Quercetin's influence on exercise-induced changes in plasma cytokines and muscle and leukocyte cytokine mRNA

2007 ◽  
Vol 103 (5) ◽  
pp. 1728-1735 ◽  
Author(s):  
David C. Nieman ◽  
Dru A. Henson ◽  
J. Mark Davis ◽  
E. Angela Murphy ◽  
David P. Jenkins ◽  
...  

Trained male cyclists ( n = 40) ingested quercetin (Q; n = 20) (1,000 mg/day) or placebo (P; n = 20) supplements under randomized, double-blinded methods for 3 wk before and during a 3-day period in which subjects cycled for 3 h/day at ∼57% maximal work rate. Blood samples were collected before and after each exercise session and assayed for plasma IL-6, IL-10, IL-1ra, IL-8, TNF-α, and monocyte chemoattractant protein 1, and leukocyte IL-10, IL-8, and IL-1ra mRNA. Muscle biopsies were obtained before and after the first and third exercise sessions and assayed for NF-κB and cyclooxygenase-2 (COX-2), IL-6, IL-8, IL-1β, and TNF-α mRNA. Postexercise increases in plasma cytokines did not differ between groups, but the pattern of change over the 3-day exercise period tended to be lower in Q vs. P for IL-8 and TNF-α ( P = 0.094 for both). mRNA increased significantly postexercise for each cytokine measured in blood leukocyte and muscle samples. Leukocyte IL-8 and IL-10 mRNA were significantly reduced in Q vs. P (interaction effects, P = 0.019 and 0.012, respectively) with no other leukocyte or muscle mRNA group differences. Muscle NF-κB did not increase postexercise and did not differ between Q and P. Muscle COX-2 mRNA increased significantly postexercise but did not differ between Q and P. In summary, 1 g/day quercetin supplementation by trained cyclists over a 24-day period diminished postexercise expression of leukocyte IL-8 and IL-10 mRNA, indicating that elevated plasma quercetin levels exerted some effects within the blood compartment. Quercetin did not, however, influence any of the muscle measures, including NF-κB content, cytokine mRNA, or COX-2 mRNA expression across a 3-day intensified exercise period.

2003 ◽  
Vol 94 (3) ◽  
pp. 1025-1032 ◽  
Author(s):  
Theodoros Vassilakopoulos ◽  
Maria-Helena Karatza ◽  
Paraskevi Katsaounou ◽  
Androniki Kollintza ◽  
Spyros Zakynthinos ◽  
...  

Exercise increases plasma TNF-α, IL-1β, and IL-6, yet the stimuli and sources of TNF-α and IL-1β remain largely unknown. We tested the role of oxidative stress and the potential contribution of monocytes in this cytokine (especially IL-1β) response in previously untrained individuals. Six healthy nonathletes performed two 45-min bicycle exercise sessions at 70% ofV˙o 2 max before and after a combination of antioxidants (vitamins E, A, and C for 60 days; allopurinol for 15 days; and N-acetylcysteine for 3 days). Blood was drawn at baseline, end-exercise, and 30 and 120 min postexercise. Plasma cytokines were determined by ELISA and monocyte intracellular cytokine level by flow cytometry. Before antioxidants, TNF-α increased by 60%, IL-1β by threefold, and IL-6 by sixfold secondary to exercise ( P < 0.05). After antioxidants, plasma IL-1β became undetectable, the TNF-α response to exercise was abolished, and the IL-6 response was significantly blunted ( P < 0.05). Exercise did not increase the percentage of monocytes producing the cytokines or their mean fluorescence intensity. We conclude that in untrained humans oxidative stress is a major stimulus for exercise-induced cytokine production and that monocytes play no role in this process.


1984 ◽  
Vol 56 (1) ◽  
pp. 145-149 ◽  
Author(s):  
H. J. Green ◽  
J. A. Thomson ◽  
M. E. Ball ◽  
R. L. Hughson ◽  
M. E. Houston ◽  
...  

To investigate the role of high-intensity intermittent exercise on adaptations in blood volume and selected hematological measures, four male subjects aged 19–23 yr [peak O2 consumption (VO2max) = 53 ml X min-1 X kg-1] performed supramaximal (120% VO2max) cycle exercise on 3 consecutive days. Each exercise session consisted of intermittent work performed as bouts of 1-min work to 4-min rest until fatigue or until a maximum of 24 repetitions had been completed. Measurements on blood samples were made before the exercise period and 24 h after the last exercise session. Plasma volume (PV) estimated using 131I-human serum albumin increased by 11.6% (3,504 vs. 3,912 ml; P less than 0.05). Total blood volume (TBV) based on PV and hematocrit (Hct) values increased by 4.5% (5,798 vs. 6,059 ml; P less than 0.05), whereas red cell volume (RCV) decreased by 6.4% (2,294 vs. 2,147 ml; P less than 0.05). Measurements of hematological indices indicated significant reductions (P less than 0.05) in whole-blood Hct (39.7 vs. 35.5%), hemoglobin concentration (15.5 vs. 13.9 g/100 ml), hemoglobin content (897 vs. 839 g), and red blood cell count (5.15 vs. 4.55 X 10(6) X mm-3). The findings of this study suggest that exercise intensity is a major factor in promoting exercise-induced hypervolemia and that rapid elevations in PV can be induced early in training.


1996 ◽  
Vol 1 (5) ◽  
pp. 262-269 ◽  
Author(s):  
PV Byskosh ◽  
AT Reder

IFN-β reduces the number and severity of exacerbations of multiple sclerosis (MS), presumably by modifying immune regulation. We used semiquantitative polymerase chain reaction (RT-PCR) to measure mRNA levels for cytokines before and after IFN β-1b therapy. mRNA was extracted from mononuclear cells of nine healthy controls and 31 patients with MS. Before therapy, IL-10 and leukemia inhibitory factor (UF) mRNA levels were elevated in stable MS compared to active MS. Twenty four hours after IFN β-1b treatment, mRNA levels for IL-1, IL-2, IL-4, IL-6, IL-10, IL-12, IL-13, IFN-γ, TNF-α and UF had not changed. At 1 week, TNF-α mRNA increased and IL-10 and UF mRNA rose in 75% of patients. IL-2, IL-4, IL-12, IL-13 and IFN-γ did not change. At 3 months, cytokine mRNA returned to baseline levels. mRNA for the IFN-induced antiviral enzyme, 2, 5-OAS, rose by 24 h, peaked at 1 week, and remained elevated thereafter. Serum triglycerides and liver enzymes rose after therapy. Increased SGPT at 3 months correlated with TNF-α mRNA levels, suggesting that cytokines may cause some side effects of IFN β-1b. Baseline cytokine mRNA levels reflect disease activity, but the therapeutic effect of IFN β-1b does not appear to be explained by changes in cytokine mRNA levels.


2016 ◽  
Vol 311 (5) ◽  
pp. R841-R850 ◽  
Author(s):  
Corinna Serviente ◽  
Lisa M. Troy ◽  
Maxine de Jonge ◽  
Daniel D. Shill ◽  
Nathan T. Jenkins ◽  
...  

Endothelial dysfunction and inflammation are characteristics of subclinical atherosclerosis and may increase through progressive menopausal stages. Evaluating endothelial responses to acute exercise can reveal underlying dysfunction not apparent in resting conditions. The purpose of this study was to investigate markers of endothelial function and inflammation before and after acute exercise in healthy low-active perimenopausal (PERI) and late postmenopausal (POST) women. Flow-mediated dilation (FMD), CD31+/CD42b− and CD62E+ endothelial microparticles (EMPs), and the circulating inflammatory factors monocyte chemoattractant protein 1 (MCP-1), interleukin 8 (IL-8), and tumor necrosis factor-α (TNF-α) were measured before and 30 min after acute exercise. Before exercise, FMD was not different between groups (PERI: 6.4 ± 0.9% vs. POST: 6.5 ± 0.8%, P = 0.97); however, after acute exercise PERI tended to improve FMD (8.5 ± 0.9%, P = 0.09), whereas POST did not (6.2 ± 0.8%, P = 0.77). Independent of exercise, we observed transient endothelial dysfunction in POST with repeated FMD measures. There was a group × exercise interaction for CD31+/CD42b− EMPs ( P = 0.04), where CD31+/CD42b− EMPs were similar before exercise (PERI: 57.0 ± 6.7 EMPs/μl vs. POST: 58.5 ± 5.3 EMPs/μl, P = 0.86) but were higher in POST following exercise (PERI: 48.2 ± 6.7 EMPs/μl vs. POST: 69.4 ± 5.3 EMPs/μl, P = 0.023). CD62E+ EMPs were lower in PERI compared with POST before exercise ( P < 0.001) and increased in PERI ( P = 0.04) but did not change in POST ( P = 0.68) in response to acute exercise. After acute exercise, MCP-1 ( P = 0.055), TNF-α ( P = 0.02), and IL-8 ( P < 0.001) were lower in PERI but only IL-8 decreased in POST ( P < 0.001). Overall, these data suggest that perimenopausal and late postmenopausal women display different endothelial and inflammatory responses to acute exercise.


Immuno ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 26-39
Author(s):  
Takaki Tominaga ◽  
Jiapeng Huang ◽  
Katsuhiko Suzuki

Although exercise-induced humoral factors known as exerkines benefit systemic health, the role of most exerkines has not been investigated. Monocyte chemoattractant protein-1 (MCP-1) is a representative chemokine whose circulating concentrations increase after exercise, and it is one of the exerkines. MCP-1 is a ligand for CC chemokine receptor 2 (CCR2), which is expressed on monocytes, macrophages, and muscle cells. However, there is no information on the role of CCR2 signaling in exercise. Therefore, to investigate the research question, we administrated CCR2 antagonist or PBS to mice to inhibit CCR2 signaling before and after exercise. Our results showed that CCR2 signaling inhibition promoted exercise-induced macrophage infiltration and inflammation 24 h after exercise in muscle. CCR2 signaling inhibition also exacerbated exercise-induced inflammation immediately after exercise in muscle. However, neutrophil infiltration and oxidative stress had no contribution to exercise-induced inflammation by CCR2 signaling inhibition. CCR2 signaling inhibition also exacerbated exercise-induced inflammation immediately after exercise in kidney, liver, and adipose tissues. To summarize, pharmacological inhibition of CCR2 signaling exacerbated exercise-induced inflammation independently of neutrophil infiltration and oxidative stress.


Perfusion ◽  
2004 ◽  
Vol 19 (3) ◽  
pp. 185-191 ◽  
Author(s):  
Jale Bengi Celik ◽  
Niyazi Gormus ◽  
Selmin Okesli ◽  
Zulfikare Işik Gormus ◽  
Hasan Solak

Objective: This study examined the correlation between tumour necrosis factor-alfa (TNF-α), interleukin (IL)-6 and IL-8, IL-10 and methylprednisolone pretreatment. Methods: This is a prospective, randomized and double-blinded study. Sixty patients undergoing coronary artery bypass grafting (CABG) were randomized to receive either intravenous methylprednisolone (n=30, Group M) or intravenous placebo (n=30, Group S). The patients received intravenously either 30 mg/kg methylprednisolone (Group M) or placebo (Group S) 10 min before and after cardiopulmonary bypass (CPB). In an intensive care unit (ICU), four additional doses were given at 6-hourly intervals. Blood samples for the measurements of TNF-α, IL-6, IL-8 and IL-10 were obtained before induction of anaesthesia (T0=control value), after induction (T1), before starting CPB (T2), after aortic declamping (T3), at the end of CPB (T4) and 6 hours (T5), 12 hours (T6) and 24 hours (T7) after skin closure. Creatine kinase (CK) and creatine kinase isoenzyme MB (CK-MB) were evaluated at the following intervals: T0, T5, T6 and T7. Results: When compared with the control value, TNF-α, IL-6 and IL-8 significantly increased in Group S and Group M (p B-0.05), but these values were significantly greater in Group S than in Group M (p B-0.05). In comparison with the control value, IL-10 increased in both groups (p B-0.05), but was significantly greater in Group M than in Group S (p B-0.05). CK and CK-MB were increased in both groups in postoperative values compared to control values. In Group S, CK and CK-MB levels were significantly lower than in Group M (p B-0.05). Conclusion: In this study, we have found that pre-operative administration of methylprednisolone has decreased TNF-α, IL-6 and IL-8 release, and increased the perfusing IL-10 levels after CPB. Thus, methylpredniso-lone may decrease the inflammatory response during the CPB procedure.


2009 ◽  
Vol 34 (6) ◽  
pp. 1098-1107 ◽  
Author(s):  
Louise Croft ◽  
Jonathan D. Bartlett ◽  
Don P.M. MacLaren ◽  
Thomas Reilly ◽  
Louise Evans ◽  
...  

This aims of this study were to investigate the effects of carbohydrate availability during endurance training on the plasma interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α response to a subsequent acute bout of high-intensity interval exercise. Three groups of recreationally active males performed 6 weeks of high-intensity interval running. Groups 1 (LOW+GLU) and 2 (LOW+PLA) trained twice per day, 2 days per week, and consumed a 6.4% glucose or placebo solution, respectively, before every second training session and at regular intervals throughout exercise. Group 3 (NORM) trained once per day, 4 days per week, and consumed no beverage during training. Each group performed 50 min of high-intensity interval running at the same absolute workloads before and after training. Muscle glycogen utilization in the gastrocnemius muscle during acute exercise was reduced (p < 0.05) in all groups following training, although this was not affected by training condition. Plasma IL-6 concentration increased (p < 0.05) after acute exercise in all groups before and after training. Furthermore, the magnitude of increase was reduced (p < 0.05) following training. This training-induced attenuation in plasma IL-6 increase was similar among groups. Plasma IL-8 concentration increased (p < 0.05) after acute exercise in all groups, although the magnitude of increase was not affected (p > 0.05) by training. Acute exercise did not increase (p > 0.05) plasma TNF-α when undertaken before or after training. Data demonstrate that the exercise-induced increase in plasma IL-6 concentration in response to customary exercise is attenuated by previous exercise training, and that this attenuation appears to occur independent of carbohydrate availability during training.


2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Tasuku Terada ◽  
Alanna Friesen ◽  
Baljot S. Chahal ◽  
Gordon J. Bell ◽  
Linda J. McCargar ◽  
...  

Aim. To explore the factors associated with exercise-induced acute capillary glucose (CapBG) changes in individuals with type 2 diabetes (T2D).Methods. Fifteen individuals with T2D were randomly assigned to energy-matched high intensity interval exercise (HI-IE) and moderate intensity continuous exercise (MI-CE) interventions and performed a designated exercise protocol 5 days per week for 12 weeks. The duration of exercise progressed from 30 to 60 minutes. CapBG was measured immediately before and after each exercise session. Timing of food and antihyperglycemic medication intake prior to exercise was recorded.Results. Overall, the mean CapBG was lowered by 1.9 mmol/L (P<0.001) with the change ranging from −8.9 to +2.7 mmol/L. Preexercise CapBG (44%;P<0.001), medication (5%;P<0.001), food intake (4%;P=0.043), exercise duration (5%;P<0.001), and exercise intensity (1%;P=0.007) were all associated with CapBG changes, explaining 59% of the variability.Conclusion. The greater reduction in CapBG seen in individuals with higher preexercise CapBG may suggest the importance of exercise in the population with elevated glycemia. Lower blood glucose can be achieved with moderate intensity exercise, but prolonging exercise duration and/or including brief bouts of intense exercise accentuate the reduction, which can further be magnified by performing exercise after meals and antihyperglycemic medication. This trial is registered with ClinicalTrial.govNCT01144078.


2021 ◽  
Vol 27 (5) ◽  
pp. 409-420
Author(s):  
A. Hugo Montes ◽  
Eulalia Valle-Garay ◽  
Guadalupe Martin ◽  
Julio Collazos ◽  
Victoria Alvarez ◽  
...  

Primary responses in sepsis-mediated inflammation are regulated by pro-inflammatory cytokines. Variations in the cytokine genes might modify their transcription or expression, plasma cytokines levels and response to sepsis. Activation protein-1 (AP-1) and NF-κB regulate cytokines gene expression in sepsis. A total of 90 severely septic and 91 non-infected patients were prospectively studied. IL-1α ( –889 C/T), IL-1β ( +3954 C/T), IL-6 ( –174 G/C), TNF-α ( –238 G/A), TNF-α ( –308G/A), IL-8 ( –251A/T) and IL-10 ( –1082 G/A) SNPs, plasma IL-1β, IL-4, IL-6, IL-8, IL-10, IL-13, IFN-γ, TNF-α and monocyte chemoattractant protein 1 (MCP-1) levels, and AP-1 and NF-κB gene expression by neutrophils were assessed. A allele carriers of TNF-α ( –238 G/A) SNP were less frequent among septic patients. IL-6, IL-8, IL-10, TNF-α and MCP-1 levels were higher, and AP-1 and NF-κB gene expressions lower in septic patients. Sepsis was independently associated with higher fibrinogen, neutrophils counts and IL-8 levels, lower prothrombin, absence of the variant A allele of the TNF-α (–238 G/A) SNP, and haemodynamic failure. Death was independently associated with a higher APACHE II score, higher IL-8 levels, and the diagnosis of sepsis. TNF-a ( –238 G/A) SNP could protect against sepsis development. Higher IL-8 levels are predictive of sepsis and mortality.


2007 ◽  
Vol 292 (1) ◽  
pp. R143-R149 ◽  
Author(s):  
Carl D. Bradford ◽  
James D. Cotter ◽  
Megan S. Thorburn ◽  
Robert J. Walker ◽  
David F. Gerrard

Exercise increases mean body temperature (T̄body) and cytokine concentrations in plasma. Cytokines facilitate PG production via cyclooxygenase (COX) enzymes, and PGE2 can mediate fever. Therefore, we used a COX-2 inhibitor to test the hypothesis that PG-mediated pyrogenicity may contribute to the raised T̄body in exercising humans. In a double-blind, cross-over design, 10 males [age: 23 yr (SD 5), V̇o2 max: 53 ml·kg−1·min−1 (SD 5)] consumed rofecoxib (50 mg/day; NSAID) or placebo (PLAC) for 6 days, 2 wk apart. Exercising thermoregulation was measured on day 6 during 45-min running (∼75% V̇o2 max) followed by 45-min cycling and 60-min seated recovery (28°C, 50% relative humidity). Plasma cytokine (TNF-α, IL-10) concentrations were measured at rest and 30-min recovery. T̄body was similar at rest in PLAC (35.59°C) and NSAID (35.53°C) and increased similarly during running, but became 0.33°C (SD 0.26) lower in NSAID during cycling (37.39°C vs. 37.07°C; P = 0.03), and remained lower throughout recovery. Sweating was initiated at T̄body of ∼35.6°C in both conditions but ceased at higher T̄body in PLAC than NSAID during recovery [36.66°C (SD 0.36) vs. 36.39°C (SD 0.27); P = 0.03]. Cardiac frequency averaged 6·min−1 higher in PLAC ( P < 0.01), whereas exercising metabolic rate was similar (505 vs. 507 W·m−2; P = 0.56). A modest increase in both cytokines across exercise was similar between conditions. COX-2 specific NSAID lowered exercising heat and cardiovascular strain and the sweating (offset) threshold, independently of heat production, indicating that PGE-mediated inflammatory processes may contribute to exercising heat strain during endurance exercise in humans.


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