Volume 15, Issue 3 (May-Jun 2021)                   mljgoums 2021, 15(3): 33-39 | Back to browse issues page

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Bahreini A, Akbarpour M, Fathi R, Goldashti H. Evaluation of Changes in Insulin Resistance and Serum Cortisol Levels after Eight Weeks of Continuous and Interval Aerobic Training in Healthy and Obese Girls. mljgoums 2021; 15 (3) :33-39
URL: http://mlj.goums.ac.ir/article-1-1297-en.html
1- Department of physical Education, Islamic Azad University, Chalous Branch, Iran , a_bahreine2@yahoo.com
2- Department of Cultivation and Plant Breeding, Faculty of Agriculture and Natural Resources, Islamic Azad University, Chalous Branch, Iran
3- Department of sport physiology, Mazandaran University, Babolsar,Iran
4- Department of Physical Education, Islamic Azad University, Chalous Branch, Iran
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INTRODUCTION
Obesity is increasing among children worldwide (1, 2). Childhood obesity is considered as a predictor of obesity in adulthood (3), so that an increase in body mass index (BMI) in childhood indicates an increase in BMI in adulthood (4). According to predictions, about 35 million children will be overweight or obese worldwide (5). About 27% of children and 21% of adolescents were obese in Iran in 2016 (1).
Proper physical activity is the easiest way to maintain good health and weight because about one-third of the daily energy is spent on physical activity (6). Childhood obesity can lead to chronic diseases such as diabetes, apnea, cardiovascular disease and high blood pressure in childhood and adulthood (7-10). Behavioral problems and reduced puberty age, especially in girls, are other complications of childhood obesity (11). In addition to obesity, secretion of growth hormone and IGF-I increases during puberty, leading to increased oxidation of free fatty acids and the resistance of peripheral tissues to glucose uptake, thereby increasing insulin resistance (12, 13). With regard to increase in insulin concentration, serum level of sex hormone-binding globulin increases the fat tissue and cortisol level and also impairs the hypothalamic-pituitary axis in obese individuals (14). Regular physical activity is a non-pharmacological treatment of obesity and insulin resistance (2). Ciolac et al. found that a 16-week intense aerobic training program in healthy young women can improve insulin sensitivity (15). Ramezani et al. reported that endurance training could significantly reduce insulin resistance in obese children aged 8-12 years (16). According to Papovic et al., the minimum intensity of endurance exercise necessary to produce cortisol response is about 60% of VO2 max (17). Tartibian et al. also observed a significant increase in creatine kinase and cortisol levels in children immediately after training (18). Paahoo et al. indicated an increase in serum cortisol levels after 12 weeks of intense periodic training (14).
Given the importance of training in weight control and reducing risk factors of diabetes and insulin resistance (14, 18), the present study aimed to investigate effects of eight weeks of continuous and interval aerobic training on some metabolic factors, insulin resistance and serum cortisol levels in obese girls aged 9-11 years.
 
MATERIALS AND METHODS
This applied and semi-experimental study was carried out in Mazandaran University in Babolsar, Iran. Thirty-six female students aged 9 to 11 years with a BMI of more than the 85th percentile were selected via convenience sampling. The participants were randomly assigned to three groups of interval training, continuous training and control. Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) and estradiol levels were also evaluated to assess the students' puberty. The study was registered in Iran Clinical Trial center (IRCT20180928041160N1) and received ethics approval (ethical code: IR.UMZ.REC.1397.015).
The experimental groups trained three days a week for eight weeks according to the training protocol introduced by Mahgoub and Aly with some modifications (19). Maximum heart rate was calculated using the equation of Tanaka, Monahan and Seals (20). Heart rate was controlled using a heartbeat monitor (Polar AXN500, Finland). The subjects were weighed using a scale (Seca, Germany) and BMI was calculated by dividing weight (kg) by square height (meters).
Fasting blood samples were taken 72 hours before the first training session and 72 hours after the last training session. The samples were centrifuged at 10,000 rpm for 10 min (Universal, BH-1200, Netherland) to separate serum. Serum glucose level was measured by enzymatic pigmentation method (peroxidase (POD)/glucose oxidase (GOD) using an autoanalyzer (Hitachi, 917, Germany). Serum levels of insulin and cortisol were measured by an electrochemiluminescence technique using an autoanalyzer (Cobas E-411, Japan). Body fat percentage was measured by Harpenden caliper (Baty, UK) and the Jackson/Pollock method using the following formula (21):
Percent body fat = (0.41563 × sum of skinfolds) – (0.00112 × square of the sum of skinfolds) + (0.03661 × age) + 4.03653, where the skinfold sites (measured in mm) are abdominal, triceps and suprailiac.
The insulin resistance index (HOMA-IR) was calculated using the following equation:
HOMA-IR= [fasting insulin (µU/mL) × Fasting glucose (mmol/ L) ÷ 22.5] (22).
HOMA-IR cut-off point was considered 4.0 for II-III stages of tanner puberty table. Normal range of cortisol, insulin and glucose in children was considered as 135-635 nmol/L, 2.6-25.9 µIU/mL and 60-110 mg/dL, respectively.
Data were presented as mean ± standard deviation. Statistical analysis was performed using the SPSS software (version 21). Normal distribution of data and equality of variances were examined by Shapiro-Wilk test and Levene's test, respectively. The paired t-test was used to examine intragroup changes, while one-way analysis of variance was used to evaluate intergroup differences. A p-value of less than 0.05 was considered as statistically significant.
 
RESULTS
Table 1 shows the demographic information of subjects in the study groups.
Table 1. Demographic information of participants in the study groups
Variables Control group (n=9) Continuous training group (n= 11) Interval training group (n= 12)
Age (year) 9.66±0.56 9.33±0.57 9.86±0.95
Height (cm) 139.55±4.91 137.63±7.52 142.75±8.66
Weight (kg) 46.95±4.98 47.76±9.88 53.57±10.42
BMI (kg/m2) 24.03±1.29 26.04±4.18 25.83±2.18
 
The mean weight of subjects in the training groups did not change significantly after the training period, but a significant weight gain (P<0.05) was observed in the control group compared to the pretest state. In addition, BMI and body fat percentage of subjects in the training groups decreased significantly after the training. However, no change in BMI was observed in the control group, and the body fat percentage showed an increasing trend. Serum glucose level increased in all groups compared to pretest (P>0.05). Serum insulin level increased slightly in the interval training group but reduce insignificantly in the continuous training group (P>0.05). Moreover, serum insulin level increased significantly in the control group (P<0.05). Insulin resistance increased significantly in the control and interval training groups (P<0.05) but reduced slightly in the continuous training group (P>0.05). Serum cortisol levels did not change significantly in the study groups (Table 2).
 
Table 2. Mean level of study variables in the pretest and posttest stages
Groups Variables Pre-test Post-test
Interval training group Weight (kg) 53.5±10.4 53.0±10.1
BMI (kg/m2) 25.8±2.1 25.1±12.1*
Body fat percentage 31.6±1.9 29.7±1.8*
Glucose (mg/dL) 81.8±4.1 87.5±5.5
Insulin (µIU/mL) 17.4±8.5 18.4±4.2
HOMA-IR 3.5±1.8 3.9±0.9
Cortisol (nmol/L) 526.811±174.905 449.301±198.512
Continuous training group Weight (kg) 52.3±19.1 52.5±19.4
BMI (kg/m2) 26.9±6.3 26.4±6.4*
Body fat percentage 31.3±4.2 30.3±4.4*
Glucose (mg/dL) 80.7±7.5 82±7.4
Insulin (µIU/mL) 17.1±12.3 15.2±5.7
HOMA-IR 3.4±2.7 3.1±1.3
Cortisol (nmol/L) 548.777±89.254 632.504±221.203
Control group Weight (kg) 46.9±4.9 47.8±5.1*
BMI (kg/m2) 24.1±1.29 24.1±1.28
Body fat percentage 31.5±1.8 32.1±1.8
Glucose (mg/dL) 91±4.2 92±5
Insulin (µIU/mL) 15.2±5.9 16.3±6.3
HOMA-IR 3.4±1.4 3.8±1.6
Cortisol (nmol/L) 402.716±108.220 477.627±203.175
 
One-way analysis of variance indicated significant differences in weight, BMI, body fat percentage and blood glucose levels between the study groups. The insulin resistance index and serum cortisol levels did not differ significantly between the study groups (Table 3).
 
Table 3. One-way analysis of variance between pretest and posttest level of target variables in the study groups
 
Degrees of freedom
 
Significance level
 
F-Value
 
Variables
2 0.005 6.03 Weight
2 0.01 4.6 BMI
2 0.0 14.7 Body Fat percentage
2 0.009 5.54 Glucose
2 0.63 0.46 Insulin
2 0.56 0.58 Insulin resistance index (HOMA)
2 1.170 1.891 Cortisol
 
DISCUSSION
Given the growing prevalence of obesity in children and its complications (16), the present study aimed to investigate the effects of aerobic training on demographic factors such as weight, BMI and body fat percentage as well as some metabolic factors such as serum glucose and insulin levels in obese girls. In the present study, the mean weight of participants in the sedentary group increased significantly after eight weeks, but no increase was seen in the continuous and interval training groups. In addition, BMI and body fat percentage decreased significantly in the training groups but remained almost unchanged in the sedentary group. Unlike the result of this research, Habibian et al. did not see any significant difference in weight and body fat percentage after eight weeks of training aerobic training groups (23). Similar to our findings, Fazelifar and Ebrahim also reported a significant reduction in body fat mass, weight and BMI after endurance-strength training, but the type and duration of the trainings were different (1). Russell et al. reported a significant reduction in BMI after moderate and high intensity interval training in adolescents (24, 25).
In all study groups, a significant increase was noted in serum glucose levels. Although the levels were still in the normal range, the changes in glucose level were more significant in the interval training group compared to the control group. Serum insulin level decreased in the continuous training group and increased in the interval training and control groups, but none of these changes were significant. Inconsistent with our findings, Habibian et al. reported a significant reduction in these two variables 48 hours after aerobic training in obese girls aged 8-12 years (23). Tang et al. also reported a reduction in serum glucose and insulin levels after a period of resistance training (26). In line with our findings, Garcia Hermoso et al. observed no significant change in serum glucose, insulin and insulin resistance index after 12 weeks of high-intensity interval training in obese/overweight individuals aged 6 to 17 years (27).
There was no significant difference in the HOMA-IR index between the training groups. Similarly, Hamedinia et al. stated that the insulin resistance index did not change significantly in obese children and adolescents after eight weeks of endurance training in water (28). Lee et al. reported that six weeks of skipping rope training improved the HOMA-IR index in obese adolescents (29). Furthermore, Nasis et al. indicated that a 12-month aerobic training program could improve insulin sensitivity in obese/overweight adolescent girls (16). Nasimento et al. found that after eight months of training without weight change, the HOMA-IR index decreased in obese/overweight children and adolescents (15). It seems that improvement of HOMA-IR requires longer training interventions. Despite the inactivity of the control group, there was an increase in the level of HOMA-IR. Owing to the fact that the subjects of this research were in the puberty period, they are not resistant to insulin because the cut-off point of HOMA-IR in these two stages was defined as 4.0 (30). In general, puberty contributes to insulin resistance due to the increased secretion of growth hormone and IGF-I, which increases the probability of temporary insulin resistance in non-diabetic children with normal weight; however, this change is irreversible in obese children (12). Abbasi et al. observed a significant increase in insulin levels in obese children with insulin resistance compared to insulin sensitive obese children, but there was no difference between two groups in terms of glucose levels (31).
In our study, serum cortisol level did not change significantly in the training groups. Paahoo et al. reported an increase in serum cortisol levels in obese children after 12 weeks of high intensity periodic training. Papovic et al. reported a significant increase in serum cortisol level after endurance training with 60% VO2max (17). Hamedinia et al. also reported an increase in peripheral cortisol production in the phenomenon of abdominal and visceral obesity (32). Foley et al. found no significant change in fasting cortisol levels in non-athletes after six and 12 weeks of aerobic training (33).
Cortisol is a catabolic hormone that can be affected by obesity (14). Organs involved in physical activity secrete corticotropin releasing hormone and activate the hypothalamic-pituitary-adrenal axis, which eventually increases cortisol secretion (10, 14). Due to the higher energy demand during physical activity, increasing cortisol concentrations can increase blood sugar levels and help break down of fats and proteins and stimulate gluconeogenesis while reducing glucose uptake in peripheral tissues. However, the extent of increase in cortisol concentration depends on the intensity, duration and type of physical activity. The highest cortisol response is achieved when the overall stress (volume and/or intensity) of the training is high (36). In exercise adaptation, cortisol prepares the body for the next bout of exercise. Following acute exercise, there is an increased tissue sensitivity to glucocorticoids that serves to counteract muscle inflammation, cytokine synthesis and muscle damage. Inactivation of cortisol to cortisone appears to be another adaptation strategy to exercise but overtraining may impair inactivation of cortisol in athletes (36, 37). Despite the fact that an increase in baseline or acute increase in cortisol in stressful conditions is detrimental to health, an increase in acute and basal levels of this hormone may be helpful in response to chronic training. 
 
CONCLUSION
In summary, the reduction in weight, BMI and fat percentage were obtained in both training groups after eight weeks of training intervention. It appears that the continuous training is more promising because of a decreasing trend in insulin level, HOMA-IR and a reasonable increase in cortisol level.
 
ACKNOWLEDGMENTS
We like to thank the experts of physiology lab at Mazandaran University for helping us in the experimental assessments.
 
CONFLICT OF INTEREST
The authors declare that there is no conflict of interest regarding publication of this article.
Research Article: Original Paper | Subject: Sport Physiology
Received: 2020/05/22 | Accepted: 2020/07/30 | Published: 2021/04/28 | ePublished: 2021/04/28

References
1. Fazelifar S, Ebrahim KH. (2012). Effects of concurrent training and detraining on leptin and insulin concentration in obese children. Physiology of Sport and Shysical Activity Journal.8:639-646. (Persian)
2. Kazemi R, Rahmani M, Taherabadi J. Effect of eight weeks High intensity Interval Training (HIT on Body weight and serum levels of TNF-α, insulin and lipid profile in obese children. RJMS. 2016; 22 (139) :1-7. [Persian] [View at Publisher] [Google Scholar]
3. Wang LY, Denniston M, Lee S, Galuska D, Lowry R. Long - term health and economic impact of preventing and reducing overweight and obesity in adolescence. Journal of Adolescent Health. 2010; 46(5): 467-73. [DOI:10.1016/j.jadohealth.2009.11.204] [PubMed] [Google Scholar]
4. Wang LY, Chyen D, Lee S, Lowry R. The association between body mass index in adolescence and obesity in adulthood. Journal of Adolescent Health. 2008; 42(5): 512-18. [DOI:10.1016/j.jadohealth.2007.10.010] [PubMed] [Google Scholar]
5. Farzanegi P, Samiee M, Sabbaghian Z. Interactive effect of regular aerobic training and milk consumption on some inflammatory markers and lipid profile in overweight boys. Koomesh. 2016; 17(3): 627-635. [View at Publisher] [Google Scholar]
6. Sedighi E, Azizi M, Parnow H. Evaluation of prevalence obesity and IT'S citation with physical activity levels in Javanroud girls students with 7-12 years old. Journal of Clinical Research in Paramedical Science. 2016; 4: 351-359. [Persian] [View at Publisher] [Google Scholar]
7. Hedleg AA, Ogden CL, Johnson CL, Carroll MD. Obesity among our children, adolescents, and adults. Jama. 2004; 291(23): 2847-50. [DOI:10.1001/jama.291.23.2847] [PubMed] [Google Scholar]
8. Wogden CL, Carroll MD, Flegal KM. High body mass index for age among our children, adolescents, and adolescents. Jama. 2005; 2401(20): 299-305. [DOI:10.1001/jama.299.20.2401] [PubMed] [Google Scholar]
9. Birch L, Rentura A. Preventing childhood obesity: what work and quest. International journal of obesity. 2009; 33: 574-581. [DOI:10.1038/ijo.2009.22] [PubMed] [Google Scholar]
10. Sajedi D, Shabani R. The effect of aerobic and resistance concurrent training on leptin and cortisol levels on overweigh and obese anxious adolescents girls. Iranian Journal of rehabilitation research in nursing. 2018; 5(1): 43-53. [Persian] [View at Publisher] [Google Scholar]
11. Mirshekar S, Safavi SM, Yadegar far GH. The relationship between food insecurity and stunting combined with obesity and overweight in children aged 7 to 11 years in Zabol. Iranian Journal of Epidemiology. 2017; 12(4): 44-54. [Persian] [View at Publisher] [Google Scholar]
12. Hannon TS, Janosky J, Arslanian SA. Longitudinal study of physiologic insulin resistance and metabolic changes of puberty. Pediatric Research. 2006; 60: 759-630. [DOI:10.1203/01.pdr.0000246097.73031.27] [PubMed] [Google Scholar]
13. Winer JC, Zem TL, Taksali SE, Dziura J, Cali AM, Wollschlager M, et al. Adiponectin in childhood and adolescent obesity and its association with inflammatory markers and components of the metabolic syndrome. Journal of clinical endocrinology metabolism. 2006; 91: 4414-23. [DOI:10.1210/jc.2006-0733] [PubMed] [Google Scholar]
14. Paahoo A, Tadibi V, and Behpoor N. Acute effect of high intensity interval training (Hilt) on testosterone levels, cortisol and testosterone on cortisol ratio in obese and overweight children untrained and trained. 2016; 17(6): 457-468. [Persian] [View at Publisher] [Google Scholar]
15. Ciolac EG, Bocchi EA, Bortolotto LA, Crvalho VO, Greve JM, Guimataes GV. Effect of high-intensity aerobic training vs.¬ moderate exercise on hemodynamic metabolic and neuro-humoral abnormalities of young normotensive women at high familial risk for hyperetension. Hyper Tension Research. 2010; 33(8): 836-43. [DOI:10.1038/hr.2010.72] [PubMed] [Google Scholar]
16. Ramezani A, Gaeini A, Hosseini M, Mohammadi J. Effect of Endurance, Strength and Combined Training on Lipid Profile, Insulin Resistance, and Serum Adiponectin Levels in Inactive Obese Children. Armaghane danesh. 2016; 21 (7) :641-654. [View at Publisher]
17. Papovic B, Papovic D, Macut D, Bozic Antic I. et al. Acute response to endurance exercise stress: focus on catabolic/anabolic interplay between cortisol, testosterone, and sex hormone binding globulin in professional athletes. Journal of Medical Biochemistry. 2019; 38(1): 6-12. [DOI:10.2478/jomb-2018-0016] [PubMed] [Google Scholar]
18. Tartibia B, Zeynali F, Mohammad Amini Khayats S, Maleki Mansourabad S, Abdollahzade N, Fakhreddin Yaghoobnezhad F. Response of inflammatory, immune and hormonal markers to incremental exercise in the healthy girls. Journal of healthy and care. 2016; 17(2): 154-165. [View at Publisher] [Google Scholar]
19. Mahgoub MD, & Aly S. The effects of continuous vs intermittent exercise on lipid profile in obese children. International Journal of Therapy and Rehabilitation. 2015; 22(6): 272-276. [DOI:10.12968/ijtr.2015.22.6.272] [Google Scholar]
20. Tanaka H, Monahan KD, and Seals DR. Age- predicted index maximal heart rate revisited. Journal of American College of Cardiology. 2001; 37(1): 153-156. [DOI:10.1016/S0735-1097(00)01054-8] [Google Scholar]
21. Jackson A S, Pollock ML, Ward A. Generalized equations for predicting body density of women. Medicine and science in sports and exercise. 1980; 12(3):175-81. [DOI:10.1249/00005768-198023000-00009] [PubMed] [Google Scholar]
22. Matthews DR, Hosker J P, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985; 28:412-19. [DOI:10.1007/BF00280883] [PubMed] [Google Scholar]
23. Habibian M, Farzanegi P, Asadi B. The effect of regular aerobic exercise along with vitamin C consumption on homocysteine levels and insulin resistance in obese girls. Armaghan-danesh. 2017; 22(1): 61-74. [View at Publisher] [Google Scholar]
24. Racil G, Ounis B, Hammouda O, Kallel A, Zouhal H, Chamari K and Amri M. Effects of high vs. moderate exercise intensity during interval training on lipids and adiponectin levels in obese young female. European Journal of Applied Physiology. 2013; 113:2531-2540. [DOI:10.1007/s00421-013-2689-5] [PubMed] [Google Scholar]
25. Racil G, Coquart JB, Elmontassar W, Haddadi M, Goebel R, Chaouachi A, Amri M, Chamari, K. Greater effects of high- compared with moderate-intensity interval training on cardio-metabolic variables, blood leptin concentration and rating of perceived exertion in obese adolescent females. Biology of sport. 2016; 33: 145-152. [DOI:10.5604/20831862.1198633] [PubMed] [Google Scholar]
26. Tong TK, Kong Z, Shi X, Shi Q. Comparable Effects of Brief Resistance Exercise and Isotime Sprint Interval Exercise on Glucose Homeostasis in Men. J Diabetes Res. 2017;2017:8083738. [DOI:10.1155/2017/8083738] [PubMed] [Google Scholar]
27. Carcia-Hermoso A, Cerrillo-Urbina A, Herrera-Vizcaino V. Is high -intensity interval training more effective on improving cardiometabolic risk and aerobic capacity than other forms of exercise in overweight and obese youth. A meta-analysis. Obesity reviews. 2016; 17:531-540. [DOI:10.1111/obr.12395] [PubMed] [Google Scholar]
28. Hamedinia MR, Sardar MA, Haghighi AH, Porjahed J. Comparison of adiponectin and leptin levels in obese children and adolescents. Journal of metabolism and endocrinology. 2009; 11(2): 169-175. (Persian). [View at Publisher] [PubMed] [Google Scholar]
29. Lee JM, Pilli S, Gebremariam A, keirns CC, Davis MM, Vijan S, et al. Getting heavier, younger trajectories of obesity over a life course. International Journal of Obesity. 2009; 34(4): 614-23. [DOI:10.1038/ijo.2009.235] [PubMed] [Google Scholar]
30. Elmaogular S, Tepe D, Ucakturk SA, Karacakara F, and Demirel F. Prevalence of dyslipidemia and associated factors in obese children and adolescents. Journal of Clinical Research in Pediatri Endocrinology. 2015; 7(3): 228-234. [DOI:10.4274/jcrpe.1867] [PubMed] [Google Scholar]
31. Abaci A, Akelma AZ, Ozdemir O, Hizli S, Razi CH, Akin KO. Relation of total homocystein level with metabolic and anthropometric variables in obese children and adolescents. Turkish Journal of Medicine Science. 2012; 42(1):69-76. [DOI] [Google Scholar]
32. Venner AA, Lyon ME, Doyle-Baker PK. Leptin: a potential biomarker for childhood obesity? Clinical Biochemistry. 2006; 39: 1047-56. [DOI:10.1016/j.clinbiochem.2006.07.010] [PubMed] [Google Scholar]
33. Foley LS, Prapavessis H, Osuch EA, De Pace JA, Murphy BA, Podolinsky NJ. An examination of potential mechanisms for exercise as a treatment for depression: a pilot study. Mental health and physical activity. 2008; 1: 69-73. [DOI:10.1016/j.mhpa.2008.07.001] [PubMed] [Google Scholar]
34. Anderson T, and Wideman L. Exercise and the cortisol awakening response: A systematic review. 2017; 3(37): 1-15. [DOI:10.1186/s40798-017-0102-3] [PubMed] [Google Scholar]
35. Azizi M, Rahmaninia F, Mohebby H, and Azarbayjani MA. The effect of physical exercise on cortisol level and energy in obese and thin men. Journal of sport biosciences. 2010; 1: 57-73. [Google Scholar]
36. Kraemer WJ, Ratamess NA, Hymer WC, Nindl BC, and Fragala MS. Growth hormone(s), testosterone, insulin-like growth factors, and cortisol: roles and integration for cellular development and growth with exercise. Frontiers in endocrinology. 2020; 11: 1-25. [DOI:10.3389/fendo.2020.00033] [PubMed] [Google Scholar]
37. Gatti R, De Palo GF. An update: Salivary hormones and physical exercise. Scandinavian Journal of Medicine and Science in Sports. 2011; 21: 157-169. [DOI:10.1111/j.1600-0838.2010.01252.x] [PubMed] [Google Scholar]
38. Anderson T, Lane AR, Hackney AC. Cortisol and testosterone dynamics following exhaustive endurance exe rcise. European Journal of Applied physiology. 2016; 116: 1503-9. [DOI:10.1007/s00421-016-3406-y] [PubMed] [Google Scholar]
39. Urhausen A, Kindermann W. Diagnosis of overtraining: what tools do we have? Sports Medicine. 2002; 32: 95-102. [DOI:10.2165/00007256-200232020-00002] [PubMed] [Google Scholar]
40. Gouarne C, Groussard C, Gratas -Delamarche A, Delamarche P, Duclos M. Overnight urinary cortisol and cortisone add new insights into adaptation to training. Medicine science sports exercise. 2005; 37: 11-57. [DOI:10.1249/01.mss.0000170099.10038.3b] [PubMed] [Google Scholar]
41. Park JY, Hwang TK, Park HK, Ahn RS. Differences in cardiovascular and hypothalamic- pituitary- adrenal axis functions between high- altitude visitors and natives during a trek on the Annapurna circuit. Neuroendocrinology. 2014; 99: 130-8. [DOI:10.1159/000363367] [PubMed] [Google Scholar]
42. Marinelli M, Roi GS, Giacometti m, Bonini P, Banfi G. Cortisol, testosterons and free testosterone in athletes performing a marathon at 4000 m altitude. Hormone Research. 1994; 41: 225-9. [DOI:10.1159/000183929] [Google Scholar]
43. Filaire E, Ferreira JP, Oliveira M, Massart A. Durnal patterns of salivary alpha-amylase and cortisol secretion in female adolescent tennis after 16 weeks of training. Psychoneuroendocrinology. 2013; 38: 1122-32. [DOI:10.1016/j.psyneuen.2012.11.001] [PubMed] [Google Scholar]

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