka et al. [51] Poland 59 (59:0) Eutrophic Daily energy expenditure $SNA; $Leptin
Racil et al. [37] France 68 (68:0) Overweight and obese Aerobic plus resistance; aerobic #Adiponectin; $ Leptin
Schranz et al. [46] Australia 56 (0:56) Overweight and obese Resistance #MM;$ BF;$BMI
Vasconcellos et al.
[34]
Brazil 20 (6:14) Overweight and obese Aerobic; none #Adiponectin;$Leptin;$ IL-6
Velez et al. [47] Spain 28 (13:15) Overweight and obese Resistance #MM;$%BF;#BMI
Zorba et al. [49] Turkey 40 (0:40) Obese Aerobic plus resistance $%BF;$CT;$TG; $LDL;$IN
Woo et al. [52] Korea 39 (19:20) Obese and eutrophic Aerobic $SNA; $Leptin; $TG;$LDL

BF: percentage body fat; AC: abdominal circumference; BMI: body mass index; BW:body weight; CL: Cardiac load; CFV: cardiac frequency variation; CRP: C reactive protein; DS: dyslipidemia; GI: glucose intolerance; HDL: high density lipoprotein; 11-6: interleukin 6; IN: insulin; IR: insulin resistance; LDL: low density lipoprotein; LPA: level of physical activity; MM: muscle mass; PAl-1:plasminogen activator inhibitor-1; SBP: systolic blood pressure;

Table 1: Main metabolic effects of physical exercise on childhood obesity (adapted from Paes 2015 and Sirico 2018).

BF: percentage body fat; AC: abdominal circumference; BMI: body mass index; BW:body weight; CL: Cardiac load; CFV: cardiac frequency variation; CRP: C reactive protein; DS: dyslipidemia; GI: glucose intolerance; HDL: high density lipoprotein; 11-6: interleukin 6; IN: insulin; IR: insulin resistance; LDL: low density lipoprotein; LPA: level of physical activity; MM: muscle mass; PAl-1:plasminogen activator inhibitor-1; SBP: systolic blood pressure;

Table 1: Main metabolic effects of physical exercise on childhood obesity (adapted from Paes 2015 and Sirico 2018).

All these benefits make PA practice a fundamental tool to mitigate the damages associated with childhood obesity, considered to be the most important aspect of the approach to prevention and treatment of childhood obesity and its consequences [30,58,59].

Conclusion

The practice of PA is effective for prevention and treatment of childhood obesity. The magnitude of the benefits may vary depending on the type and volume of activity and extends well beyond the effects on body weight.

In obese children, the practice of PA leads to: improvement in body composition (reduction of fat mass and increase of lean mass), improvement in cardiorespiratory fitness, strength gain, proprioception, increased caloric expenditure, increased resting metabolic rate, increased tolerance to the use of glucose as an energy substrate, increased insulin sensitivity, improvement in lipid metabolism, and reduction of the inflammatory status.

It is fundamental for every health professional to be aware of PA benefits for prevention and treatment of childhood obesity. Even though achieving compliance with WHO recommendations can be difficult, it is our duty to simulate and encourage the practice of PA in childhood and adolescence.

References

  1. WHO (2009) Population-based prevention strategies for childhood obesity: Report of a WHO forum and technical meeting, Geneva :15-17.
  2. Lazarus R, Baur L, Webb K, Blyth F (1996) Body mass index in screening for adiposity in children and adolescents: Systematic evaluation using receiver operating characteristic curves. Am J Clin Nutr 63: 500-506.
  3. Danford LC, Schoeller DA, Kushner RF (1992) Comparison of two bioelectrical impedance analysis models for total body water measurement in children. Ann Hum Biol 19: 603-607.
  4. Phillips SM, Bandini LG, Compton DV, Must A (2003) A longitudinal comparison of body composition by total body water and bioelectrical impedance in adolescent girls. J Nutr 133: 1419-1425.
  5. Bell CG, Walley AW, Froguel P (2005) The genetics of human obesity. Nat Rev Gene 6: 221-234.
  6. www.odi.org.uk/future-diets
  7. Kelishadi R, Pour MH, Sarraf-Zadegan N, Sadry GH, Ansari R, et al. (2003) Obesity and associated modifiable environmental factors in Iranian adolescents: Isfahan healthy heart program-Heart health promotion from childhood. Pediatr Int 45: 435-442.
  8. Lobstein T, Baur LA, Jackson-Leach R (2010) The childhood obesity epidemic: Preventing childhood obesity. Oxford: Wiley-Blackwell: 3-14.
  9. Gurnani M, Birken C, Hamilton J (2015) Childhood obesity: Causes, consequences, and management. Pediatr Clin North Am 62: 821-840.
  10. Ogden CL, Carroll MD, Kit BK, Flegal KM (2014) Prevalence of childhood and adult obesity in the United States, 2011-2012. JAMA 311: 806-814.
  11. Skinner AC, Skelton JÁ (2014) Prevalence and trends in obesity and severe obesity among children in the United States, 1999-2012. JAMA Pediatr 168: 561-566.
  12. Pinto RM, Cominetti C, da Cruz AD (2016) Basic and genetic aspects of food intake control and obesity: Role of dopamin receptor D2 TAQIA polymorphism. Obes Res Open J 2: 119-127.
  13. Gungor NK (2014) Overweight and obesity in children and adolescents. J Clin Res Pediatr Endocrinol 6: 129-43.
  14. Crinò A, Greggio NA, Beccaria L, Schiaffini R, Pietrobelli A, et al. (2003) Diagnosis and differential diagnosis of obesity in childhood. Minerva Pediatr 55: 461-470.
  15. Barker DJ, Eriksson JG, Forsén T, Osmond C (2002) Fetal origins of adult disease: Strength of effects and biological basis. Int J Epidemiol 31: 1235-1239.
  16. Skelton JA, Irby MB, Grzywacz J, Miller G (2011) Etiologies of obesity in children: Nature and nurture. Pediatr Clin North Am 58: 1333-1354.
  17. Wrotniak BH, Shults J, Butts S, Stettler N (2008) Gestational weight gain and risk of overweight in the offspring at age 7 y in a multicenter, multiethnic cohort study. Am J Clin Nutr 87: 1818-1824.
  18. Bergmann KE, Bergmann RL, Von Kries R, Böhm O, Richter R, et al. (2003) Early determinants of childhood overweight and adiposity in a birth cohort study: Role of breast-feeding. Int J Obes Relat Metab Disord 27: 162-172.
  19. Aranceta-Bartrina J, Pérez-Rodrigo C (2016) Determinants of childhood obesity: ANIBES study. Nutr Hosp 33: 17-20.
  20. Boone JE, Gordon-Larsen P, Adair LS, Popkin BM (2016) Screen time and physical activity during adolescence: Longitudinal effects on obesity in young adults. Int J Behav Nutr Phys Act 4: 26.
  21. Temple JL, Giacomelli AM, Kent KM, Roemmich JN, Epstein LH, et al. (2007) Television watching increased motivated responding for food and energy intake in children. Am J Clin Nutr 85: 355-361.
  22. Kubo T (2014) Common approach to childhood obesity in Japan. J Pediatr Endocrinol Metab 27: 581-592.
  23. Barquera S, Hernández-Barrera L, Rothenberg SJ, Cifuentes E (2018) The obesogenic environment around elementary schools: Food and beverage marketing to children in two Mexican cities. BMC Public Health18: 461.
  24. Caspersen CJ, Powell KE, Christenson GM (1985) Physical activity, exercise, and physical fitness: Definitions and distinctions for health-related research. Public Health Rep 100: 126-31.
  25. www.cdc.gov/nccdphp/sgr/pdf/sgrfull.pdf
  26. World Health Organization (WHO) (2010) Global recommendations on physical activity for health, Geneva, Switzerland.
  27. World Health Organization (WHO) (2013) Global Action plan for the prevention and control of non-communicable disease 2013-2020, Geneva, Switzerland.
  28. Landry BW, Driscoll SW (2012) Physical activity in children and adolescents. PM R 4: 826-832.
  29. Brambilla P, Pozzobon G, Pietrobelli A (2011) Physical activity as the main therapeutic tool for metabolic syndrome in childhood. Int J Obes 35: 16-28.
  30. Kelley GA, Kelley KS (2013) Effects of exercise in the treatment of overweight and obese children and adolescents: A systematic review of meta-analyses. J Obes 2013: 783103.
  31. Lima JG, Galeno Y (2015) O papel do exercício físico no tratamento da obesidade. In: Sociedade Brasileira de Endocrinologia e Metabologia; Czepielewski M, Meireles R, Carvalho GA, organizadores. PROENDOCRINO: Ciclo7. Porto Alegre: Artmed Panamericana 97-123.
  32. Kim Y, Park H (2013) Does regular exercise without weight loss reduce insulin resistance in children and adolescents? Int J Endocrinol 2013: 402592.
  33. Monteiro PA, Chen KY, Lira FS, Saraiva BT, Antunes BM, et al. (2015) Concurrent and aerobic exercise training promote similar benefits in body composition and metabolic profiles in obese adolescents. Lipids Health Dis 14: 153.
  34. Vasconcellos F, Seabra A, Cunha F, Montenegro R, Penha J, et al. (2016) Health markers in obese adolescents improved by a 12-week recreational soccer program: A randomised controlled trial. J Sports Sci 34: 564-575.
  35. Huang CJ, Zourdos MC, Jo E, Ormsbee M (2013). Influence of physical activity and nutrition on obesity-related immune function. ‎Sci World J 752071.
  36. Fazelifar S, Ebrahim K, Sarkisian V (2013) Effect of concurrent training and detraining on anti-inflammatory biomarker and physical fitness levels in obese children. Rev Bras Med Esporte 19: 349-354.
  37. Racil G, Zouhal H, Elmontassar W, Ben Abderrahmane A, De Sousa MV, et al. (2016) Plyometric exercise combined with high-intensity interval training improves metabolic abnormalities in young obese females more so than interval training alone. Appl Physiol Nutr Metab 41: 103-109.
  38. Sirico F, Bianco A, D'Alicandro G, Castaldo C, Montagnani S, et al. (2018) Effects of physical exercise on adiponectin, leptin, and inflammatory markers in childhood obesity: Systematic review and meta-analysis. Child Obes 14: 207-217.
  39. Corte de Araujo AC, Roschel H, Picanço AR, do Prado DM, Villares SM, et al. (2012) Similar health benefits of endurance andhigh-intensity interval training in obese children. PlosOne 7: e42747.
  40. Laguna M, Aznar S, Lara MT, Lucía A, Ruiz JR, et al. (2013) Heart rate recovery is associated with obesity traits and related cardiometabolic risk factors in children and adolescents. Nutr Metab Cardiovasc Dis 10: 995-1001.
  41. Lai A, Chen W, Helm K (2013) Effects of visfatin gene polymorphism RS4730153 on exercise-induced weight loss of obese children and adolescents of Han Chinese. Int J Biol Sci 9: 16-21.
  42. Lee S, Bacha F, Hannon T, Kuk JL, Boesch C, et al. (2012) Effects of aerobic versus resistance exercise without caloric restriction on abdominal fat, intrahepatic lipid, and insulin sensitivity in obese adolescent boys: A randomized, controlled trial. Diabetes 61: 2787-2795.
  43. Legantis CD, Nassis GP, Dipla K, Vrabas IS, Sidossis LS, et al. (2012) Role of cardiorespiratory fitness and obesity on hemodynamic responses in children. J Sports Med Phys Fitness 52: 311-318.
  44. Makni E, Moalla W, Trabelsi Y, Lac G, Brun JF, et al. (2012) Six-minute walking test predicts maximal fat oxidation in obesechildren. Int J Obes 36: 908-913.
  45. Park J, Miyashita M, Kwon Y, Park H, Kim E, et al. (2012) A 12-week after-school physical activity programme improves endothelial cell function in overweight and obese children: A randomized controlled study. BMC Pediatr 12: 111.
  46. Schranz N, Tomkinson G, Parletta N, Petkov J, Olds T, et al. (2014) Can resistance training change the strength, body composition and self-concept of overweight and obese adolescent males? A randomised controlled trial. Br J Sports Med 48: 1482-1488.
  47. Velez A, Golem DL, Arent SM (2010) The impact of a 12-week resistance training program on strength, body composition, and self-concept of Hispanic adolescents. J Strength Cond Res 24: 1065-1073.
  48. Davis CL, Pollock NK, Waller JL, Allison JD, Dennis BA, et al. (2012) Exercise dose and diabetes risk in overweight and obese children: A randomized controlled trial. JAMA 308: 1103-1112.
  49. Zorba E, Cengiz T, Karacabey K (2011) Exercise training improves body composition, blood lipid profile and serum insulin levels in obese children. J Sports Med Phys Fitness 51: 664-669.
  50. Karacabey K (2009) The effect of exercise on leptin, insulin, cortisol and lipid profiles in obese children. J Int Med Res 37: 1472-1478.
  51. Plonka M, Toton-Morys A, Adamski P, Suder A, Bielanski W, et al. (2011) Association of the physical activity with leptinblood serum level, body mass indices and obesity in school girls. J Phys and Pharm 62: 647-656.
  52. Woo J, Shin KO, Yoo JH, Park S, Kang S, et al. (2012) The effects of detraining on blood adipokines and antioxidant enzyme in Korean overweight children. Eur J Pediatr 171: 235-243.
  53. Militão AG, De Oliveira Karnikowski MG, Da Silva FR, Gar-cez Militão ES, Dos Santos Pereira RM, et al. (2013) Effects of a recreational physical activity and healthy habits orientation program, using an illustrated diary, on the cardiovascular risk profile of overweight and obese scho-olchildren: A pilot study in a public school in Brasilia, Federal District, Brazil. Diabetes Metab Syndr Obes 6: 445-451.
  54. Pauli JR, Cintra DE, Souza CT, Ropelle ER (2009) New mechanisms by which physical exercise improves insulin resistance in the skeletal muscle. Arq Bras Endocrinol Metabol 53: 399-408.
  55. Silveira LR, Pinheiro CH, Zoppi CC, Hirabara SM, Vitzel KF, et al. (2011) Regulation of glucose and fatty acid metabolismo in skeletal muscle during contraction. Arq Bras Endocirnol Metabol 55: 303-313.
  56. Elsen M, Raschke S, Eckel J (2014) Browning of white fat: Does irisin play a role in humans? J Endocrinol 222: 25-38.
  57. Rodrigues KCC, Pereira RM, Campos TDP, Moura RF, Silva ASR, et al. (2018) The role of physical exercise to improve the browning of white adipose tissue via POMC neurons. Front Cell Neurosci 12: 88.
  58. Guinhouya BC, Hubert H (2011) Insight into physical activity in combating the infantile metabolic syndrome. Environ Health Prev Med 16: 144-147.
  59. Velez A, Golem DL, Arent SM (2010) The impact of a 12-week resistance training program on strength, body composition, and self-concept of Hispanic adolescents. J Strength Cond Res 24: 1065-1073.
  60. Paes ST (2015) Efeitos metabólicos do exercício físico na obesidade infantil: Uma visão atual. Rev Paul Pediatr 33: 122-129.