Search tips
Search criteria 


Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
J Adolesc Health. Author manuscript; available in PMC 2013 January 1.
Published in final edited form as:
PMCID: PMC3245515

Depressive Symptoms and Cardiorespiratory Fitness in Obese Adolescents

Lauren B. Shomaker, PhD,a,b Marian Tanofsky-Kraff, PhD,a,b Jaclyn M. Zocca, BA,a Sara E. Field, BA,a,b Bart Drinkard, MSPT, CCS,c and Jack A. Yanovski, MD, PhDa,*



Adolescent depressive symptoms have been associated with reduced physical activity. However, existing studies have relied on questionnaire measures of physical activity, which may not necessarily reflect actual energy expenditures. We sought to evaluate the relationship between depressive symptoms and objectively-measured cardiorespiratoryfitness among severely obese adolescents.


One hundred thirty-four obese (body mass index [BMI; kg/m2] ≥ 95th percentile) adolescent girls and boys (ages 12–17 years) reported their depressive symptoms on the Children’s Depression Inventory. Adolescents also participated in a maximal cycle ergometry exercise test to measure cardiorespiratory fitness. Body composition was assessed with dual-energy x-ray absorptiometry (DXA) scanning.


Among the 103 adolescents who reached maximal exertion, those with elevated depressive symptoms (16%) displayed poorer cardiorespiratory fitness than those without elevated depressive symptoms (VO2max 1873.2 ± 63.6 vs. 2012.9 ± 28.6 mL/min, p < .05). Symptoms of anhedonia also were related to lower fitness (p < .05). These effects were observed after accounting for age, sex, race, and lean mass.


Among obese adolescents, elevated depressive symptoms are associated with poorer objectively-measured cardiorespiratory fitness. Future experimental tests should investigate whether cardiorespiratory fitness acts as a mediator of adolescent depressive symptoms’ impact on obesity or obesity-related health co-morbidities.

Keywords: Adolescent, Depression, Physical fitness, Obesity, Body composition


Depression and obesity are two of our nation’s most widespread public health concerns, particularly during adolescence [1, 2]. Elevated symptoms of depression affect over 25% of adolescents [1]. Even elevated symptoms at levels that do not reach the threshold for a major depressive disorder are related to significant psychosocial impairment [3]. Adolescent obesity is similarly widespread and has major health implications. Approximately 32% of youth are overweight (body mass index [BMI; kg/m2] ≥ 85th percentile), and 17% are obese (≥ 95th percentile) [2, 4]. Overweight and obese adolescents are at heightened risk for a host of serious medical problems. These include type 2 diabetes, hypertension, dyslipidemia, impaired glucose homeostasis, steatohepatitis, sleep apnea, and intracranial hypertension [5, 6], as well as medical concerns unique to youth such as accelerated pubertal and skeletal development and orthopedic disorders [7, 8]. In spite of their common prevalence, it is only recently that the association between depression and obesity has been examined. Several meta-analyses support a relationship between symptoms of depression and obesity [911], and further indicate that depressive symptoms predict the development of obesity [9, 11]. In particular, among adolescent girls, elevated symptoms of depression are associated with an over 2.5 greater likelihood of becoming obese compared to girls without elevated symptoms [9]. Conversely, the experience of being obese may increase individuals’ depressive symptoms [11].

The mechanisms that explain the relationship between symptoms of depression and obesity remain unclear. One possibility is that symptoms of depression promote excess weight gain during adolescence via reduced physical activity and consequently, lower energy expenditure. From a cognitive-behavioral theoretical framework, elevated symptoms of depression develop and are maintained as a result of a negative view of the self, one’s experiences, and the future [12]. In particular, anhedonia—which refers to loss of pleasure in activities that one previously found enjoyable—ensues from these cognitions, and is theorized to prompt behavioral withdrawal from activities such as physical exercise, which further exacerbates depressed mood [13]. In support of this notion, a number of cross-sectional studies have found an inverse association between adolescents’ symptoms of depression and self-reported physical activity, exercise, or sports participation [1418]. In contrast, in a large sample of young adolescent girls, depressive symptoms were not significantly associated with physical activity assessed by accelerometer, an ambulatory device used to objectively monitor moderate-to-vigorous physical activity [19]. Longitudinal data indicate that increases in adolescents’ depressive symptoms are associated with decreases in self-reported leisure-time, physical activity [20]. Results of another prospective study of adolescent girls found that depressive symptoms predicted reduced self-reported physical activity, and likewise, low self-reported physical activity predicted increased depressive symptoms [21]. However, some longitudinal studies have failed to find a significant relationship between depressive symptoms and physical activity in either direction [22, 23].

In light of these mixed results, it is noteworthy that the existing literature on depression and physical activity primarily has relied upon self-report assessments of physical activity. Although convenient, such questionnaire measures are limited by poor validity [24]. Therefore, it is crucial to determine the relationship between symptoms of depression and objective measurements. Cardiorespiratory fitness, also called maximal aerobic power, reflects an individual’s ability to carry out prolonged, strenuous physical exercise [25]. Cardiorespiratory fitness is the major component of physical fitness most relevant to an individual’s risk of developing obesity health-related co-morbidities such as cardiovascular disease and type 2 diabetes [26]. Children and adolescents’ cardiorespiratory fitness is highly influenced by regular engagement in moderate-to-high intensity physical exercise, and, as such, may be a valid integrated marker of recent physical activity [27]. We, therefore, examined whether symptoms of depression were related to objective assessments of cardiorespiratory fitness among a population of adolescents at heightened risk for adult obesity: obese adolescents seeking weight-loss treatment [28].



Participants were a convenience sample of obese (BMI ≥ 95th percentile) adolescents studied prior to taking part in a weight loss treatment study ( ID: NCT00001723). Youth were recruited from the Washington, DC metropolitan area with a range of methods including newspaper advertisements, flyers posted in local commercial venues, and through physician referrals. Inclusion criteria were age 12–17 years, BMI ≥ 95th percentile, non-Hispanic White or Black race/ethnicity, and good general health other than ≥ 1 quantifiable obesity-related health co-morbidity such as systolic or diastolic hypertension, type 2 diabetes, impaired glucose tolerance, hyperinsulinemia, hyperlipidemia, hepatic steatosis, or sleep apnea. For purposes of the current study, adolescents were included if they completed a depression screening questionnaire, exercise test, and body composition measurement. Exclusion criteria were other hepatic, renal, gastrointestinal, most endocrinologic, or pulmonary disorders, current pregnancy or breastfeeding, regular use of prescription medications unrelated to obesity-related health complications (not including oral contraceptives), recent use of anorexiant medication for the purpose of weight loss, or the presence of a psychiatric diagnosis in the adolescent or parent that would have impaired study compliance.


For the purposes of the current study, adolescents were studied at baseline, prior to the initiation of treatment. All assessments were conducted at the NIH Warren Grant Magnuson Clinical Research Center. Adolescents completed questionnaire measures assessing psychosocial adjustment, completed dual-energy x-ray absorptiometry (DXA) scanning, and took part in a maximal cycle ergometry test. Before exercise testing, participants were evaluated with a medical history, physical examination, and 12-lead electrocardiogram. All participants were free of a significant musculoskeletal injury, as determined by a physician. American Heart Association guidelines for exercise testing were observed [29]. Participants and their parents provided signed assent and consent, respectively. All procedures were approved by the Institutional Review Board of the Eunice Kennedy Shriver National Institute of Child Health and Human Development.


Body measurements

Height and weight were obtained after an overnight fast. Participants were clothed but with shoes removed. Height was measured three times to the nearest millimeter by a stadiometer (Holtain, Crymmych, Wales), calibrated before each adolescent’s measurement. Weight was measured to the nearest 0.1 kg with a calibrated digital scale (Scale-Tronix, Wheaton, IL). Participant’s height and weight were used to compute BMI. Body lean mass (kg) and percent body fat mass were assessed with DXA using a Hologic (Waltham, MA) QDR-4500A instrument.

Depressive symptoms

Participants completed the Ch ildren’s Depression Inventory (CDI), a reliable and well-validated 27-item self-report questionnaire, to assess depressive symptoms [30]. Participants were deemed to have elevated depressive symptoms if their total raw score, derived from the sum of all items, exceeded twelve. This cut-off has been proposed for screening for youth at-risk for clinical depression [31, 32]. The CDI’s total score also was broken down into its five continuous sub-scales tapping different aspects of depressive symptoms: a) negative mood, b) interpersonal problems, c) ineffectiveness, d) anhedonia, and e) negative self-esteem. The CDI has demonstrated adequate internal consistency, test-re-test reliability, discriminative validity, and concurrent validity [33, 34].

Cardiorespiratory fitness

Cardiorespiratory fitness was determined with cycle ergometry testing. Participants were familiarized with the cycle ergometer (Ergoline 800; SensorMedics, Yorba Linda, CA) prior to testing. Adolescents were instructed to pedal at a cadence of 60–65 revolutions per minute. Exercise began with a 4-minute warm-up period with no resistance applied to the pedals. After the warm-up, participants were encouraged to exercise to the limit of their tolerance. Predicted maximal power was used to adjust the rate of workload increase for each participant [35]; workload was increased until either the participant could no longer continue or could no longer maintain the prescribed pedaling cadence. Expired gas exchange was measured breath by breath throughout exercise using a metabolic cart (Sensormedics Vmax, Yorba Linda, CA). Maximal oxygen uptake during exercise (VO2max) was calculated as the 20-second average of values achieved at the end of exercise, with higher values reflecting better cardiorespiratory fitness. Participants who met at least two of four criteria during cycle ergometry were considered to have achieved a maximal VO2 test and reached their VO2max: i) maximal heart rate of ≥ 185 beats per minute achieved during the last minute of exercise, measured with a 12-lead electrocardiogram; ii) respiratory exchange rate of 1.02, calculated as the 20-second average of values achieved at the end of exercise; iii) peak rating of perceived exertion during exercise of ≥ 18, measured with the 20-point Borg Rating of Perceived Exertion Scale [36]; and iv) achievement of an oxygen plateau, defined as ≤ 2.0 mL/kg per minute change in oxygen uptake during the last minute of exercise [37].

Analytic Plan

Data were screened for problems of skew, kurtosis, and outliers. Descriptive statistics were generated on study variables. Validity criteria for measuring VO2max during cycle ergometry testing were examined. The primary independent variable was depressive symptoms status defined as no elevated symptoms (CDI < 13) vs.elevated symptoms (CDI ≥ 13). We also considered depressive symptoms continuously as CDI total score and negative mood, interpersonal problems, ineffectiveness, anhedonia, and negative self-esteem. The dependent variable was VO2max (maximal oxygen uptake, mL/min). Independent samples t-tests, correlations, or chi-square analyses were used to describe the bivariate relationships among depressive symptoms status or VO2max with demographic characteristics (age in years, sex, and race as non-Hispanic White vs.non-Hispanic Black) and anthropom etric characteristics (lean body mass in kg, percent body fat, height in cm, weight in kg, BMI z score, and number of obesity-related health co-morbidities). Analysis of covariance (ANCOVA) was conducted to test the relationship between depressive symptoms status (0 = no elevated symptoms vs.1 = elevated symptoms) and VO2max. A series of multiple hierarchical regressions was performed to test the relationships between continuous measures of total depressive symptoms, negative mood, interpersonal problems, ineffectiveness, anhedonia, or negative self-esteem and VO2max. Covariates considered in all ANCOVA and regression models were age (years), sex (dummy-coded: 0 = male vs.1 = female), race (dummy-coded: 0 = non-Hispanic White vs. 1 = non-Hispanic Black), lean mass (kg), percent fat mass, weight (kg), height (cm), and number of obesity-related health co-morbidities. Only age, sex, race, and lean mass were retained, as the other covariates were not significantly related to VO2max in any multivariate model. There were no apparent violations of homogeneity of variance (ANCOVA) or homoskedasticity (multiple regression) using Levine’s test and plotted residuals/predicted values, respectively. Finally, the interaction between sex and depressive symptoms was tested to explore whether the relationship between depressive symptoms and VO2max differed for boys and girls. In these analyses, the independent variables were depressive symptoms (mean-centered for continuous scales), sex, and their interaction. Age, sex, race, and lean mass were included as covariates.


All variables approximated a normal distribution (skew < 3, kurtosis < |10|). Outliers (approximately 1.5% of all data points) were recoded to fall within three standard deviations of the mean [38]. One hundred thirty-four adolescents participated. Descriptive information on demographic and anthropometric characteristics is provided in Table 1. Approximately 16% of adolescents (n = 16) endorsed elevated depressive symptoms (CDI total score ≥ 13). Those with elevated depressive symptoms did not differ from those without elevated depressive symptoms in age, sex, race, lean mass, percent fat mass, weight, height, BMI z score or number of obesity-related health co-morbidities.

Table 1
Demographic Characteristics of Adolescent Study Participants by Depressive Symptoms Status

One-hundred three adolescents met criteria for reaching VO2max on their cycle ergometry test. Of the 31 youth whose cycle tests did not meet validity criteria, approximately 96% did not achieve an oxygen plateau, 97% had a maximal heart rate < 185 beats per minutes, 90% did not endorse the criterion cut-off for perceived exertion, and 41% did not meet the respiratory exchange rate criterion. Compared to those who achieved a valid cycle test, adolescents who did not achieve a valid cycle test were more likely to be younger (p < .01),non-Hispanic Black (vs. non-Hispanic White; p < .05), and to have a greater BMI z score (p < .05). There were no significant differences between those with and without a valid cycle test on any other variable, including depressive symptoms, sex, lean mass, percent fat mass, weight, height, or number of obesity-related health co-morbidities.

The remaining sample was comprised of 103 obese adolescent girls (68%) and boys with an average age of 14.6 ± 1.4 years. Average VO2max was 1975.2 ± 349.6 mL/min and ranged from 1238 to 2894 mL/min. Maximal heart rate was similar among adolescents with and without elevated depressive symptoms (186.2 ± 13.6 beats/min vs. 188.8 ±11.7 beats/min, p = .43), as was respiratory exchange rate (1.17 ± .07 vs. 1.16 ± .06, p = .51). VO2max was positively correlated with age (r = .24, p < .01), lean mass (r = .64, p < .001), weight (r = .54, p < .001), and height (r = .42, p < .001). Also, boys displayed greater VO2max than girls (M ± SE 2154.9 ± 70.8 mL/min vs. 1890.5 ± 34.1 mL/min, p < .01).

Adjusting for age, sex, race, and lean mass, adolescents with elevated depressive symptoms displayed poorer VO2max than adolescents without elevated symptoms (p = .04; Figure 1). Depressive symptoms status accounted for 4% of the variance in VO2max2 = .04). In analyses examining depressive symptoms continuously, the association between total depressive symptoms and VO2max did not reach significance (β = −.11, p = .12), accounting for age, sex, race, and lean mass. Adjusting for the same covariates, there was a significant, inverse association between anhedonia and VO2max (p < .05), such that higher reports of anhedonia were related to poorer exercise performance (Figure 2). Above and beyond the contribution of age, sex, race, and lean mass (R2 = .50, p < .001), anhedonia explained a unique 3% of the variance in VO2max (ΔR2 = .03, p = .016). The relationships between other continuous dimensions of depressive symptoms and VO2max did not reach statistical significance (ps = .06 to .81).

Figure 1
Adolescents with elevated depressive symptoms (CDI Total Score ≥ 13) displayed lower VO2max (mL/min) during maximal cycle ergometry testing than adolescents with low depressive symptoms (CDI < 13), adjusting for age (years), sex, race, ...
Figure 2
Adolescents’ self-reported anhedonia was inversely associated with VO2max (mL/min) during maximal cycle ergometry testing, adjusting for age (years), sex, race, and lean mass (kg), β (standardized regression coefficient) = −.17, ...

Exploratory analyses tested sex as a potential moderator of the relationship between depressive symptoms and VO2max. The only significant effect was an interaction of sex by negative mood (p = .026). Negative mood scale score was associated with poorer VO2max among boys only (β= −.22, p = .024), but not among girls (β= .06, p = .56). Sex did not act as a significant moderator in any other model.


Among obese, weight loss treatment-seeking adolescents, those with elevated depressive symptoms displayed significantly poorer cardiorespiratory fitness, as assessed with cycle ergometry, than those without elevated depressive symptoms. Notably, the association between depressive symptoms status and cardiorespiratory fitness was observed after accounting for differences in lean mass, an important contributor to fitness levels, even among uniformly obese individuals [39]. Also, the relationship between depressive symptoms and fitness was not moderated by sex. In other words, obese girls, as well as boys, with elevated depressive symptoms were less fit relative to their counterparts without depressive symptoms.

Results from the present study are consistent with previous studies reporting a significant cross-sectional association between depressive symptoms and lower self-reported physical activity among non-treatment seeking samples of adolescents and young adults [14, 1618]. The current findings’ reliance on objectively-measured cardiorespiratory fitness, as opposed to self-report measures of physical activity that may be limited by poor validity [24], lend support to the notion that elevated depressive symptoms may exert an impact on voluntary energy expenditures such as engagement in leisure-time physical activities. Indeed, when types of depressive symptoms were examined, anhedonia was related to adolescent girls’ and boys’ poorer cardiorespiratory fitness, after accounting for lean mass and other relevant covariates. Negative mood also was related to poorer cardiorespiratory fitness, although only among boys. This sex by negative mood interaction is curious in light of data supporting a stronger relationship between depressive symptoms and obesity in girls compared to boys [9]. Yet, it should be considered with caution given the exploratory nature of these analyses and the null interaction effects observed for the other variables.

Taken together, these findings converge with cognitive-behavioral theories of depression that emphasize that depressed mood states prompt behavioral withdrawal from activities such as exercise, which in turn further exacerbates depressed mood [13]. Conversely, it is possible that engagement in physical activity affects depressive symptoms through a variety of potential mechanisms. Participation in physical activity or sports might decrease depressive symptoms through cognitive factors such as enhancing physical self-concept and self-esteem [15]. Similarly, exercise has been posited to increase positive affect through operating on neurotransmitters involved in emotion regulation such as serotonin, dopamine, acetylcholine, and norepinephrine [40]. Several longitudinal studies examining adolescent depression and self-reported physical activity support a cyclical interaction between depressive symptoms and physical activity over time [20, 21].

Nonetheless, the cross-sectional, observational nature of the current data limits the ability to make causal inferences about the depressive symptoms-cardiorespiratory fitness relationship. Also, while VO2max is a criterion-measure of cardiorespiratory fitness, depressive symptoms were assessed with questionnaire, which although reliable and valid as a screening tool [33, 34], cannot distinguish between those with and without clinical depression. Further study of the relationship between depressive symptoms and cardiorespiratory fitness using interview-based measures of adolescent depression is warranted. Indeed, we only found an association of cardiorespiratory fitness with elevated depressive symptoms rather than total depressive symptoms considered continuously, calling for replication in adolescent samples enriched for clinical depression. The current sample studied was comprised of weight loss treatment-seeking obese adolescents with at least one obesity-related health co-morbidity. Individuals who required or who already were engaged in ongoing psychiatric treatment were excluded from participation. Consequently, a shortcoming of the current study is that the findings are limited in their generalizability to other populations. Finally, it is important to recognize that the effects of elevated depressive symptoms or anhedonia on cardiorespiratory fitness were small relative to the effects of demographic/anthropometric variables.

The present findings are hypothesis-generating with regard to the potential mechanisms involved in the relationship between elevated depressive symptoms and obesity. Elevated depressive symptoms or major depression have been shown to predict the development of obesity [9, 11]; yet, there is much to be determined about how depressive symptoms lead to excess weight gain in adolescents who are still physically and affectively developing. The current results support the possibility that poor cardiorespiratory fitness, resulting from reduced physical activity, may be one such mechanism. Mechanistic research delving into the factors, such as cardiorespiratory fitness, that may help to explain how elevated depressive symptoms influence physical health outcomes is crucial to the design and implementation of effective obesity prevention and intervention efforts.


Research support: National Research Service Award 1F32HD056762 from the NICHD (to L. Shomaker), and Intramural Research Program grant 1ZIAHD000641 from the NICHD with supplemental funding from NIMHD and OBSSR (to J. Yanovski).


Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.


1. Lewinsohn PM, Shankman SA, Gau JM, et al. The prevalence and co-morbidity of subthreshold psychiatric conditions. Psychol Med. 2004;34(4):613–622. [PubMed]
2. Flegal KM, Ogden CL, Yanovski JA, et al. High adiposity and high body mass index-forage in US children and adolescents overall and by race-ethnic group. Am J Clin Nutr. 2010;91(4):1020–1026. [PubMed]
3. Gonzalez-Tejera G, Canino G, Ramirez R, et al. Examining minor and major depression in adolescents. J Child Psychol Psychiatry. 2005;46(8):888–899. [PubMed]
4. Ogden CL, Flegal KM. Changes in terminology for childhood overweight and obesity. Natl Health Stat Report. 2010;(25):1–5. [PubMed]
5. Must A, Strauss RS. Risks and consequences of childhood and adolescent obesity. Int J Obes Relat Metab Disord. 1999;23:S2–S11. [PubMed]
6. Weiss R, Dziura J, Burgert TS, et al. Obesity and the metabolic syndrome in children and adolescents. N Engl J Med. 2004;350(23):2362–2374. [PubMed]
7. Russell DL, Keil MF, Bonat SH, et al. The relation between skeletal maturation and adiposity in African American and Caucasian children. J Pediatr. 2001;139:844–848. [PubMed]
8. Taylor ED, Theim KR, Mirch MC, et al. Orthopedic complications of overweight in children and adolescents. Pediatrics. 2006;117:2167–2174. [PMC free article] [PubMed]
9. Blaine B. Does depression cause obesity?: a meta-analysis of longitudinal studies of depression and weight control. J Health Psychol. 2008;13(8):1190–1197. [PubMed]
10. de Wit L, Luppino F, van Straten A, et al. Depression and obesity: a meta-analysis of community-based studies. Psychiatry Res. 2010;178(2):230–235. [PubMed]
11. Luppino FS, de Wit LM, Bouvy PF, et al. Overweight, obesity, and depression: a systematic review and meta-analysis of longitudinal studies. Arch Gen Psychiatry. 2010;67(3):220–229. [PubMed]
12. Beck AT. Cognitive therapy and the emotional disorders. New York: International Universities Press; 1976.
13. Lewinsohn PM, Youngren MA, Grosscup SJ. Reinforcement and depression. In: Dupue RA, editor. The psychobiology of depressive disorders: implications for the effects of stress. New York: Academic Press; 1979. pp. 291–316.
14. Field T, Diego M, Sanders C. Adolescent depression and risk factors. Adolescence. 2001;36(143):491–498. [PubMed]
15. Dishman RK, Hales DP, Pfeiffer KA, et al. Physical self-concept and self-esteem mediate cross-sectional relations of physical activity and sport participation with depression symptoms among adolescent girls. Health Psychol. 2006;25(3):396–407. [PubMed]
16. Haarasilta LM, Marttunen MJ, Kaprio JA, et al. Correlates of depression in a representative nationwide sample of adolescents (15–19 years) and young adults (20–24 years) Eur J Public Health. 2004;14(3):280–285. [PubMed]
17. Kirkcaldy BD, Shephard RJ, Siefen RG. The relationship between physical activity and self-image and problem behaviour among adolescents. Soc Psychiatry Psychiatr Epidemiol. 2002;37(11):544–550. [PubMed]
18. Norris R, Carroll D, Cochrane R. The effects of physical activity and exercise training on psychological stress and well-being in an adolescent population. J Psychosom Res. 1992;36(1):55–65. [PubMed]
19. Johnson CC, Murray DM, Elder JP, et al. Depressive symptoms and physical activity in adolescent girls. Med Sci Sports Exerc. 2008;40(5):818–826. [PubMed]
20. Motl RW, Birnbaum AS, Kubik MY, et al. Naturally occurring changes in physical activity are inversely related to depressive symptoms during early adolescence. Psychosom Med. 2004 May–Jun;66(3):336–342. [PubMed]
21. Jerstad SJ, Boutelle KN, Ness KK, et al. Prospective reciprocal relations between physical activity and depression in female adolescents. J Consult Clin Psychol. 2010;78(2):268–272. [PMC free article] [PubMed]
22. Birkeland MS, Torsheim T, Wold B. A longitudinal study of the relationship between leisure-time physical activity and depressed mood among adolescents. Psychol Sport Exerc. 2009;10(1):25–34.
23. Rothon C, Edwards P, Bhui K, et al. Physical activity and depressive symptoms in adolescents: a prospective study. BMC Med. 2010;8:32. [PMC free article] [PubMed]
24. Chinapaw MJ, Mokkink LB, van Poppel MN, et al. Physical activity questionnaires for youth: a systematic review of measurement properties. Sports Med. 2010;40(7):539–563. [PubMed]
25. U.S. Department of Health and Human Services. Physical activity and health: a report of the surgeon general. Atlanta: 1996.
26. LaMonte MJ, Blair SN, Church TS. Physical activity and diabetes prevention. J Appl Physiol. 2005;99(3):1205–1213. [PubMed]
27. Ortega FB, Ruiz JR, Castillo MJ, et al. Physical fitness in childhood and adolescence: a powerful marker of health. Int J Obes (Lond) 2008;32(1):1–11. [PubMed]
28. Whitaker RC, Wright JA, Pepe MS, et al. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med. 1997;337(13):869–873. [PubMed]
29. Washington RL, Bricker JT, Alpert BS, et al. Guidelines for exercise testing in the pediatric age group. From the Committee on Atherosclerosis and Hypertension in Children, Council on Cardiovascular Disease in the Young, the American Heart Association. Circulation. 1994;90(4):2166–2179. [PubMed]
30. Kovacs M. Unpublished manuscript. Vol. 1992. 2003. The children’s depression inventory.
31. Lobovits DA, Handal PJ. Childhood depression: prevalence using DSM-III criteria and validity of parent and child depression scales. J Pediatr Psychol. 1985;10(1):45–54. [PubMed]
32. Kazdin, Colbus, Rodgers Assessment of depression and diagnosis or depressive disorder among psychiatrically disturbed children. J Abnorm Child Psychol. 1986;14(4):499–515. [PubMed]
33. Costello EJ, Angold A. Scales to assess child and adolescent depression: checklists, screens, and nets. J Am Acad Child and Adolesc Psychiatry. 1988;27(6):726–737. [PubMed]
34. Curry JF, Craighead WE. Depression. In: Ollendick TH, Hersen M, editors. Handbook of child and adolescent assessment. Nedham Heights: Allyn and Bacon; 1993. pp. 251–268.
35. Wasserman K, Hansen JE, Sue DY, et al. Principles of exercise testing and interpretation. 3. Philadelphia, PA: Lippincott, Williams & Wilkins; 1999.
36. Chen MJ, Fan X, Moe ST. Criterion-related validity of the Borg ratings of perceived exertion scale in healthy individuals: a meta-analysis. J Sports Sci. 2002;20(11):873–899. [PubMed]
37. Rowland TW. Developmental exercise physiology. Champaign, IL: Human Kinetics; 1996.
38. Behrens JT. Principles and procedures of exploratory data analysis. Psychol Methods. 1997;2:131–160.
39. Norman AC, Drinkard B, McDuffie JR, et al. Influence of excess adiposity on exercise fitness and performance in overweight children and adolescents. Pediatrics. 2005;115(6):e690–696. [PMC free article] [PubMed]
40. Deslandes A, Moraes H, Ferreira C, et al. Exercise and mental health: many reasons to move. Neuropsychobiology. 2009;59(4):191–198. [PubMed]