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Journal of Exercise Rehabilitation logoLink to Journal of Exercise Rehabilitation
. 2025 Dec 22;21(6):284–291. doi: 10.12965/jer.2550690.345

Eight weeks of moderate aerobic exercise on body composition and markers of inflammation and oxidative stress in middle-aged obese females

Kyung-Shin Park 1,*, Paola Canales Gonzalez 1, Miguel Nieto 1, Brett S Nickerson 2
PMCID: PMC12765893  PMID: 41497242

Abstract

This study investigated the effects of 4-week and 8-week moderate-intensity aerobic exercise on body composition and markers of inflammation and oxidative stress in middle-aged obese Hispanic females, with a particular focus on assessing these changes independently of fat mass reduction. A total of 35 participants were randomly assigned to either an exercise group or a control group for an eight-week intervention. The exercise group performed treadmill-based aerobic training at 55% of maximal oxygen consumption, with a fixed workload adjusted for body mass and a progression from three to four weekly sessions. Body composition was assessed using dual-energy x-ray absorptiometry, and blood samples were collected at baseline, 4 weeks, and 8 weeks to analyze tumor necrosis factor-alpha (TNF-α), C-reactive protein, adiponectin, total antioxidant status (TAS), and 8-hydroxydeoxyguanosine (8-OHdG). After 8 weeks, the exercise group showed significant reductions in body fat percentage, TNF-α, and 8-OHdG, alongside an increase in TAS. Notably, by week 4, significant decreases in TNF-α and increases in TAS were observed despite no measurable changes in body weight or fat mass, indicating an early anti-inflammatory and antioxidative response to exercise independent of adiposity reduction. The findings at 4 weeks suggest that moderate aerobic exercise can independently reduce inflammation and oxidative stress, even before measurable fat loss occurs. These improvements were further enhanced by fat loss after 8 weeks, indicating that moderate aerobic exercise may reduce the risk of obesity-related disorders in middle-aged obese females, both through direct anti-inflammatory effects and by promoting fat loss.

Keywords: Inflammation, Oxidative stress, Obesity, Aerobic exercise, Middle-aged women

INTRODUCTION

Obesity has emerged as a major global public health concern, reaching pandemic levels over the past two decades (Abd El-Kader et al., 2013; Khanna et al., 2022). In the United States, the Hispanic population bears a disproportionately higher prevalence of obesity compared to White Caucasians (Howell et al., 2022), placing this group at increased risk for obesity-related metabolic complications. Beyond its impact on body weight, obesity contributes to broader health disparities due to its strong association with cardiometabolic disorders and reduced quality of life (Ellulu et al., 2017; Khanna et al., 2022).

Excess body fat plays an active role in disease progression by functioning as an endocrine organ that elevates circulating proinflammatory cytokines and oxidative stress (Beavers et al., 2015; Khanna et al., 2022). These biological disturbances are implicated in the pathogenesis of insulin resistance, cardiovascular disease, and other obesity-related conditions (Ellulu et al., 2017). As a result, inflammation and oxidative stress are recognized as key therapeutic targets in lifestyle interventions aimed at mitigating disease risk in obese individuals (Krause et al., 2014; Papagianni et al., 2023; You et al., 2004).

Aerobic exercise is a widely recognized strategy for preventing and managing chronic diseases. Numerous studies have shown that regular aerobic training can reduce cardiovascular risk factors and improve insulin sensitivity (Balducci et al., 2010; Beavers et al., 2013; Kelly et al., 2007). Exercise has also been associated with reductions in systemic inflammation and oxidative stress among overweight and obese individuals (Krause et al., 2014; Papagianni et al., 2023), suggesting potential benefits beyond weight control.

Although exercise benefits are well established, some studies suggest that improvements in inflammatory and oxidative markers depend primarily on reductions in body fat (Beavers et al., 2013; Kelly et al., 2007; Marcell et al., 2005). They reported that significant decreases in proinflammatory cytokines and oxidative stress occurred only when fat mass was reduced, supporting the view that fat loss is a prerequisite for measurable improvements in metabolic health.

In contrast, emerging evidence suggests that exercise may exert anti-inflammatory and antioxidative effects independent of changes in adiposity. For instance, Starkie et al. (2003) demonstrated that exercise can suppress TNF-α production through the transient release of muscle-derived cytokines, while You et al. (2013) reported enhanced anti-inflammatory activity following exercise without accompanying fat loss. These findings challenge the assumption that body fat reduction is necessary for improvements in inflammatory status.

Given the ongoing debate regarding whether exercise-induced benefits require fat loss, it is critical to determine if moderate-intensity exercise can improve systemic inflammation and oxidative stress before significant changes in body composition occur. Therefore, the purpose of this study was to investigate the effects of an 8-week moderate-intensity aerobic exercise program, including a midpoint assessment at 4 weeks, on inflammatory cytokines and oxidative stress, independent of weight or fat loss.

MATERIALS AND METHODS

Study participants

A total of 38 obese Hispanic females aged 34–46 years were recruited from the Hispanic community in the United States. Eligibility criteria included being a non-smoker, premenopausal, obese (body mass index [BMI]>30 kg/m2), physically inactive, and free from chronic diseases. Participants were excluded if they were on medications that could affect metabolic, cardiovascular, or immune functions or if they had any musculoskeletal limitations. The study was approved by the Institutional Review Board (TAMIU-IRB-20131203), and all participants provided written informed consent and completed medical history forms before any study procedures.

Experimental design

At the initial visit, participants were stratified into three subgroups based on their baseline BMI (≤35.0, 35.1–40.0, and ≥40.1 kg/m2). Within each BMI stratum, participants were randomly assigned to either the exercise (EX: n=19) or control (CON: n=19) group using a computer-generated randomization procedure. Group allocation was determined after completion of baseline testing to minimize selection bias.

Assessments were conducted at 3 time points: before the intervention (PRE), after 4 weeks (4W POST), and after 8 weeks (8W POST) of intervention. Participants were instructed to maintain their usual dietary habits and to refrain from engaging in any additional aerobic or anaerobic exercise outside of the assigned program throughout the study period. Testing sessions were held between 8:00 a.m. and 10:00 a.m. following a 12-hr overnight fast. Each session included anthropometric measurements, assessment of body fat and visceral adipose tissue (VAT) mass, a maximal oxygen consumption (VO2max) test, and venous blood collection.

Measurements

Anthropometric measurements

Measurements were performed in duplicate by a trained technician. Height and weight were recorded to the nearest 0.1 cm and 0.1 kg, respectively, with participants dressed in indoor clothing and without shoes.

Body composition assessment

Total and regional body composition were assessed using dual- energy x-ray absorptiometry (Hologic Discovery Series, USA) at PRE, 4W POST, and 8W POST. This method estimated total lean mass and fat mass in specific regions, including visceral fat. Participants lay supine on the scanning table for the duration of the scan, which was performed according to standard clinical protocols. They wore a gown and removed all metal objects, such as glasses, jewelry, and cell phones.

VO2max test

The VO2max test was conducted 3 times at PRE, 4W POST, and 8W POST. The result from the PRE test was used to set the exercise intensity (55% of VO2max) for the exercise group. VO2max was measured during a continuous, progressive treadmill protocol, starting at 4 km/hr with speed increments of 0.8 km/hr every 2 min.

Blood collection and analyses

Five milliliters of venous blood were drawn from an antecubital vein immediately after body fat measurement on each testing day. The blood was centrifuged in serum-separating vacutainer tubes at 1,000×g for 15 min (Allegra X-15R Refrigerated Centrifuge, Beckman Coulter, USA). Serum samples were stored at −80°C until analysis. Enzyme-linked immunosorbent assays were used to measure tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), adiponectin, total antioxidant status (TAS), and 8-hydroxydeoxyguanosine (8-OHdG). Measurements were conducted with commercial kits (Cayman Chemical Co., USA) using a microplate reader (EL 808, BioTek Co., USA). The mean intra-assay coefficients of variation (CVs) were 5.7% for TNF-α, 6.1% for CRP, 6.6% for adiponectin, 6.3% for TAS, and 6.6% for 8-OHdG; inter-assay CVs were 6.5%, 7.4%, 8.1%, 6.9%, and 7.3%, respectively.

Exercise intervention

The exercise group engaged in walking sessions on a treadmill at an intensity corresponding to 55% VO2max using the target heart rate obtained during VO2max testing at PRE. This intensity was selected within the range recommended by the American College of Sports Medicine (American College of Sports Medicine, 2018) for moderate-intensity aerobic exercise, considering participants’ body weight, safety, and adherence.

Each participant performed exercises and expended 14.2 kcal/kg/wk for the first 4 weeks (3 sessions per week) and 18.9 kcal/kg/wk for weeks 5–8 (4 sessions per week). The duration of each exercise session was adjusted according to each participant’s VO2-velocity relationship. Heart rate was monitored with a Polar heart rate monitor (Polar, USA) and recorded every 10 min to ensure adherence to the target intensity. As participants’ fitness improved, treadmill speed was adjusted based on heart rate, with increases implemented if the average heart rate decreased by more than 5 beats per minute over two consecutive sessions. All exercise sessions were supervised by research assistants. Control group participants did not engage in any physical activity during the study. Exercise sessions for the exercise group were scheduled at participants’ convenience, and missed sessions were rescheduled.

Data analysis

Sample size calculations were performed using G*Power 3.1.0 software, with an alpha level of 0.05, an effect size of 0.40, and a power of 0.80, estimating a required sample size of 15 participants. Statistical analyses were conducted using IBM SPSS Statistics ver. 28.0 (IBM Co., USA). Two-way analysis of variance (ANOVA) was employed to analyze changes in body composition, inflammatory cytokines, and oxidative stress markers. Post hoc analyses were performed using the Bonferroni correction, with statistical significance set at P<0.05.

RESULTS

The flow of participants throughout the study is illustrated in Fig. 1. A total of 45 individuals were screened for eligibility, of whom 38 met the inclusion criteria and were randomized into the exercise (EX, n=19) and control (CON, n=19) groups. During the 8-week intervention, three participants from the EX group were excluded for missing more than three training sessions, resulting in 35 participants (EX, n=16; CON, n=19) who completed the study and were included in the final analysis. No adverse events occurred during the intervention.

Fig. 1.

Fig. 1

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CONSORT (Consolidated Standards of Reporting Trials)-style flow diagram showing participant enrollment, allocation, follow-up, and analysis.

Physical characteristics

At baseline, there were no significant differences between the EX and CON in age, body weight, height, or VO2max. The mean age, body weight, and height were 39.4±3.2 years (mean±standard deviation), 89.8±16 kg, and 160.5±4.3 cm in the EX and 40.3±3.7 years, 90.4±15.6 kg, 162.1±5.2 cm in the CON, respectively. Baseline VO2max values were 23.2±4.4 mL/kg/min for EX and 22.9±4.1 for CON.

A two-way repeated-measures ANOVA revealed significant time×group interactions for body weight (F [1, 33]=24.18, P< 0.001, ηp2=0.423), BMI (F [1, 33]=23.10, P<0.001, ηp2=0.412), and body fat percentage (F [1, 33]=41.97, P<0.001, ηp2=0.560), whereas no significant interaction was found for VAT.

The changes in body composition of the 35 participants, at PRE, 4W POST and 8W POST of the exercise intervention, are detailed in Table 1. Within-group analyses showed that, in the exercise group, body weight (P=0.01), BMI (P=0.023), and body fat percentage (P=0.015) significantly decreased after the 8-week intervention compared with baseline, whereas VAT showed no significant change (P=0.062). None of these variables showed significant difference at 4W POST as compared to PRE. In contrast, the control group exhibited no significant changes in any body-composition variable through 8 weeks of intervention.

Table 1.

Changes in body composition within and between groups during 8 weeks of intervention

Variable Group PRE 4W POST 8W POST Δ (8W–PRE) Within-group P (8W–PRE) Between-group P Effect size (η2, Cohen d)
Weight (kg) EX 89.8±16.0 89.5±15.3 87.6±14.8 −2.2±2.1 0.010* 0.478 (0.297, 1.20)
CON 90.4±15.6 90.3±16.1 90.9±16.6 0.5±1.4 0.812
BMI (kg·m−2) EX 34.9±5.5 34.7±5.3 33.8±5.2 −1.1±0.8 0.023* 0.672 (0.238, 0.75)
CON 34.4±5.8 34.4±6.0 34.6±6.2 0.2±0.9 0.873
Body Fat (%) EX 42.1±5.2 41.9±5.4 40.4±5.3 −1.7±1.2 0.015* 0.180 (0.255, 1.10)
CON 42.6±5.6 42.5±5.7 42.4±5.7 00.2±0.9 0.735
VAT (kg) EX 0.87±0.23 0.86±0.28 0.83±0.31 −0.04±0.02 0.062 0.627 (0.021, 0.30)
CON 0.87±0.25 0.87±0.26 0.88±0.26 0.01±0.01 0.826
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Values are means±standard deviation.

PRE, before the intervention; EX, exercise group; CON, control group; BMI, body mass Index; VAT, visceral adipose tissue mass.

*

P<0.05, significantly different from PRE within group.

Markers of inflammation and oxidative stress

Significant time×group interactions were observed for TNF-α (F [1, 33]=7.93, P<0.001, ηp2=0.19), TAS (F [1, 33]=15.39, P<0.001, ηp2=0.32), 8-OHdG (F [1, 33]=4.73, P=0.012, ηp2= 0.13), whereas no interactions were found for CRP or adiponectin.

Changes in inflammatory cytokines and markers of oxidative stress are presented in Figs. 2 and 3. In the exercise group, significant within-group improvements were observed. Post hoc comparisons showed that TAS increased from PRE to 4W POST (P<0.001) and further to 8W POST (P<0.001), whereas TNF-α decreased progressively from PRE to 4W POST (P=0.009) and 8 weeks (P<0.001). Additionally, 8-OHdG decreased significantly from PRE to 8W POST (P=0.039). In contrast, CRP and adiponectin showed no significant changes. No significant changes were observed in these variables for the CON group.

Fig. 2.

Fig. 2

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Changes of inflammatory cytokines at baseline (PRE) and after 4-weeks (4W POST) and 8-weeks (8W POST) of aerobic exercise intervention. Values are means±standard deviation. PRE, before the intervention; EX, exercise group; CON, control group; TNF-α, tumor necrosis factor-alpha; CRP, C-reactive protein. *P<0.05, significantly different from PRE within group.

Fig. 3.

Fig. 3

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Changes of markers of oxidative stress at baseline (PRE) and after 4 weeks (4W POST) and 8 weeks (8W POST) of aerobic exercise intervention. Values are means±standard deviation. PRE, before the intervention; EX, exercise group; CON, control group; TAS, total antioxidant status; 8-OHdG, 8-hydroxydeoxyguanosine. *P<0.05, significantly different from PRE within group.

DISCUSSION

This study examined the effects of 4- and 8-week moderate-intensity treadmill exercise on changes in body fat percentage, VAT mass, and markers of inflammation and oxidative stress in middle- aged Hispanic obese females. After 8 weeks of training, significant reductions were observed in body fat percentage, TNF-α, and 8-OHdG, along with an increase in TAS. However, no significant changes were found in VAT mass, CRP, or adiponectin. Notably, measurements taken at 4W POST revealed decreases in TNF-α and increases in TAS, despite no changes in body weight, body fat percentage, or VAT mass at that time. These findings suggest that exercise may induce early improvements in inflammatory and oxidative markers prior to measurable changes in adiposity.

Obesity is widely recognized as a major risk factor for cardiovascular and metabolic diseases, contributing to elevated levels of circulating inflammatory cytokines (Beavers et al., 2013; Ellulu et al., 2017; Khanna et al., 2022) and increased oxidative stress (Dennis et al., 2013; Squillacioti et al., 2019; Zguira et al., 2019). Regular exercise, particularly at low to moderate intensity, is considered as an effective strategy to counteract these adverse effects (Alcazar et al., 2019; Jeong and Yoon, 2012; Pimenta et al., 2015; Simioni et al., 2018). Previous research has reported improvements in oxidative stress markers and antioxidant status following endurance training in both young and older adults (Abd El-Kader and Saiem Al-Dahr, 2016; Mota et al., 2019; Park et al., 2005). However, it remains unclear whether these benefits are dependent on reductions in fat mass, as some studies reported concurrent weight loss (Abd El-Kader and Saiem Al-Dahr, 2016), while other did not measured changes in body composition (Mota et al., 2019).

Reductions in body fat are generally associated with lower oxidative stress. For example, Kelly et al. (2007) observed that 8 weeks of endurance training in overweight children did not alter oxidative stress markers, such as 8-isoprostane, when no reductions in fat mass occurred, implying that improvements in oxidative balance may depend on fat loss. Similarly, Kanikowska et al. (2021) demonstrated that caloric restriction reduced oxidative stress alongside decreases in fat mass and body fat percentage. However, other studies have reported improvements in oxidative stress independent of fat loss (Krause et al., 2014; Samjoo et al., 2013), suggesting that factors beyond changes in body composition, such as enhanced antioxidant capacity or exercise-induced physiological adaptations, may contribute to redox regulation. In the present study, TAS increased as early as 4W POST, prior to detectable changes in adiposity, supporting the hypothesis that exercise may improve oxidative balance through mechanisms independent of fat loss.

Proinflammatory cytokines are closely associated with obesity, as increased adiposity promotes a chronic low-grade inflammatory state (Beavers et al., 2013; Khanna et al., 2022). Many studies concluded that reductions in inflammatory cytokines are primarily driven by fat loss rather than exercise alone (Abd El-Kader and Al-Jiffri, 2018; Beavers et al., 2013; Marcell et al., 2005). Beavers et al. (2013) suggested that significant cytokine reductions occur only when fat mass decreases by more than 5%. This aligns with findings from Abd El-Kader and Al-Jiffri (2018) and Marcell et al. (2005), who noted that changes in adiponectin are linked to weight loss rather than improvements in fitness, concluding that regular exercise does not alter inflammatory cytokine levels. Moreover, most studies reporting significant changes in inflammatory cytokines following exercise also observed weight and/or fat loss (Abd El-Kader and Saiem Al-Dahr, 2016; Dekker et al., 2007; Kadoglou et al., 2007). Therefore, it is challenging to attribute changes in inflammatory cytokines to the effects of exercise.

Nonetheless, a growing body of evidence supports the idea that changes in inflammatory cytokines can occur independently of alterations in body weight or fat mass. Balducci et al. (2010) found that a 12-month high-intensity exercise program (aerobic or aerobic+resistance) significantly reduced proinflammatory markers such as CRP and TNF-α and increased adiponectin levels, even without weight or fat loss, suggesting that high-intensity exercise can reduce mortality risk in obese individuals without fat reduction. Similarly, Markofski et al. (2014) observed that resistance training lowered circulating inflammatory monocytes and decreased lipopolysaccharide-stimulated TNF-α, indicating that exercise may reduce proinflammatory cytokines by targeting inflammatory monocytes. Lambert et al. (2008) also reported that 12 weeks of combined exercise training reduced fat mass, increased fat-free mass, and decreased interleukin-6 (IL-6) and TNF-α mRNA expression in muscle, effects not seen in the diet-only group. Additionally, You et al. (2004) found that a diet plus exercise intervention lowered CRP and TNF-α levels, while the diet-only group did not achieve the same results despite similar fat loss.

While these studies support the anti-inflammatory effects of exercise independent of fat loss, most have been conducted in older or clinical populations, leaving uncertainty as to whether similar responses occur in healthy adults. The present study addresses this gap by examining the association between exercise and inflammatory cytokines in middle-aged Hispanic women, a group that has been underrepresented in prior exercise and inflammation research.

The present study aligns with emerging evidence that exercise may exert anti-inflammatory effects independent of fat loss. Although the precise mechanisms were not directly examined, several biological pathways may explain the early reduction in TNF-α observed after 4 weeks of training. One plausible mechanism involves the role of skeletal muscle-derived IL-6. Starkie et al. (2003) demonstrated that exercise-induced elevations in IL-6 were accompanied by decreases in TNF-α, suggesting that transient increases in IL-6 released from contracting skeletal muscle may acutely suppress systemic TNF-α production. Therefore, the early decline in TNF-α found in this study could reflect such IL-6–mediated anti-inflammatory signaling. In addition, moderate aerobic exercise enhances sympathetic nervous system activity and catecholamine release, particularly epinephrine, which has been shown to promote anti-inflammatory cytokines (IL-4, IL-10) and inhibit TNF-α synthesis (Shaw et al., 2018). This mechanism may further contribute to the rapid improvement in inflammatory status during the early phase of exercise training. Finally, increased blood flow to adipose tissue during exercise may alleviate local hypoxia and reduce hypoxia-induced cytokine production, even in the absence of fat loss (Czarkowska-Paczek et al., 2011; Hatano et al., 2011). Although these mechanisms are supported by indirect evidence from animal and experimental studies, further human research is needed to confirm the pathways through which exercise exerts its anti-inflammatory effects independent of fat loss.

This study had several key strengths. First, it was a randomized controlled trial with a 12-week duration of supervised, individualized one-on-one training sessions conducted in a cardio training room specifically designed for this research. Additionally, weekly energy expenditure was normalized relative to body weight using metabolic equivalent of task·hour/week, which ensured that participants engaged in equivalent levels of exercise regardless of their body weight. This approach enhances confidence that the exercise intervention was consistently applied across participants.

There are three notable limitations to consider. First, daily dietary intake and additional physical activities were not controlled in this study, although participants were instructed to maintain their usual lifestyle during the 8-week intervention period. This lack of control might have influenced body weight and body fat percentage, especially in the initial 4 weeks, as participants might have increased their caloric intake to compensate for the elevated energy expenditure. Second, the intervention period was relatively short, which may limit the interpretation of longer-term adaptations. However, the 8-week duration was deliberately chosen to capture the independent effects of exercise on inflammation and oxidative stress before substantial fat loss occurs. Finally, as this study was conducted predominantly among middle-aged Hispanic female adults in a largely Hispanic region, ethnic generalizability is limited, and the findings may not be directly applicable to other populations.

In conclusion, this study provides evidence that moderate-intensity aerobic exercise can improve markers of inflammation and oxidative stress in obese middle-aged women, even before measurable reductions in body fat or visceral adiposity occur. These findings highlight the therapeutic value of physical activity as a strategy to enhance metabolic health and reduce systemic inflammation, independent of weight loss. From a practical perspective, the results also suggest that informing individuals with obesity about the early physiological benefits of exercise—such as reductions in inflammation and oxidative stress even without fat loss—may help improve adherence to exercise programs. Emphasizing these internal health improvements, rather than focusing solely on visible weight changes, could motivate participants to maintain regular exercise, ultimately promoting long-term metabolic and cardiovascular health. Future studies should further explore the optimal exercise duration and intensity required to sustain these adaptations and examine whether similar benefits occur across different populations.

Footnotes

CONFLICT OF INTEREST

No potential conflict of interest relevant to this article was reported.

ACKNOWLEDGMENTS

This study was supported by Texas A&M International University Research Grant.

REFERENCES

  1. Abd El-Kader S, Gari A, Salah El-Den A. Impact of moderate versus mild aerobic exercise training on inflammatory cytokines in obese type 2 diabetic patients: a randomized clinical trial. Afr Health Sci. 2013;13:857–863. doi: 10.4314/ahs.v13i4.1. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Abd El-Kader SM, Al-Jiffri OH. Impact of weight reduction on insulin resistance, adhesive molecules and adipokines dysregulation among obese type 2 diabetic patients. Afr Health Sci. 2018;18:873–883. doi: 10.4314/ahs.v18i4.5. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Abd El-Kader SM, Saiem Al-Dahr MH. Impact of weight loss on oxidative stress and inflammatory cytokines in obese type 2 diabetic patients. Afr Health Sci. 2016;16:725–733. doi: 10.4314/ahs.v16i3.12. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Alcazar J, Losa-Reyna J, Rodriguez-Lopez C, Navarro-Cruz R, Alfaro-Acha A, Ara I, García-García FJ, Alegre LM, Guadalupe-Grau A. Effects of concurrent exercise training on muscle dysfunction and systemic oxidative stress in older people with COPD. Scand J Med Sci Sports. 2019;29:1591–1603. doi: 10.1111/sms.13494. [DOI] [PubMed] [Google Scholar]
  5. American College of Sports Medicine . ACSM’s guidelines for exercise testing and prescription. 10th ed. Philadelphia (PA): Wolters Kluwer; 2018. [Google Scholar]
  6. Balducci S, Zanuso S, Nicolucci A, Fernando F, Cavallo S, Cardelli P, Fallucca S, Alessi E, Letizia C, Jimenez A, Fallucca F, Pugliese G. Anti-inflammatory effect of exercise training in subjects with type 2 diabetes and the metabolic syndrome is dependent on exercise modalities and independent of weight loss. Nutr Metab Cardiovasc Dis. 2010;20:608–617. doi: 10.1016/j.numecd.2009.04.015. [DOI] [PubMed] [Google Scholar]
  7. Beavers KM, Ambrosius WT, Nicklas BJ, Rejeski WJ. Independent and combined effects of physical activity and weight loss on inflammatory biomarkers in overweight and obese older adults. J Am Geriatr Soc. 2013;61:1089–1094. doi: 10.1111/jgs.12321. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Beavers KM, Beavers DP, Newman JJ, Anderson AM, Loeser RF, Jr, Nicklas BJ, Lyles MF, Miller GD, Mihalko SL, Messier SP. Effects of total and regional fat loss on plasma CRP and IL-6 in overweight and obese, older adults with knee osteoarthritis. Osteoarthritis Cartilage. 2015;23:249–256. doi: 10.1016/j.joca.2014.11.005. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Czarkowska-Paczek B, Zendzian-Piotrowska M, Bartlomiejczyk I, Przybylski J, Gorski J. The influence of physical exercise on the generation of TGF-β1, PDGF-AA, and VEGF-A in adipose tissue. Eur J Appl Physiol. 2011;111:875–881. doi: 10.1007/s00421-010-1693-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Dekker MJ, Lee S, Hudson R, Kilpatrick K, Graham TE, Ross R, Robinson LE. An exercise intervention without weight loss decreases circulating interleukin-6 in lean and obese men with and without type 2 diabetes mellitus. Metabolism. 2007;56:332–338. doi: 10.1016/j.metabol.2006.10.015. [DOI] [PubMed] [Google Scholar]
  11. Dennis BA, Ergul A, Gower BA, Allison JD, Davis CL. Oxidative stress and cardiovascular risk in overweight children in an exercise intervention program. Child Obes. 2013;9:15–21. doi: 10.1089/chi.2011.0092. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Ellulu MS, Patimah I, Khaza’ai H, Rahmat A, Abed Y. Obesity and inflammation: the linking mechanism and the complications. Arch Med Sci. 2017;13:851–863. doi: 10.5114/aoms.2016.58928. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Hatano D, Ogasawara J, Endoh S, Sakurai T, Nomura S, Kizaki T, Ohno H, Komabayashi T, Izawa T. Effect of exercise training on the density of endothelial cells in the white adipose tissue of rats. Scand J Med Sci Sports. 2011;21:e115–e121. doi: 10.1111/j.1600-0838.2010.01176.x. [DOI] [PubMed] [Google Scholar]
  14. Howell CR, Juarez L, Agne AA, Nassel AF, Scarinci IC, Ayala GX, Cherrington AL. Assessing Hispanic/Latino and Non-Hispanic White social determinants of obesity among a community sample of residents in the rural southeast US. J Immigr Minor Health. 2022;24:1469–1479. doi: 10.1007/s10903-022-01334-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Jeong S, Yoon M. Swimming’s prevention of ovariectomy-induced obesity through activation of skeletal-muscle PPARα. Int J Sport Nutr Exerc Metab. 2012;22:1–10. doi: 10.1123/ijsnem.22.1.1. [DOI] [PubMed] [Google Scholar]
  16. Kadoglou NP, Perrea D, Iliadis F, Angelopoulou N, Liapis C, Alevizos M. Exercise reduces resistin and inflammatory cytokines in patients with type 2 diabetes. Diabetes Care. 2007;30:719–721. doi: 10.2337/dc06-1149. [DOI] [PubMed] [Google Scholar]
  17. Kanikowska D, Kanikowska A, Swora-Cwynar E, Grzymisławski M, Sato M, Bręborowicz A, Witowski J, Korybalska K. Moderate caloric restriction partially improved oxidative stress markers in obese humans. Antioxidants (Basel) 2021;10:1018. doi: 10.3390/antiox10071018. [DOI] [PMC free article] [PubMed] [Google Scholar]
  18. Kelly AS, Steinberger J, Olson TP, Dengel DR. In the absence of weight loss, exercise training does not improve adipokines or oxidative stress in overweight children. Metabolism. 2007;56:1005–1009. doi: 10.1016/j.metabol.2007.03.009. [DOI] [PubMed] [Google Scholar]
  19. Khanna D, Khanna S, Khanna P, Kahar P, Patel BM. Obesity: a chronic low-grade inflammation and its markers. Cureus. 2022;14:e22711. doi: 10.7759/cureus.22711. [DOI] [PMC free article] [PubMed] [Google Scholar]
  20. Krause M, Rodrigues-Krause J, O’Hagan C, Medlow P, Davison G, Susta D, Boreham C, Newsholme P, O’Donnell M, Murphy C, De Vito G. The effects of aerobic exercise training at two different intensities in obesity and type 2 diabetes: implications for oxidative stress, low-grade inflammation and nitric oxide production. Eur J Appl Physiol. 2014;114:251–260. doi: 10.1007/s00421-013-2769-6. [DOI] [PubMed] [Google Scholar]
  21. Lambert CP, Wright NR, Finck BN, Villareal DT. Exercise but not diet-induced weight loss decreases skeletal muscle inflammatory gene expression in frail obese elderly persons. J Appl Physiol (1985) 2008;105:473–478. doi: 10.1152/japplphysiol.00006.2008. [DOI] [PMC free article] [PubMed] [Google Scholar]
  22. Marcell TJ, McAuley KA, Traustadóttir T, Reaven PD. Exercise training is not associated with improved levels of C-reactive protein or adiponectin. Metabolism. 2005;54:533–541. doi: 10.1016/j.metabol.2004.11.008. [DOI] [PubMed] [Google Scholar]
  23. Markofski MM, Flynn MG, Carrillo AE, Armstrong CL, Campbell WW, Sedlock DA. Resistance exercise training-induced decrease in circulating inflammatory CD14+CD16+ monocyte percentage without weight loss in older adults. Eur J Appl Physiol. 2014;114:1737–1748. doi: 10.1007/s00421-014-2902-1. [DOI] [PubMed] [Google Scholar]
  24. Mota MP, Dos Santos ZA, Soares JFP, de Fátima Pereira A, João PV, O’Neil Gaivão I, Oliveira MM. Intervention with a combined physical exercise training to reduce oxidative stress of women over 40 years of age. Exp Gerontol. 2019;123:1–9. doi: 10.1016/j.exger.2019.05.002. [DOI] [PubMed] [Google Scholar]
  25. Papagianni G, Panayiotou C, Vardas M, Balaskas N, Antonopoulos C, Tachmatzidis D, Didangelos T, Lambadiari V, Kadoglou NPE. The anti-inflammatory effects of aerobic exercise training in patients with type 2 diabetes: a systematic review and meta-analysis. Cytokine. 2023;164:156157. doi: 10.1016/j.cyto.2023.156157. [DOI] [PubMed] [Google Scholar]
  26. Park JY, Ferrell RE, Park JJ, Hagberg JM, Phares DA, Jones JM, Brown MD. NADPH oxidase p22phox gene variants are associated with systemic oxidative stress biomarker responses to exercise training. J Appl Physiol (1985) 2005;99:1905–1911. doi: 10.1152/japplphysiol.00380.2005. [DOI] [PubMed] [Google Scholar]
  27. Pimenta M, Bringhenti I, Souza-Mello V, Dos Santos Mendes IK, Aguila MB, Mandarim-de-Lacerda CA. High-intensity interval training beneficial effects on body mass, blood pressure, and oxidative stress in diet-induced obesity in ovariectomized mice. Life Sci. 2015;139:75–82. doi: 10.1016/j.lfs.2015.08.004. [DOI] [PubMed] [Google Scholar]
  28. Samjoo IA, Safdar A, Hamadeh MJ, Raha S, Tarnopolsky MA. The effect of endurance exercise on both skeletal muscle and systemic oxidative stress in previously sedentary obese men. Nutr Diabetes. 2013;3:e88. doi: 10.1038/nutd.2013.30. [DOI] [PMC free article] [PubMed] [Google Scholar]
  29. Shaw DM, Merien F, Braakhuis A, Dulson D. T-cells and their cytokine production: the anti-inflammatory and immunosuppressive effects of strenuous exercise. Cytokine. 2018;104:136–142. doi: 10.1016/j.cyto.2017.10.001. [DOI] [PubMed] [Google Scholar]
  30. Simioni C, Zauli G, Martelli AM, Vitale M, Sacchetti G, Gonelli A, Neri LM. Oxidative stress: role of physical exercise and antioxidant nutraceuticals in adulthood and aging. Oncotarget. 2018;9:17181–17198. doi: 10.18632/oncotarget.24729. [DOI] [PMC free article] [PubMed] [Google Scholar]
  31. Squillacioti G, Bellisario V, Grignani E, Mengozzi G, Bardaglio G, Dalmasso P, Bono R. The Asti Study: the induction of oxidative stress in a population of children according to their body composition and passive tobacco smoking exposure. Int J Environ Res Public Health. 2019;16:490. doi: 10.3390/ijerph16030490. [DOI] [PMC free article] [PubMed] [Google Scholar]
  32. Starkie R, Ostrowski SR, Jauffred S, Febbraio M, Pedersen BK. Exercise and IL-6 infusion inhibit endotoxin-induced TNF-alpha production in humans. FASEB J. 2003;17:884–886. doi: 10.1096/fj.02-0670fje. [DOI] [PubMed] [Google Scholar]
  33. You T, Arsenis NC, Disanzo BL, Lamonte MJ. Effects of exercise training on chronic inflammation in obesity : current evidence and potential mechanisms. Sports Med. 2013;43:243–256. doi: 10.1007/s40279-013-0023-3. [DOI] [PubMed] [Google Scholar]
  34. You T, Berman DM, Ryan AS, Nicklas BJ. Effects of hypocaloric diet and exercise training on inflammation and adipocyte lipolysis in obese postmenopausal women. J Clin Endocrinol Metab. 2004;89:1739–1746. doi: 10.1210/jc.2003-031310. [DOI] [PubMed] [Google Scholar]
  35. Zguira MS, Slimani M, Bragazzi NL, Khrouf M, Chaieb F, Saïag B, Tabka Z. Effect of an 8-week individualized training program on blood biomarkers, adipokines and endothelial function in obese young adolescents with and without metabolic syndrome. Int J Environ Res Public Health. 2019;16:751. doi: 10.3390/ijerph16050751. [DOI] [PMC free article] [PubMed] [Google Scholar]

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