Objective: evaluate the impact of concurrent training (CT) on biochemical parameters and obesity-related cardiometabolic risk factors.

Methods: case report of a sedentary 23-year-old male, classified as class 1 obese. Blood sample collected: glucose (GLU), glycated hemoglobin (HbA1c), total cholesterol (TC), triglycerides (TG), HDL-cholesterol fraction (HDL), LDL-cholesterol fraction (LDL), tumor necrosis factor alpha (TNF-α), C-reactive protein (CRP), interleukin-6 (IL-6), leptin (LEP) and adiponectin (ADP). In addition, VO2max, resting heart rate (HR), resting systolic and diastolic blood pressure (SBP and DBP), body mass (BM), height (HT), waist circumference (WC) and hip circumference (HC) were measured. The body mass index (BMI) and body adiposity index (BAI) were obtained by anthropometric measurements. All variables were evaluated before and after eight weeks of TC with progressive intensity, performed in three non-consecutive weekly sessions.

Results: a reduction was observed in blood GLU (Δ%=-5.56), HbA1c (Δ%=-13.46), TC (Δ%=-19.05), TG (Δ%=-9.64), LDL (Δ%=-32.98), TNF-α (Δ%=-23.2), CRP (Δ%=-67.03), IL-6 (Δ%=-21.2) and LEP (Δ%=-37.5). The variables HDL (Δ%=10.5) and ADP (Δ%=152.73) exhibited an increase. A decline was observed in BM (Δ%=-1.69), WC (Δ%=-9.55), HC (Δ%=-9.17), BMI (Δ%=-1.7), BAI (Δ%=-14.24), SBP (Δ%=-4.96) and HR (Δ%=-18.67). The VO₂max showed an increase (Δ%=16.83).

Conclusion: a concurrent 8-week training program had beneficial effects on biochemical parameters and obesity-related cardiometabolic risk factors.

Keywords: obesity, concurrent training, metabolic syndrome, prevention, treatment

HT, height; BM, body mass; WC, waist circumference; HC, hip circumference.

Obesity, characterized by excessive accumulation of body fat,¹ is considered a chronic and progressive disease due to associated comorbidities.^2,3 These include metabolic syndrome (MS), a complex disorder characterized by cardiometabolic risk factors such as abdominal obesity, insulin resistance, glucose intolerance and dyslipidemia.⁴ Individuals with MS are at increased risk of developing type II diabetes, coronary artery disease, arterial hypertension, atherosclerosis, some types of cancer and early death.^3,5 Because it is strongly associated with obesity, the prevalence of MS has increased rapidly in both developed and developing countries.⁶ In a systematic review, Vidigal et al.,⁷ found a prevalence of MS in the Brazilian adult population between 28.9 and 29.6%, according to the criteria used to define it.

The regional distribution of fat plays an important role in the etiology of adiposity-related diseases in several populations.⁸ A number of studies suggest that adipose tissue stored in specific body areas can differentially affect metabolic health.⁹ In this respect, the literature reports an adverse risk of metabolic disorder with visceral adiposity,¹⁰ although femoral adiposity is associated with a decreased risk of having two or more cardiometabolic risk factors in African American and white adults.¹¹ Thus, besides acting as a risk factor for the onset of MS, the excessive deposit of adipose tissue can be harmful to health for other reasons. Historically considered only a fat storage site, adipose tissue (AT) has been classified as an endocrine organ due to its bioactive substances.^13,14 These substances, known as adipokines or adipocytokines,^14,15 are involved in a wide variety of physiological processes, including insulin action, endothelial function, and energy balance regulation.^16,17 However, the increase in some proinflammatory adipocytokines is related to the immune system and increased inflammatory response, prompting some researchers to view obesity as a chronic state of systemic inflammation.¹⁸

Obesity and its comorbidities should not be treated separately. Treatment involves a lifestyle change and multidisciplinary intervention in the areas of internal medicine, physical education, nutrition and psychology.¹⁹ Cardiorespiratory and strength training performed successively during the same training session is characterized as concurrent training (CT),^20,21 and is an important strategy for weight loss in overweight and obese individuals. Reducing total body fat, increasing lean body mass and basal metabolic rate,^22,23 and lowering proinflammatory adipocytokine levels²⁴ result in positive responses. Thus, both types of training induce adaptations in skeletal muscles that will combat a range of disorders affecting functional capacity and metabolic health, including sarcopenia, type II diabetes and obesity.²⁵ As such, the present study aimed to evaluate the impact of concurrent training on biochemical parameters and obesity-related cardiometabolic risk factors.

Design

The present investigation is a case report.²⁶ The study described and interpreted data with the primary purpose of assessing the merit of a physical exercise program.

Sample

The criterion-based sample²⁶ consisted of an individual who did not engage in regular physical exercise, had no history of osteomyoarticular lesions that could interfere with their participation, did not use ergogenic / nutritional / pharmacological resources that could interfere with the dependent variables, and were in the class 1 obesity range.³

Ethics

The volunteer gave his informed consent in accordance with the Declaration of Helsinki,²⁷ and Resolution 510 of the National Health Council, Brazil (2016). The project was approved by the Research Ethics Committee of the Federal University of the State of Rio de Janeiro under protocol number 983.976/15.

Body composition

The following pre- and post-intervention body composition variables were measured: total body mass (BM), height (HT), waist circumference (WC), and hip circumference (HC). To assess total body mass and height, we used a mechanical balance with capacity of 150kg and accuracy of 100 g and a Filizola® stadiometer (Brazil) respectively. Waist and hip circumference were measured with a Sanny® anthropometric tape (Brazil). The procedures followed International Society for the Advancement of Kinanthropometry (ISAK) guidelines.^25,28

Body mass index (BMI) and body adiposity index (BAI) were calculated using the anthropometric measures obtained. BMI was obtained by the ratio of body mass in kilograms to height in meters squared.³ BAI was calculated using the WC and HP measurements in centimeters, and HT in meters in the following formula: $BAI=\left[WC-to-HCratio/\left(HTx\surd HT\right)\right]-18$ .²⁹

Blood pressure

Systolic and diastolic blood pressure (SBP and DBP) were measured on the day anthropometric measurements were collected using an OMRON HEM-7200 digital electronic sphygmomanometer.

Strength test

With a view to measuring the maximum load and determining training intensity, the 1RM tests³⁰ were performed in the following exercises: chest-supported row, 45° leg press, supine straight leg raise, knee flexion (flexor table), high pulley elbow extension and low pulley elbow flexion. A lower limb and upper limb exercise were performed on each strength testing day. There was an interval of at least 48h between each test session.

Cardio respiratory test

Cardio respiratory fitness was evaluated using the 12-minute Cooper test, which consists of the subject walking/running as far as possible in 12 min. Maximum oxygen consumption (VO_2max) is then calculated based on the distance traveled. The Cooper test was performed on a 400-meter athletics track. The course was demarcated by cones every 50 meters and controlled by the research team to evaluate the distance traveled in 12 minutes. Thus, it was possible to predict maximum VO₂ using Cooper’s equation.³¹ Prior to the test, the volunteer rested in a quiet environment for 10 minutes to measure resting heart rate (HR) using a Polar® FT1 digital heart monitor.

Biochemical variables

After a 12-hour fast and eight hours sleep, blood samples were collected to analyze the following parameters: glucose (GLU); glycated hemoglobin (HbA1c); (LDL), tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), interleukin-6 (IL- 6), leptin (LEP) and adiponectin (ADP). The biochemical parameters HbA1c and CRP were analyzed using the turbidimetry method. TC, TG, HDL, LDL, and GGT were analyzed by the enzymatic colorimetric method. Glucose was determined by the enzymatic method. The chemiluminescence method was applied to analyze TNF-α and IL-6, the kinetic-UV method to determine ALT and AST and the enzyme immunoassay technique to assess LEP and ADP.

LDL concentration was estimated using the Friedewald formula: LDL=TC-HDL- (TG/5).³² Blood sample collection, biochemical parameter analysis and disposal of the biological material were carried out by qualified personnel from the Sérgio Franco laboratory in Rio de Janeiro, Brazil.

Food frequency questionnaire (QFA)

In order to ascertain the volunteer’s dietary habits, he completed the food frequency questionnaire (FFQ)³³ in the week prior to the beginning of the intervention and in the following eight weeks.

Intervention

The intervention involved eight weeks of physical exercise, totaling 24 sessions of concurrent training (CT), performed on three nonconsecutive days per week, in the following order: strength training (ST) followed by aerobic training (AT). The ST started with a warm-up of 15 repetitions and overload of approximately 50%, which was used for the first series in the different exercises of the program. The weekly characteristics of the ST phase are presented in Table 1. Immediately after strength training, aerobic training was performed using continuous treadmill walking, with the characteristics presented in Table 2. The intensity of aerobic training was controlled by a Polar FT1 digital cardiac monitor, and the target training zone was calculated using heart rate reserve (HRR).³⁰

Data analysis

The difference between the measures was calculated as well as the percentage difference between pre-intervention (Baseline) and post-intervention (Post). Data were processed in Microsoft Excel software, 2007.

The results of cardiometabolic risk factors at baseline and post-intervention are presented in Table 3. BM, WC, HC, BMI, BAI, SBP and HRrest decreased, VO2max increased and HT and DBP remained unchanged. The biochemical parameter results at pre-intervention (Baseline) and post-intervention (Post) are presented in Table 4. With respect to biochemical markers, a decline was observed in all parameters analyzed, except for HDL and ADP, which showed an increase. In relation to the food frequency questionnaire, no change was found in the volunteer's eating habits throughout the intervention period.^31–33

The results of the present study showed a positive impact on the variables studied as a result of concurrent training in a 23-year-old man with grade 1 obesity. All the biochemical, hemodynamic and anthropometric parameters related to cardiometabolic risk improved with the training used. The choice of strength training followed by aerobic exercise in concurrent training is due to literature reports suggesting that aerobic exercise performed first alters the molecular events that regulate muscle proteins during subsequent resistance exercise, impairing strength gain. In this respect, activation of the tuberous sclerosis complex 2 (TSC2) acts negatively on the mTOR signaling pathway, blocking proteins from binding with their respective receptors, which, in turn, prevents hypertrophy.³⁴

Results similar to those obtained here were reported in a systematic review involving 12 trials with 555 young people, where the authors investigated whether the combination of aerobic and resistance exercise (concurrent training) was better than aerobic exercise alone for the health of obese children and adolescents. Compared with aerobic exercise alone, concurrent training resulted in greater reductions in body mass ($\overline{x}$ =-2.28kg), fat ($\overline{x}$ =-3.49%) and LDL cholesterol ($\overline{x}$ =-10.20mg/dL), and an increase in both lean body mass ($\overline{x}$ =2.20kg) and ADP levels ($\overline{x}$ =2.59μg/mL). However, it is important to underscore that the differences were greater for long-term programs (>24 weeks). In the present study, there was a decline in LDL cholesterol (Δ%=-32.98) and a rise in ADP (Δ%=152.73). With respect to the other variables, there was a decrease in BM (Δ%=-1.69) and BAI (Δ%=-14.24).³⁵

A study of sixteen patients with type II diabetes (DM2) investigated the effects of a concurrent training program on inflammatory status and metabolic parameters. The patients were randomly assigned to an experimental group (EG; n=8), who underwent a concurrent aerobic and resistance program (3 times a week for 16 weeks) or a control group (CG; n=8) who followed the traditional model of diabetes care. The EG significantly improved body composition, blood pressure, total cholesterol, and overall fitness level. After training, plasma leptin levels (-33.9%), pro-inflammatory markers IL-6 (-25.3%), TNF-α (-19.8%) and monocyte chernotactic protein-1 (MCP -1) (-15.3%) decreased, while IGF-1, an anabolic hormone, increased (+16.4%). On the other hand, there was no significant change in ADP or CRP.³⁶ In the present study, ADP levels (+152.73%) increased, and leptin (-37.5%), IL-6 (-21.21%), TNF- α (-23.2%) and CRP (-67.03%) decreased.

Interestingly, Colato et al.,³⁷ found increased levels of TNF-α and CRP after 12 weeks of concurrent training in 41 overweight / obese patients. Although there was an improvement in body composition and an increase in T-cell proliferation, the authors emphasize that exercise progression may be physiologically stressful for these patients, as demonstrated by inflammatory markers.

Another study carried out in DM2 patients also compared the effects of three different exercise modalities on metabolic control, insulin resistance, inflammatory markers, adipocytokines, hemodynamic parameters and tissue expression of the insulin receptor substrate 1 (IRS-1) after 12weeks of training. Forty-eight patients were randomized into 4 training groups (3 times per week/60 minutes per session): aerobic group (AG; n=12), resistance group (RG; n=12), experimental group (EG; n=12) and control group (CG; n=12). (HbA1c), lipid profile, insulin resistance index (HOMA), adipocytokines (adiponectin, visfatin and resistin), TNF-α, interleukin, high-sensitivity CRP (hs-CRP) and glycated hemoglobin (HbA1c) were measured at baseline and at the end of the study. All 4 groups exhibited a decrease in blood pressure, fasting plasma glucose, postprandial plasma glucose, lipid profile and hs-CRP; however, only resistance training (RT) and aerobic + resistance training (ART) produced increased IRS-1 expression after training. Improvements in aerobic capacity were demonstrated by the significant increase (16.3%) in VO₂max³⁸ These findings corroborate those of the present research in biochemical parameters, and it should be noted that the positive variation of VO₂max in both studies was very similar (16.3% x 16.8%).

With respect to hemodynamic parameters, the present study found a 5% decrease in SBP; however, DBP remained unchanged. A study conducted by Niño et al.,³⁹ aimed to evaluate the effects of aerobic (AT), resistance (RT) and concurrent (ART) training programs on systolic and diastolic blood pressure, both at rest and during submaximal exercise in healthy young people. Thirty-nine healthy active individuals were randomized to all three types of training and one control group. Exercise groups were trained for 60 minutes, three times a week for six weeks and a submaximal cycle ergometer test was performed before, at the end and three weeks after training. Blood pressure was measured before and during the test. In the submaximal test, SBP and DBP decreased significantly (p <0.05) after "detraining" (three weeks after) in the three exercise groups. However, significant reductions were observed at rest between pre-training and detraining only in the ART group (p <0.05). The difference in these findings from those of the present study is that only SBP decreased, while DBP remained unchanged.

An eight-week concurrent training program reduced cardiometabolic risk and positively altered biophysical and biochemical variables in this individual case report. So, further studies are indicated to confirm the positive aspects of concurrent training on active lifestyle.

None.

The author declares there are no conflicts of interest.

None.

1. Marti A, Marcos A, Martinez J. Obesity and immune function relationships. Obes Rev. 2001;2(2):131–40.
2. Klein-Platat C, Oujaa M, Wagner A, et al. Physical activity is inversely related to waist circumference in 12-y-old French adolescents. International Journal of Obesity. 2005;29(1):9–14.
3. Godoy-Matos A, Oliveira J, Guedes E, et al. Brazilian obesity guidelines 2009/2010. Brazilian Association for the Study of Obesity and Metabolic Syndrome (ABESO). 2009;(3):11–30.
4. Xavier H, Izar M, Faria Neto J, et al. Brazilian guideline for dyslipidemia and prevention of atherosclerosis. Brazilian Archives of Cardiology. 2013;101(4):1–20.
5. Cardoso G, Silva A, De Lavor W, et al. Resistance exercise does not change components and markers of metabolic syndrome in pre- and postmenopausal period. Med Sport. 2016;69:13–23.
6. Riley L, Cowan M. Noncommunicable diseases country profiles 2014. Geneva: World Health Organization. 2014.
7. Vidigal FC, Bressan J, Babio N, et al. Prevalence of metabolic syndrome in Brazilian adults: a systematic review. BMC public health. 2013;13(1):1198.
8. Zhang X, Hu EA, Wu H, et al. Associations of leg fat accumulation with adiposity‐related biological factors and risk of metabolic syndrome. Obesity. 2013;21(4):824–830.
9. Choi SI, Chung D, Lim JS, et al. Relationship between Regional Body Fat Distribution and Diabetes Mellitus: 2008 to 2010 Korean National Health and Nutrition Examination Surveys. Diabetes Metab J. 2017;41(1):51–59.
10. Shimabukuro M, Kozuka C, Taira S-i, et al. Ectopic fat deposition and global cardiometabolic risk: new paradigm in cardiovascular medicine. J Med Invest. 2013;60(1.2):1–14.
11. Lemieux I. Energy Partitioning in Gluteal-Femoral Fat: Does the Metabolic Fate of Triglycerides Affect Coronary Heart Disease Risk? Arterioscler Thromb Vasc Biol. 2004;24:795–797.
12. Lima F. Fat tissue: a brief historical perspective and the current moment. Brazilian Archives of Endocrinology & Metabology. 2008;52(6):927–928.
13. Guimarães D, Sardinha F, Mizurini D, et al. Adipocytokines: A New View of Adipose Tissue. Rev Nutr. 2007;20(5):549–559.
14. Prado W, Lofrano M, Oyama L, et al. Obesity and inflammatory adipokines: practical implications for exercise prescription: [review]. Rev Bras Med Sport. 2009;15(5):378–383.
15. Madeira I, Carvalho C, Gazolla F, et al. Impact of obesity on metabolic syndrome components and adipokines in prepubertal children. J Pediatr. 2009;85(3):261–268.
16. Matsuda M, Shimomura L, Sata M, et al. Role of adiponectin in preventing vascular stenosis The missing link of adipo-vascular axis. J Biol Chem.2002;277(40):37487–37491.
17. Elissondo N, Gómez Rosso L, Maidana P, et al. Adiponectin: an adipocytokine with multiple protective functions. Latin American Clinical Biochemistry Act. 2008;42(1):17–33.
18. Rosa G, Mello D, Fortes M, et al. Adipose tissue, metabolic hormones and physical exercise. Revista Andaluza de Medicina del Deporte. 2013;6(2):78–84.
19. Dâmaso A, Tock L, Tufik S, et al. Multidisciplinary treatment reduces visceral adiposity tissue, leptin, ghrelin and the prevalence of non-alcoholic fat liver disease (NAFLD) in obese adolescents. Revista Brasileira de Medicina do Esporte. 2006;12(5):263–267.
20. Rosa G, Dantas E, Biehl C, et al. Leptin, Cortisol and Distinct Concurrent Training Sequences. Int J Sports Med. 2012;33:177–80.
21. Mirzaei B, Rahmani-Nia J, Mehrabani M, et al. Effect of serial and integrated concurrent exercise on selected physical fitness factors of young men handball players. Med Sport. 2013;66:47–59.
22. Dolezal B, Potteiger J. Concurrent resistance and endurance training influence basal metabolic rate in nondieting individuals. J Appl Physiol. 1998;85(2):695–700.
23. Ho S, Dhaliwal S, Hills A, et al. The effect of 12 weeks of aerobic, resistance or combination exercise training on cardiovascular risk factors in the overweight and obese in a randomized trial. BMC Public Health. 2012;12(1):704.
24. Golbidi S, Mesdaghinia A, Laher I. Exercise in theMetabolic Syndrome. Oxid Med Cell Longev. 2012. p. 1–13.
25. Fyfe JJ, Bishop DJ, Stepto NK. Interference between concurrent resistance and endurance exercise: molecular bases and the role of individual training variables. Sports Med. 2014;44(6):743–762.
26. Thomas JR, Nelson JK, Silverman SJ. Research methods in physical activity: Human Kinetics Publishers; 2013.
27. W.M.A. Declaration of Helsinki. Ethical Principles for Medical Research Involving Human Subjects. 59th WMA General Assembly, Seoul. 2008.
28. Marfell-Jones T, Stewart A, Carter L. International standards for anthropometric assessment. South Africa: International Society for the Advancement of Kinanthropometry. 2006.
29. Bergman R, Stefanovski D, Buchanan T, et al. A better index of body adiposity. Obesity. 2011;19(5):1083–1089.
30. Baechle TR, Earle RW. Essencials of strength training and conditioning: Champaign: human kinetics; 2000.
31. ACSM. Guidelines For Exercise Testing and Prescreption. 10th ed. Lippincott Williams & Wilkins. 2017.
32. Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin chem. 1972;18(6):499–502.
33. Mannato L, Pereira T, Veslaquez-Melen G, et al. Elsa-Brasil Food Frequency Questionnaire: Proposal for Reduction and Validation of the Reduced Version. Nutrire. 2013;38(Suplemento):55.
34. Fyfe J, Bishop D, Stepto N. Interference between concurrent resistance and endurance exercise: molecular bases and the role of individual training variables. Sports Med. 2014;44(6):743–762.
35. García-Hermoso A, Ramírez-Vélez R, Ramírez-Campillo R, et al. Concurrent aerobic plus resistance exercise versus aerobic exercise alone to improve health outcomes in paediatric obesity: a systematic review and meta-analysis. Br J Sports Med. 2016.
36. Annibalini G, Lucertini F, Agostini D, et al. Concurrent Aerobic and Resistance Training Has Anti-Inflammatory Effects and Increases Both Plasma and Leukocyte Levels of IGF-1 in Late Middle-Aged Type 2 Diabetic Patients. Oxidative Medicine and Cellular Longevity. 2017;2017:10.
37. Colato A, Abreu F, Medeiros N, et al. Effects of concurrent training on inflammatory markers and expression of CD4, CD8, and HLA-DR in overweight and obese adults. Journal of Exercises science & Fitness. 2014;12(2):55–61.
38. Jorge M, de Oliveira V, Resende N, et al. The effects of aerobic, resistance, and combined exercise on metabolic control, inflammatory markers, adipocytokines, and muscle insulin signaling in patients with type 2 diabetes mellitus. Metabolism. 2011;60(9):1244–12552.
39. Niño O, Balagué N, Aragonés D, et al. Different training programs decrease blood pressure during submaximal exercise. Eur J Appl Physiol. 2017;117(11):2181–2189.