Physical fitness attenuates leukocyte-endothelial adhesion in response to acute exercise

2006 ◽  
Vol 101 (3) ◽  
pp. 785-788 ◽  
Author(s):  
Paul J. Mills ◽  
Suzi Hong ◽  
Laura Redwine ◽  
Steven M. Carter ◽  
Albert Chiu ◽  
...  

Studies suggest that physical fitness promotes cardiovascular health, including improved endothelial function and possibly reduced inflammatory responses to stressors. This study examined the effects of fitness on leukocyte-endothelial adhesion in response to an acute exercise challenge. Peripheral blood mononuclear cell (PBMC) adhesion to human umbilical venous endothelial cells (HUVEC) was examined in 18 more-fit and 19 less-fit individuals [mean age 39 yr (SD 11)] before and after a 20-min treadmill exercise at 65–70% peak oxygen consumption. PBMC were isolated from whole blood (Ficoll-Paque) at rest and immediately after exercise. HUVEC were incubated for 4 h in the presence of cytokines IL-1 and IL-8 to activate endothelial adhesion molecule expression. Fit subjects showed a significant reduction in PBMC-HUVEC adhesion after exercise ( P < 0.01) compared with less-fit subjects, who showed no significant change. Regardless of fitness levels, both at rest and in response to exercise, soluble ICAM-1 in the incubation media attenuated PBMC-HUVEC adhesion by ∼81% ( P < 0.001). The findings indicate that immune cells that demarginate in response to exercise have reduced ability to adhere in individuals who are physically fit, an effect apparently independent of ICAM-1 binding. The findings provide evidence of how physical fitness might protect individuals from inflammatory responses to exercise.

2020 ◽  
Author(s):  
Kévin Contrepois ◽  
Si Wu ◽  
Kegan J Moneghetti ◽  
Daniel Hornburg ◽  
Sara Ahadi ◽  
...  

AbstractExercise testing is routinely used in clinical practice to assess fitness - a strong predictor of survival - as well as causes of exercise limitations. While these studies often focus on cardiopulmonary response and selected molecular pathways, the dynamic system-wide molecular response to exercise has not been fully characterized. We performed a longitudinal multi-omic profiling of plasma and peripheral blood mononuclear cells including transcriptome, immunome, proteome, metabolome and lipidome in 36 well-characterized volunteers before and after a controlled bout of acute exercise (2, 15, 30 min and 1 hour in recovery). Integrative analysis revealed an orchestrated choreography of biological processes across key tissues. Most of these processes were dampened in insulin resistant participants. Finally, we discovered biological pathways involved in exercise capacity and developed prediction models revealing potential resting blood-based biomarkers of fitness.


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.


2017 ◽  
Vol 25 (4) ◽  
pp. 559-569 ◽  
Author(s):  
André L. Estrela ◽  
Aline Zaparte ◽  
Jeferson D. da Silva ◽  
José Cláudio Moreira ◽  
James E. Turner ◽  
...  

To examine whether the volume of previous exercise training in older athletes influences inflammatory, redox, and hormonal profiles, 40 trained marathon runners were divided into higher-volume (HVG, ∼480 min/week) and lower-volume groups (LVG, ∼240 min/week). Plasma inflammatory proteins, redox biomarkers, salivary testosterone, and cortisol were assessed at restand following two maximal acute exercise bouts. At rest, the LVG exhibited higher CRP, higher protein carbonyls, and lower SOD activity compared to the HVG (p’s < .05). In response to exercise, TNF-α declined similarly in both groups whereas CRP increased differentially (+60% LVG; +24% HVG; p’s < .05). Protein carbonyls decreased and thiols increased similarly in both groups, but SOD declined differentially between groups (−14% LVG; −20% HVG; p’s < .05). Salivary testosterone decreased similarly in both groups, whereas cortisol did not change. A higher volume of training is associated with favorable inflammatory and redox profiles at rest, perhaps mediated by small inflammatory responses to acute exercise.


Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 930 ◽  
Author(s):  
Xavier Capó ◽  
Miquel Martorell ◽  
Miguel D. Ferrer ◽  
Antoni Sureda ◽  
Victoria Pons ◽  
...  

Our aim was to characterize the effects of calorie restriction on the anthropometric characteristics and physical performance of sportsmen and to evaluate the effects of calorie restriction and acute exercise on mitochondria energetics, oxidative stress, and inflammation. Twenty volunteer taekwondo practitioners undertook a calorie restriction of 30–40% on three alternate days a week for one month. Eleven volunteer sportsmen participated as controls. Both groups performed an energy efficiency test to evaluate physical performance, and samples were taken before and after exercise. The total weight of participants significantly decreased (5.9%) after calorie restriction, while the efficiency of work and the contributions of fat to obtain energy were enhanced by calorie restriction. No significant differences induced by acute exercise were observed in individual non-esterified fatty acid percentage or oxidative stress markers. Calorie restriction downregulated the basal gene expression of nitric oxide synthase, antioxidant enzymes, mitochondrial uncoupling proteins, and repairing stress proteins, but it enhanced the expression of sirtuins in peripheral blood mononuclear cells. In conclusion, one month of calorie restriction decreases body weight and increases physical performance, enhancing energy efficiency, moderating the antioxidant and inflammatory basal gene expression, and influencing its response to acute exercise.


2021 ◽  
Author(s):  
Tiffany R. Bellomo ◽  
Noah L. Tsao ◽  
Hillary Johnston-Cox ◽  
Kamil Borkowski ◽  
Gabrielle Shakt ◽  
...  

Abstract Background: The progression of peripheral arterial disease (PAD) and the metabolome’s response to supervised exercise therapy (SET) has not yet been investigated. Results: When analyzing individual time points during exercise, we found high levels of anandamide (AEA) before any exercise interventions were associated with a shorter, or worse, walking time. We also found increased arachidonic acid (AA) and decreased levels of AA precursors dihomo-γ-linolenic acid and diacylglycerol before any exercise was associated with shorter walking times. Participants who were able to tolerate large increases in AA during acute exercise had longer, or better, walking times both before and after SET. Significance: We identified two pathways of relevance to individual response to SET: AEA synthesis may increase the activity at endocannabinoid receptors, resulting in worse treadmill test performance. SET may help train patients withstand higher levels of AA and inflammatory signaling, resulting in longer walking times.


1991 ◽  
Vol 69 (8) ◽  
pp. 1217-1221 ◽  
Author(s):  
Christine Jean ◽  
Gilles Tancrède ◽  
Suzanne Rousseau-Migneron ◽  
André Nadeau

Even if it is well established that epinephrine is a hormone originating from the adrenal medullae, the reappearance of circulating epinephrine has been reported in rats a few days after adrenodemedullation. To verify if the extra-adrenal tissue responsible for this epinephrine production can be stimulated, sham-operated or adrenodemedullated rats, either trained or kept sedentary, were submitted to an acute exercise stimulation test. Blood sampling was done before and after the test in precannulated rats for the determination of plasma epinephrine, norepinephrine, and corticosterone levels. Basal epinephrine levels were significantly reduced in trained and sedentary adrenodemedullated rats compared with their sham-operated counterparts. In response to exercise, there was no significant rise in epinephrine levels in both groups of adrenodemedullated rats. The norepinephrine levels in the basal state and in response to exercise were not altered by adrenodemedullation nor by physical conditioning. Basal corticosterone levels were similar between adrenodemedullated and sham-operated animals, either trained or kept sedentary. In response to exercise, corticosterone levels increased significantly in each group of rats but to a lesser extent in both groups of adrenodemedullated animals. These data indicate that the extra-adrenal epinephrine secretion that develops in the absence of adrenal medullae is not influenced by acute exercise nor by physical training.Key words: adrenodemedullation, extra-adrenal epinephrine, rat, physical training, acute exercise.


2001 ◽  
Vol 91 (4) ◽  
pp. 1808-1813 ◽  
Author(s):  
Miguel A. Rivera ◽  
Marcos Echegaray ◽  
Tuomo Rankinen ◽  
Louis Pérusse ◽  
Treva Rice ◽  
...  

We examined the possible association between a transforming growth factor (TGF)-β1 gene polymorphism in codon 10 and blood pressure (BP) at rest, in acute response to exercise in the pretrained (sedentary) and trained states, as well as in its training response (Δ) to 20 wk of endurance exercise. Subjects were 257 black and 480 white, healthy sedentary normotensive subjects from the HERITAGE Family Study. The polymorphism was detected by polymerase chain reaction and digestion with the Msp A1 I endonuclease yielding a wild (leucine-10) and a mutant (proline-10) allele. Resting and exercise [50 W plus 60, 80, and 100% maximal oxygen consumption (V˙o 2 max)] BP were determined before and after training. Significant ( P < 0.05) race-genotype interactions were found for systolic (S) BP in both the sedentary and trained states. Among whites but not in blacks, the TGF-β1 genotypes were significantly ( P < 0.05) associated with sedentary-state SBP at rest, at 50 W, and at 60 and 100% V˙o 2 max as well as with trained-state SBP at rest and at 80 and 100%V˙o 2 max. The leucine-10 homozygotes had significantly ( P < 0.05) lower SBP than proline-10 homozygotes. ΔBP was not significantly associated with genotype. These results support the hypothesis of an association between the TGF-β1 marker in codon 10 and SBP at rest and in response to acute exercise in whites but not in blacks.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Nan Xiao ◽  
Meng Nie ◽  
Huanhuan Pang ◽  
Bohong Wang ◽  
Jieli Hu ◽  
...  

AbstractCytokine release syndrome (CRS) is a major cause of the multi-organ injury and fatal outcome induced by SARS-CoV-2 infection in severe COVID-19 patients. Metabolism can modulate the immune responses against infectious diseases, yet our understanding remains limited on how host metabolism correlates with inflammatory responses and affects cytokine release in COVID-19 patients. Here we perform both metabolomics and cytokine/chemokine profiling on serum samples from healthy controls, mild and severe COVID-19 patients, and delineate their global metabolic and immune response landscape. Correlation analyses show tight associations between metabolites and proinflammatory cytokines/chemokines, such as IL-6, M-CSF, IL-1α, IL-1β, and imply a potential regulatory crosstalk between arginine, tryptophan, purine metabolism and hyperinflammation. Importantly, we also demonstrate that targeting metabolism markedly modulates the proinflammatory cytokines release by peripheral blood mononuclear cells isolated from SARS-CoV-2-infected rhesus macaques ex vivo, hinting that exploiting metabolic alterations may be a potential strategy for treating fatal CRS in COVID-19.


Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 936
Author(s):  
Olga Witkowska-Piłaszewicz ◽  
Rafał Pingwara ◽  
Jarosław Szczepaniak ◽  
Anna Winnicka

Clenbuterol, the β2-adrenoceptor agonist, is gaining growing popularity because of its effects on weight loss (i.e., chemical liposuction). It is also popular in bodybuilding and professional sports, due to its effects that are similar to anabolic steroids. However, it is prohibited by anti-doping control. On the other hand, it is suggested that clenbuterol can inhibit the inflammatory process. The cells from 14 untrained and 14 well-trained race horses were collected after acute exercise and cultured with clenbuterol. The expressions of CD4, CD8, FoxP3, CD14, MHCII, and CD5 in PBMC, and reactive oxygen species (ROS) production, as well as cell proliferation, were evaluated by flow cytometry. In addition, IL-1β, IL-4, IL-6, IL-10, IL-17, INF-γ and TNF-α concentrations were evaluated by ELISA. β2-adrenoceptor stimulation leads to enhanced anti-inflammatory properties in well-trained horses, as do low doses in untrained animals. In contrast, higher clenbuterol doses create a pro-inflammatory environment in inexperienced horses. In conclusion, β2-adrenoceptor stimulation leads to a biphasic response. In addition, the immune cells are more sensitive to drug abuse in inexperienced individuals under physical training.


2005 ◽  
Vol 288 (3) ◽  
pp. R591-R599 ◽  
Author(s):  
Mitsuharu Okutsu ◽  
Kenji Ishii ◽  
Kai Jun Niu ◽  
Ryoichi Nagatomi

The aim of this study was to elucidate the mechanism responsible for lymphopenia after exercise. Seven young healthy men volunteered for this study. Peripheral blood mononuclear cells (PBMC) were cultured with cortisol and analyzed for C-X-C motif chemokine receptor 4 (CXCR4) expression by flow cytometry. To determine the effects of exercise, subjects performed exhaustive cycling exercise. PBMC were cultured with plasma obtained before and after the cycling exercise. Alternatively, PBMC obtained before and after exercise were cultured without plasma or glucocorticoid to examine whether PBMC were primed in vivo for CXCR4 expression. We analyzed cortisol- or plasma-treated PBMC to determine their ability to migrate through membrane filters in response to stromal cell-derived factor 1α/CXCL12. Cortisol dose- and time-dependently augmented CXCR4 expression on T lymphocytes, with <6 h of treatment sufficient to augment CXCR4 on T lymphocytes. Postexercise plasma also augmented CXCR4 expression. Cortisol or postexercise plasma treatment markedly enhanced migration of T lymphocytes toward CXCL12. Augmentation of CXCR4 on T lymphocytes by cortisol or plasma was effectively blocked by the glucocorticoid receptor antagonist RU-486. Thus exercise-elicited endogenous cortisol effectively augments CXCR4 expression on T lymphocytes, which may account for lymphopenia after exercise.


Sign in / Sign up

Export Citation Format

Share Document