scholarly journals The Role of Exercise Training on Low-Grade Systemic Inflammation in Adults with Overweight and Obesity: A Systematic Review

2021 ◽  
Vol 18 (24) ◽  
pp. 13258
Author(s):  
Paola Gonzalo-Encabo ◽  
Gonzalo Maldonado ◽  
David Valadés ◽  
Carmen Ferragut ◽  
Alberto Pérez-López
Keyword(s):  
Exercise Training ◽  
Systemic Inflammation ◽  
Fat Mass ◽  
Overweight And Obesity ◽  
Concurrent Training ◽  
Low Grade ◽  
Mass Reduction ◽  
Tnf Α ◽  
Exercise Induced ◽  
Low Grade Inflammation

Low-grade systemic inflammation leads to critical alterations of several tissues and organs that can promote the appearance of non-communicable diseases, a risk that is increased in adults with obesity. Exercise training may counteract low-grade systemic inflammation, but there is a lack of consensus on how cytokines are modulated by training in adults with obesity. This study aimed of examining the effects of exercise training on circulating pro- and anti-inflammatory cytokines in adults with overweight and obesity, and whether exercise-induced fat mass reduction could mediate that effect. The search was conducted on Medline (Pubmed), SPORTDiscus and Web of Science databases from January 1998 to August 2021, using keywords pertaining to inflammation, exercise, and obesity. A total of 27 studies were selected, in which the circulating concentration levels of cytokines were analyzed. Endurance training (ET) decreased circulating CRP, IL-6 and TNF-α levels. TNF-α was reduced after resistance and concurrent training (CT), while IL-10 increased after resistance training (RT). Changes in IL-10 and CRP coincided with fat mass reduction, while decreased TNF-α levels were concomitant with changes in IL-6 and IL-10. Exercise training may reduce systemic low-grade inflammation profile in adults with overweight and obesity.

scholarly journals Resistance Exercise Training-Induced Muscle Hypertrophy Was Associated with Reduction of Inflammatory Markers in Elderly Women

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Kishiko Ogawa ◽  
Kiyoshi Sanada ◽  
Shuichi Machida ◽  
Mitsuharu Okutsu ◽  
Katsuhiko Suzuki
Keyword(s):  
Exercise Training ◽  
Resistance Exercise ◽  
Elderly Women ◽  
Muscle Thickness ◽  
The Elderly ◽  
Low Grade ◽  
Resistance Exercise Training ◽  
Tnf Α ◽  
Low Grade Inflammation ◽  
Circulating Levels

Aging is associated with low-grade inflammation. The benefits of regular exercise for the elderly are well established, whereas less is known about the impact of low-intensity resistance exercise on low-grade inflammation in the elderly. Twenty-one elderly women (mean age ± SD, 85.0 ± 4.5 years) participated in 12 weeks of resistance exercise training. Muscle thickness and circulating levels of C-reactive protein (CRP), serum amyloid A (SAA), heat shock protein (HSP)70, tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, monocyte chemotactic protein (MCP-1), insulin, insulin-like growth factor (IGF)-I, and vascular endothelial growth factor (VEGF) were measured before and after the exercise training. Training reduced the circulating levels of CRP, SAA (P<.05), HSP70, IGF-I, and insulin (P<.01). The training-induced reductions in CRP and TNF-α were significantly (P<.01,P<.05) associated with increased muscle thickness (r=−0.61,r=−0.54), respectively. None of the results were significant after applying a Bonferroni correction. Resistance training may assist in maintaining or improving muscle volume and reducing low-grade inflammation.

Exercise training, inflammatory cytokines, and other markers of low-grade inflammation in breast cancer survivors: A systematic review and meta-analysis.

2014 ◽  
Vol 32 (26_suppl) ◽  
pp. 121-121 ◽  
Author(s):  
Jose F Meneses-Echavez ◽  
Robinson Ramirez-Velez ◽  
Emilio Gonzalez-Jimenez ◽  
Jacqueline Schmidt Rio-Valle ◽  
Maria Jose Sanchez Perez ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Exercise Training ◽  
Cancer Survivors ◽  
Breast Cancer Survivors ◽  
Serum Levels ◽  
Low Grade ◽  
Exercise Interventions ◽  
Randomized Controlled ◽  
Tnf Α ◽  
Low Grade Inflammation

121 Background: Low-grade inflammation, characterized by high cytokine activity, plays a crucial role in tumorigenesis. Further, cytokines and other inflammatory biomarkers are closely implicated in tumor growth, angiogenesis, and metastasis. This metaanalysis of randomized controlled trials estimates the effects of exercise training in the control of the serum levels of cytokines and other inflammatory markers in breast cancer survivors. Methods: PRISMA statement and the Cochrane Handbook were followed. We searched MEDLINE, CENTRAL, EMBASE, Scopus and DARE database to retrieve randomized controlled trials published between 1980- March 2014 providing effect estimates of exercise interventions in the serum levels of cytokines, such as interleukin (IL) -2, IL-6, IL-8, tumoral necrosis factor alpha (TNF-α) and C-reactive protein (CRP) in breast cancer survivors. An Inverse of variance (IV) fixed-effects model was conducted in absence of heterogeneity (I2<50%); otherwise a random-effects model was selected. Mean Differences (MD) were calculated to estimate differences between groups (p<0.05 with 95% Confidence interval). Heterogeneity was measured with the Chi2 test (p<0.10) and I2 statistics. Results: A total of 15 studies were included (n=1,447; mean age= 51.6 years old). Exercise interventions resulted in positive effects for CRP (MD= 0.37, 95%CI, 0.04 to 0.71; p= 0.03; I2=15%), IL-2 (MD= -6.04, 85%CI, -11.41 to -0.67; p=0.03; I2=0%), IL-10 (-22.90, 95%CI, -41.27 to -4.53; p=0.001, I2=0%) and waist circumference as indicator of body composition (MD= -1.12, 95%CI, -2.06 to -0.18; p=0.02; I2=45%). Non-significant differences were observed for IL-6 and TNF-α. There was no evidence of publication bias. Conclusions: These findings suggest that exercise training improves the systemic pro-inflammatory profile in breast cancer survivors and consequently the immunological responses and the carcinogenic processes related to tumoral environment. The effects observed for IL-10 provide a novel focus of evidence for the role of exercise as an effective anti-inflammatory intervention in cancer survivors.

scholarly journals Fourteen days of smoking cessation improves muscle fatigue resistance and reverses markers of systemic inflammation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mohammad Z. Darabseh ◽  
Thomas M. Maden-Wilkinson ◽  
George Welbourne ◽  
Rob C. I. Wüst ◽  
Nessar Ahmed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Smoking Cessation ◽  
Muscle Fatigue ◽  
Fatigue Resistance ◽  
Systemic Inflammation ◽  
Muscle Function ◽  
Low Grade ◽  
Skeletal Muscle Function ◽  
Tnf Α

AbstractCigarette smoking has a negative effect on respiratory and skeletal muscle function and is a risk factor for various chronic diseases. To assess the effects of 14 days of smoking cessation on respiratory and skeletal muscle function, markers of inflammation and oxidative stress in humans. Spirometry, skeletal muscle function, circulating carboxyhaemoglobin levels, advanced glycation end products (AGEs), markers of oxidative stress and serum cytokines were measured in 38 non-smokers, and in 48 cigarette smokers at baseline and after 14 days of smoking cessation. Peak expiratory flow (p = 0.004) and forced expiratory volume in 1 s/forced vital capacity (p = 0.037) were lower in smokers compared to non-smokers but did not change significantly after smoking cessation. Smoking cessation increased skeletal muscle fatigue resistance (p < 0.001). Haemoglobin content, haematocrit, carboxyhaemoglobin, total AGEs, malondialdehyde, TNF-α, IL-2, IL-4, IL-6 and IL-10 (p < 0.05) levels were higher, and total antioxidant status (TAS), IL-12p70 and eosinophil numbers were lower (p < 0.05) in smokers. IL-4, IL-6, IL-10 and IL-12p70 had returned towards levels seen in non-smokers after 14 days smoking cessation (p < 0.05), and IL-2 and TNF-α showed a similar pattern but had not yet fully returned to levels seen in non-smokers. Haemoglobin, haematocrit, eosinophil count, AGEs, MDA and TAS did not significantly change with smoking cessation. Two weeks of smoking cessation was accompanied with an improved muscle fatigue resistance and a reduction in low-grade systemic inflammation in smokers.

scholarly journals An intensified training schedule in recreational male runners is associated with increases in erythropoiesis and inflammation and a net reduction in plasma hepcidin

2018 ◽  
Vol 108 (6) ◽  
pp. 1324-1333 ◽  
Author(s):  
Diego Moretti ◽  
Samuel Mettler ◽  
Christophe Zeder ◽  
Carsten Lundby ◽  
Anneke Geurts-Moetspot ◽  
...  
Keyword(s):  
Exercise Training ◽  
Iron Absorption ◽  
Iron Status ◽  
Geometric Mean ◽  
Iron Bioavailability ◽  
Oral Iron ◽  
Low Grade ◽  
Hemoglobin Mass ◽  
Low Grade Inflammation ◽  
Iron Utilization

ABSTRACT Background Iron status is a determinant of physical performance, but training may induce both low-grade inflammation and erythropoiesis, exerting opposing influences on hepcidin and iron metabolism. To our knowledge, the combined effects on iron absorption and utilization during training have not been examined directly in humans. Objective We hypothesized that 3 wk of exercise training in recreational male runners would decrease oral iron bioavailability by increasing inflammation and hepcidin concentrations. Design In a prospective intervention, nonanemic, iron-sufficient men (n = 10) completed a 34-d study consisting of a 16-d control phase and a 22-d exercise-training phase of 8 km running every second day. We measured oral iron absorption and erythroid iron utilization using oral 57Fe and intravenous 58Fe tracers administered before and during training. We measured hemoglobin mass (mHb) and total red blood cell volume (RCV) by carbon monoxide rebreathing. Iron status, interleukin-6 (IL-6), plasma hepcidin (PHep), erythropoietin (EPO), and erythroferrone were measured before, during, and after training. Results Exercise training induced inflammation, as indicated by an increased mean ± SD IL-6 (0.87 ± 1.1 to 5.17 ± 2.2 pg/mL; P < 0.01), while also enhancing erythropoiesis, as indicated by an increase in mean EPO (0.66 ± 0.42 to 2.06 ± 1.6 IU/L), mHb (10.5 ± 1.6 to 10.8 ± 1.8 g/kg body weight), and mean RCV (30.7 ± 4.3 to 32.7 ± 4.6 mL/kg) (all P < 0.05). Training tended to increase geometric mean iron absorption by 24% (P = 0.083), consistent with a decreased mean ± SD PHep (7.25 ± 2.14 to 5.17 ± 2.24 nM; P < 0.05). The increase in mHb and erythroid iron utilization were associated with the decrease in PHep (P < 0.05). Compartmental modeling indicated that iron for the increase in mHb was obtained predominantly (>80%) from stores mobilization rather than from increased dietary absorption. Conclusions In iron-sufficient men, mild intensification of exercise intensity increases both inflammation and erythropoiesis. The net effect is to decrease hepcidin concentrations and to tend to increase oral iron absorption. This trial was registered at clinicaltrials.gov as NCT01730521.

IL-6 as a Surrogate Biomarker: The IL-6 Clinical Value for the Diagnosis of Insulin Resistance and Type 2 Diabetes.

2021 ◽  
pp. 1-13
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Molecular Mechanisms ◽  
Diagnostic Value ◽  
Low Grade ◽  
Clinical Value ◽  
Insulin Resistant ◽  
Tnf Α ◽  
Low Grade Inflammation

1. Abstract Insulin Resistance is the leading cause of Type 2 diabetes mellitus (T2D). It occurs as a result of lipid disorders and increased levels of circulating free fatty acids (FFAs). FFAs accumulate within the insulin sensitive tissues such as muscle, liver and adipose tissues exacerbating different molecular mechanisms. Increased levels fatty acid has been documented to be strongly associated with insulin resistant states and obesity causing inflammation that eventually causes type 2-diabetes. Among the biomarkers that are accompanying low grade inflammation include IL-1β, IL-6 and TNF-α. The current review point out the importance of measuring the inflammatory biomarkers especially focusing on the conductance and measurement for IL-6 as a screening laboratory test and its diagnostic value in clinical practice.

scholarly journals Exercise training promotes a GDF15-associated reduction in fat mass in older adults with obesity

2019 ◽  
Vol 316 (5) ◽  
pp. E829-E836 ◽  
Author(s):  
Hui Zhang ◽  
Ciarán E. Fealy ◽  
John P. Kirwan
Keyword(s):  
Exercise Training ◽  
Fat Mass ◽  
Animal Studies ◽  
Acute Exercise ◽  
Exercise Intervention ◽  
Resting Energy Expenditure ◽  
Human Obesity ◽  
Total Fat ◽  
Exercise Induced ◽  
Response To Exercise

Obesity is a major risk factor for metabolic disease. Growth differentiation factor 15 (GDF15) has shown promise as a weight loss agent for obesity in animal studies. In healthy lean humans, fasting plasma GDF15 increases after acute exercise. However, the role of GDF15 in human obesity and the response of plasma GDF15 to exercise training in patients with obesity is unknown. Here, 24 sedentary volunteers with obesity [age: 65 ± 1 yr; body mass index (BMI): 35.3 ± 0.9 kg/m2] participated in a supervised 12-wk aerobic exercise intervention: 1 h/day, 5 days/wk at ~85% maximum heart rate with controlled isocaloric diet. As a result, plasma GDF15 was significantly increased (PRE: 644.1 ± 42.6 pg/ml, POST: 704.4 ± 47.2 pg/ml, P < 0.01) after the exercise intervention. Inconsistent with animal models, ΔGDF15 was not correlated with change in weight, BMI, or resting energy expenditure. However, ΔGDF15 was correlated with a reduction in total fat mass ( P < 0.05), abdominal fat mass ( P < 0.05), and android fat mass ( P ≤ 0.05). Participants with a positive GDF15 response to exercise had increased total fat oxidation (PRE: 0.25 ± 0.05 mg·kg−1·min−1, POST: 0.43 ± 0.07 mg·kg−1·min−1, P ≤ 0.05), metabolic flexibility [PRE: −0.01 ± 0.01 delta respiratory quotient (RQ), POST: 0.06 ± 0.01 delta RQ, P < 0.001], and insulin sensitivity (PRE: 0.33 ± 0.01 QUICKI index, POST: 0.34 ± 0.01 QUICKI index, P < 0.01), suggesting a link between GDF15 and fat mass loss as well as exercise-induced metabolic improvement in humans with obesity. We conclude that the exercise-induced increase in plasma GDF15 and the association with reduced fat mass may indicate a role for GDF15 as a therapeutic target for human obesity.

scholarly journals The Cooperative Induction of CCL4 in Human Monocytic Cells by TNF-α and Palmitate Requires MyD88 and Involves MAPK/NF-κB Signaling Pathways

2019 ◽  
Vol 20 (18) ◽  
pp. 4658 ◽  
Author(s):  
Sindhu ◽  
Kochumon ◽  
Shenouda ◽  
Wilson ◽  
Al-Mulla ◽  
...  
Keyword(s):  
Low Grade ◽  
Monocytic Cells ◽  
Signaling Mechanism ◽  
Blocking Antibody ◽  
Metabolic Inflammation ◽  
Qrt Pcr ◽  
Signaling Mechanisms ◽  
Tnf Α ◽  
Low Grade Inflammation ◽  
Tlr4 Receptor

: Chronic low-grade inflammation, also known as metabolic inflammation, is a hallmark of obesity and parallels with the presence of elevated circulatory levels of free fatty acids and inflammatory cytokines/chemokines. CCL4/MIP-1β chemokine plays a key role in the adipose tissue monocyte recruitment. Increased circulatory levels of TNF-α, palmitate and CCL4 are co-expressed in obesity. We asked if the TNF-α/palmitate could interact cooperatively to augment the CCL4 production in human monocytic cells and macrophages. THP-1 cells/primary macrophages were co-treated with TNF-α/palmitate and CCL4 mRNA/protein expression was assessed using qRT-PCR/ELISA. TLR4 siRNA, a TLR4 receptor-blocking antibody, XBlue™-defMyD cells and pathway inhibitors were used to decipher the signaling mechanisms. We found that TNF-α/palmitate co-stimulation augmented the CCL4 expression in monocytic cells and macrophages compared to controls (p < 0.05). TLR4 suppression or neutralization abrogated the CCL4 expression in monocytic cells. Notably, CCL4 cooperative induction in monocytic cells was: (1) Markedly less in MyD88-deficient cells, (2) IRF3 independent, (3) clathrin dependent and (4) associated with the signaling mechanism involving ERK1/2, c-Jun, JNK and NF-κB. In conclusion, TNF-α/palmitate co-stimulation promotes the CCL4 expression in human monocytic cells through the mechanism involving a TLR4-MyD88 axis and MAPK/NF-κB pathways. These findings unravel a novel mechanism of the cooperative induction of CCL4 by TNF-α and palmitate which could be relevant to metabolic inflammation.

Betaine reduces the expression of inflammatory adipokines caused by hypoxia in human adipocytes

2012 ◽  
Vol 109 (1) ◽  
pp. 43-49 ◽  
Author(s):  
K. Olli ◽  
S. Lahtinen ◽  
N. Rautonen ◽  
K. Tiihonen
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Markers ◽  
Mrna Level ◽  
Low Grade ◽  
Human Adipocytes ◽  
Low Oxygen ◽  
Hypoxic Conditions ◽  
Tnf Α ◽  
Oxygen Conditions ◽  
Low Grade Inflammation

Obesity is characterised by a state of chronic low-grade inflammation and the elevated circulating and tissue levels of inflammatory markers, including inflammation-related adipokines, released from white adipose tissue. The expression and release of these adipokines generally rises as the adipose tissue expands and hypoxic conditions start to develop within the tissue. Here, the effect of betaine, a trimethylglycine having a biological role as an osmolyte and a methyl donor, on the expression of inflammation-related markers was tested in human adipocytes under hypoxia. Differentiated adipocytes were cultivated under low (1 %) oxygen tension for 8–20 h. The expression of different adipokines, including IL-6, leptin, PPARγ, TNF-α and adiponectin, was measured by quantitative PCR by determining the relative mRNA level from the adipocytes. Hypoxia, in general, led to a decrease in the expression of PPARγ mRNA in human adipocytes, whereas the expression levels of leptin and IL-6 mRNA were substantially increased by hypoxia. The cultivation of adipocytes under hypoxia also led to a reduction in the expression of TNF-α mRNA. The results showed that hypoxia increased the relative quantification of leptin gene transcription, and that betaine (250 μmol/l) reduced this effect, caused by low oxygen conditions. Under hypoxia, betaine also reduced the mRNA level of the pro-inflammatory markers IL-6 and TNF-α. These results demonstrate that the extensive changes in the expression of inflammation-related adipokines in human adipocytes caused by hypoxia can be diminished by the presence of physiologically relevant concentrations of betaine.

Digital three-dimensional anthropometry detection of exercise-induced fat mass reduction in obese women

2014 ◽  
Vol 11 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Chiara Milanese ◽  
Andrea Giachetti ◽  
Valentina Cavedon ◽  
Francesco Piscitelli ◽  
Carlo Zancanaro
Keyword(s):  
Fat Mass ◽  
Three Dimensional ◽  
Obese Women ◽  
Mass Reduction ◽  
Exercise Induced
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