Mechanism Of Aerobic Exercise Research Articles

PC 18:1/18:1 mediates the anti-inflammatory effects of exercise and remodels tumor microenvironment of hepatocellular carcinoma

AimPhosphatidylcholine (PC) is essential for membrane structural integrity and lipid-dependent signaling pathways, and is an essential component required for cancer cell growth. Using hepatocellular carcinoma (HCC) as a tumor model, this study aims to further screen phospholipid biomarkers of the tumor microenvironment and explore the anti-tumor effects and mechanisms of aerobic exercise. Main methodsThe HCC of C57BL/6J mice was induced by the injection of the carcinogen diethylnitrosamine (DEN). Exercise was performed on an ungraded treadmill for weeks. The inflammation-related markers were detected by ELISA, PCR and immunohistochemistry, hepatic metabolic profile was analyzed by GC/MS, and lipid metabolism profile was further detected by lipid-targeted LC/MS. Cell culture was used to verify the anti-inflammatory effect of PC. Key findingsExercise reduced hepatic inflammation, tumor incidence and volume. Metabolomics analysis showed that palmitic acid is a key metabolic marker for exercise to improve tumor microenvironment. Injection of exogenous palmitic acid following exercise impaired the anti-inflammatory and anti-tumor effects of exercise. Lipid metabolomics analysis further showed that metabolites for exercise were enriched in glycerol phospholipid metabolism, including 14 phosphatidylcholines (PCs), 18 phosphatidylethanolamines (PEs), and 6 triglycerides (TGs). These biomarkers contain different lengths of fatty acid chains and different numbers of unsaturated bonds, respectively. Cell culture verified that PC (18:1/18:1) mediated lipopolysaccharide (LPS)-induced inflammation in HepG2 cell. SignificanceOur results suggest that exercise remodels glycerophospholipid metabolism and reduces hepatic palmitic acid loading and PC (18:1/18:1) level, thereby reconstructing a microenvironment that is hostile to HCC.

Mechanisms of aerobic exercise in attenuating obesity-induced cognitive impairment: A brief review

Obesity is associated with cognitive deficits. With the increasing rates of obesity and negative consequences of cognitive impairments, an understanding of interventions that may reduce cognitive impairment is of utmost importance. One intervention that has been proposed to mitigate cognitive deficits in individuals with obesity is the use of aerobic exercise. Despite the evidence that aerobic exercise may improve cognition in individuals with obesity, the exact mechanisms responsible for the cognitive improvements remain to be elucidated. This review explores three possible mechanisms that contribute to aerobic exercise-induced cognitive improvements in individuals with obesity including: 1) Improved cerebral blood flow, 2) Reduced neuroinflammation, and 3) Increased neurogenesis. Future directions will also be discussed.

Role of aerobic exercise in ameliorating NASH: Insights into the hepatic thyroid hormone signaling and circulating thyroid hormones.

Triiodothyronine (T3) administration significantly eliminates hepatic steatosis and also has a therapeutic effect on non-alcoholic steatohepatitis (NASH). However, the potential mechanism by which T3-mediated exercise improves NASH is unknow. This study aimed to explore the effect of aerobic exercise on liver injury in NASH. Aerobic exercise was conducted to explore the effects of exercise on liver injury in NASH model induced by Atherosclerotic (Ath) diet. Biochemical evaluations, histological staining and real-time PCR were first applied to confirm the amelioration effects of exercise on NASH. RNA-sequencing (RNA-seq) analysis for livers of each group were further used to identify the underlying mechanisms of aerobic exercise. Bioinformatics methods were used to explore the key functional pathways involved in the improvement of liver tissue in NASH mice by aerobic exercise. Aerobic exercise improved hepatic steatosis, lobular inflammation and fibrosis in NASH mice. multiple inflammation-related pathways were significantly enriched in the liver of NASH group and improved by aerobic exercise. The results of gene set variation analysis (GSVA) showed a higher enrichment score of T3 response signature in NASH mice with exercise. Increased Dio1 expression in the liver of NASH with exercise mice and increased circulating FT3 and FT4 levels upon aerobic exercise were confirmed. We found that aerobic exercise could significantly reduce hepatic lipid accumulation, inflammatory infiltration and fibrosis progression in the liver of NASH mice. Hepatic thyroid hormone signaling activation and circulating thyroid hormones is potentially involved in the amelioration effect of aerobatic exercise on NASH progression.

Aerobic exercise alleviates ventilator-induced lung injury by inhibiting NLRP3 inflammasome activation

BackgroundVentilator-induced lung injury (VILI) is caused by stretch stimulation and other factors related to mechanical ventilation (MV). NOD-like receptor protein 3 (NLRP3), an important innate immune component, is strongly associated with VILI. This study aimed to investigate the effect and mechanisms of aerobic exercise (EX) on VILI.MethodsTo test the effects of the PKC inhibitor bisindolylmaleimide I on PKC and NLRP3, male C57BL/6 mice (7 weeks old, 19 ~ 23 g) were randomly divided into four groups: control group(C), bisindolylmaleimide I-pretreated group(B), MV group, and bisindolylmaleimide I-pretreated + MV (B + MV) group. The mice were pretreated with bisindolylmaleimide I through intraperitoneal injection (0.02 mg/kg) 1 h before MV. MV was performed at a high tidal volume (30 ml/kg). To explore the ameliorative effect of EX on VILI, the mice were randomly divided into C group, MV group, EX group and EX + MV group and subjected to either MV or 5 weeks of EX training. After ventilation, haematoxylin-eosin (HE) staining and wet/dry weight ratio was used to assess lung pathophysiological changes. PKCɑ, P-PKCɑ, ASC, procaspase-1, caspase-1, pro-IL-1β, IL-1β, NLRP3 and occludin (tight junction protein) expression in lung tissues was determined by Western blotting. The level of IL-6 in alveolar lavage fluid was determined by ELISA.ResultsNLRP3, P-PKCɑ, and PKCɑ levels were inceased in MV group, but bisindolylmaleimide I treatment reversed these changes. Inhibition of PKC production prevented NLRP3 activation. Moreover, MV increased ASC, procaspase-1, caspase-1, pro-IL-1β, and IL1β levels and decreased occludin levels, but EX alleviated these changes. HE staining and lung injury scoring confirmed an absence of obvious lung injury in C group and EX group. Lung injury was most severe in MV group but was improved in EX + MV group. Overall, these findings suggest that MV activates the NLRP3 inflammasome by activating PKCɑ and inducing occludin degradation, while Exercise attenuates NLRP3 inflammasome and PKCɑ activation. Besides, exercise improves cyclic stretch-induced degradation of occludin.ConclusionPKC activation can increase the level of NLRP3, which can lead to lung injury. Exercise can reduce lung injury by inhibiting PKCɑ and NLRP3 activation. Exercise maybe a potential measure for clinical prevention of VILI.

Amelioration of Ambient Particulate Matter (PM2.5)-Induced Lung Injury in Rats by Aerobic Exercise Training.

Ambient particulate matter (PM2.5), as an inflammation-inducing factor, increases the prevalence of lung injury. The aim of this study was to examine the protective effect and mechanism of aerobic exercise on PM2.5 exposure-induced lung injury. Forty Wistar rats were randomly divided into four groups: sedentary+PM2.5 exposure, exercise+PM2.5 exposure, sedentary, and exercise groups. All rats in the exercise-related groups underwent 8-week aerobic interval treadmill training (5daysweek−1, 1hday−1). PM-exposed rats were exposed to ambient PM2.5 (6h day−1) for 3weeks after the 8-week exercise intervention. Then, ventilation function, histopathological changes, and inflammation responses of pulmonary tissue were examined. Results showed that PM2.5 exposure induced lung injury as manifested by decreased pulmonary function, abnormal histopathological changes, and increased pro-inflammatory cytokine levels (tumor necrosis factor-α and Interleukin-1α). Aerobic exercise alleviated the airway obstruction, reduced respiratory muscle strength, bronchial mucosal exfoliation, ultrastructure damage, and inflammatory responses induced by PM2.5 in exercise-related groups. The benefits of exercise were related with the downregulation of p38-mitogen-activated protein kinase (MAPK), and the subsequent inhibition of the pathways of the cyclooxygenase 2 (COX-2) product, prostaglandin E2 (PGE2). Thus, pre-exercise training may be an effective way to protect against PM2.5-induced lung inflammatory injury in rats.

EFFECT OF SPORTS MEDICINE ON REDUCING BODY FAT PERCENTAGE AND LEAN BODY MASS

ABSTRACT Introduction: Aerobic exercise has begun to be widely recognized as a reasonable means of preventing fat and losing weight. Scholars have confirmed that sports can help the human body lose weight and lose fat. Objective: This article measures the exercise performance indicators of subjects in different body fat percentage groups and studies the relationship between body fat percentage and exercise performance indicators. Methods: The study uses experimental methods to determine the percentage of body fat of the subjects. After physical exercise and aerobic exercise, the volunteers were tested for aerobic capacity indicators. Results: The body fat percentage of physically inactive persons was negatively correlated with aerobic and anaerobic exercise capacity indexes. Conclusion: The mechanism of aerobic exercise in weight loss treatment has the effect of promoting lipolysis and regulating blood lipid metabolism. At the same time, it has a significant influence on the number and activity of fat cells. Level of evidence II; Therapeutic studies - investigation of treatment results.

Effect and Mechanism of Aerobic Exercise on Prevention and Control of Adult Obesity in Young Rats

Effect and Mechanism of Aerobic Exercise on Prevention and Control of Adult Obesity in Young Rats

Improvement of hyperlipidemia by aerobic exercise in mice through a regulatory effect of miR-21a-5p on its target genes

Hyperlipidemia is a risk factor for cardiovascular disease, and miR-21a-5p plays an important role in the occurrence and progression of hyperlipidemia. Here, we aimed to investigate the mechanism of aerobic exercise improved hyperlipidemia through enhancing miR-21a-5p expression. In this study, high-fat/high-cholesterol diet mice received 8 weeks of aerobic exercise intervention, then we collected plasma and liver samples, we found that there had a notable improvement in weight gain, blood lipid level, and liver steatosis in hyperlipidemia mice after 8 weeks of aerobic exercise intervention. Besides, aerobic exercise significantly up-regulated the expression of miR-21a-5p and provoked favorable changes in the expression of target genes. Knockdown of miR-21a-5p resulted in dysregulation of lipid metabolism and increased expression of FABP7, HMGCR, ACAT1, and OLR1. While aerobic exercise could alleviate miR-21a-5p knock-down induced lipid metabolism disorder. Taken together, these results demonstrated that aerobic exercise improved hyperlipidemia through miR-21a-5p-induced inhibition of target genes FABP7, HMGCR, ACAT1, and OLR1.

Prospects of physical prehabilitation for prevention of postoperative cognitive dysfunction in patients undergoing coronary artery bypass grafting

The review encompasses the latest literature on the prevention of postoperative cognitive dysfunction after coronary artery bypass grafting. We performed an attempt to provide all existing data on the prospects of using physical prehabilitation, particularly aerobic exercise, for prevention of cerebrovascular complications during coronary artery bypass grafting. The article summarizes recent studies on the effects of exercise trainings on wellbeing and cognitive functions. Particular attention has been paid to the review of the studies stating the presence of cerebroprotective effects and mechanisms of aerobic exercise on cognitive function. The prospects of aerobic prehabilitation before coronary artery bypass grafting for prevention of postoperative cognitive dysfunction are discussed.

OR-035 Effect of Aerobic Training on the Exercise Capacity of Apelin Knock-out Mice

Objective Aerobic training is considered to be an effective way to enhance the body’s exercise capacity which is closely related to the improvement of skeletal muscle energy metabolism. And as a new myokine, apelin has been found to play a key role in regulating the energy metabolism of skeletal muscle. However, whether the loss of apelin gene affects exercise capacity and what role aerobic training play in it remains unknown. This study was designed to investigate the effect of apelin on exercise capacity during aerobic training and to provide a theoretical basis for the mechanism of aerobic exercise affecting exercise capacity.
 Methods Male C57BL/6J wild type mouse(n=20) and apelin knock-out mouse(n=20) were assigned by random allocation to four groups(n=10): wild type control(WC), wild type exercised(WE), apelin knock-out control(KC) and apelin knock-out exercised(KE). Exercise training consisted of treadmill running 60 minutes/day ×6 days/week for 4 weeks. The training intensity corresponded to the 70-75% maximum oxygen uptake of mice. The running speed was 15m/min with an incline of +5° in the first 2 weeks and subsequently adjusted to 20m/min according to the maximum oxygen uptake in the last 2 weeks. On the day after training, all groups were forced to perform a incremental exercise test to exhaustion. This test was started with an incline of +5°and a speed of 10 m/min for 5 min. After this initial phase, the speed was progressively increased by 3m/min every 3 min until animal exhausted. The maximum running speed, movement time and distance were recorded during the test.
 Results Compared with group WC, the maximum running speed, movement time and distance of group KC were significantly decreased(P<0.01). And the maximum running speed, movement time and distance of group KE were clearly higher than those of group KC(P<0.01). There is no significant difference between group WE and group WC, and between group KE and group WE.
 Conclusions The exercise capacity of mice was significantly decreased because of knocking out the apelin gene, and the exercise ability of apelin knock-out mice can be clearly enhanced by aerobic training.

PO-023 The Effects of Aerobic Exercise on Alternative Splicing of PKC δI pre-mRNA

Objective Alternative splicing of genes is the main way to produce large numbers of proteins, but the mechanism is unclear. The aim of this study was to evaluated the effect of aerobic exercise on PKC δI pre-mRNA alternative splicing. Further, to explore the effect of aerobic exercise on SFRS10 concentration. Because the PKCδ1 is involved in the regulation of adipocyte differentiation and splice factor SFRS10 regulates alternative of PKCδ1, explore the mechanism of PKCδ1 alternative splicing, understand the role of the alternative splicing variants, to provide the theory basis for the mechanism of aerobic exercise reduce the incidence of obesity.
 Methods C57BL/6 male mice were randomly divided into normal quiet group, normal exercise group, obese and quiet group, and obese exercise group. The exercise group performed aerobic exercise for 8 weeks. The intensity of aerobic exercise was: running platform slope is 0, speed 10 m/min, 1 h/time, 1 time/day, 6 times/week for a total of 8 weeks. Immediately after exercise, the cDNA was extracted from liver and adipose tissue. The contents of PKCδ1 and SFRS10 in liver and adipose tissue were determined by PCR and RT-PCR. Liver and fat were stained by oil red O staining to observe lipid droplet changes. And the mouse's Lee's index and blood lipids were determined.
 Results Lee's index = 3√ (body weight * 1000) / body length, Lee's index of obese mice decreased significantly after aerobic exercise, in addition, after aerobic exercise, total cholesterol (TC), triglyceride (TG) and low density Lipoprotein cholesterol (LDL-C) also showed a downward trend (P < 0.05), while high-density lipoprotein cholesterol (HDL-C) increased (P < 0.05); oil red O staining results showed lipid droplets become smaller after aerobic exercise. The results of PCR and RT-PCR showed in the obese and quiet group than in the normal quiet group, the content of PKCδ1-FL decreased, the content of PKCδ1-△Exon9 increased, and the content of SFRS10 decreased. In the normal exercise group than in the normal quiet group and in the obese exercise group than in the obese and quiet group, the PKCδ1-FL content increased, the PKCδ1-△Exon9 content decreased, and the SFRS10 content increased.
 Conclusions Aerobic exercise can significantly increase the content of PKCδ1-FL and SFRS10. PKCδ1-FL inhibits the formation of adipocytes, SFRS10 promotes the inclusion of PKCδ1 exon 9, and there is a molecular mechanism of alternative splicing between PKCδ1 and SFRS10.

Efficacy and Mechanisms of Aerobic Exercise on Cancer Initiation, Progression, and Metastasis: A Critical Systematic Review of In Vivo Preclinical Data.

A major objective of the emerging field of exercise-oncology research is to determine the efficacy of, and biological mechanisms by which, aerobic exercise affects cancer incidence, progression, and/or metastasis. There is a strong inverse association between self-reported exercise and the primary incidence of several forms of cancer; similarly, emerging data suggest that exercise exposure after a cancer diagnosis may improve outcomes for early-stage breast, colorectal, or prostate cancer. Arguably, critical next steps in the development of exercise as a candidate treatment in cancer control require preclinical studies to validate the biological efficacy of exercise, identify the optimal "dose", and pinpoint mechanisms of action. To evaluate the current evidence base, we conducted a critical systematic review of in vivo studies investigating the effects of exercise in cancer prevention and progression. Studies were evaluated on the basis of tumor outcomes (e.g., incidence, growth, latency, metastasis), dose-response, and mechanisms of action, when available. A total of 53 studies were identified and evaluated on tumor incidence (n = 24), tumor growth (n = 33), or metastasis (n = 10). We report that the current evidence base is plagued by considerable methodologic heterogeneity in all aspects of study design, endpoints, and efficacy. Such heterogeneity precludes meaningful comparisons and conclusions at present. To this end, we provide a framework of methodologic and data reporting standards to strengthen the field to guide the conduct of high-quality studies required to inform translational, mechanism-driven clinical trials. Cancer Res; 76(14); 4032-50. ©2016 AACR.

The influence of aerobic exercise on the level of advanced glyclation end products in plasma in type 2 diabetic rats

Objective To determine the influence of aerobic exercise on advanced glycation end products (AGEs)in plasma using a rat model of type 2 diabetes,and to provide an experimental basis for explaining the rehabilitative mechanism of aerobic exercise in type 2 diabetes.Methods Fifty-two healthy 8-week-old male SpragueDawley rats were allocated at random into a normal control group(n=10)and a type 2 diabetes model group(n=42).The latter were overfed with a high-sugar,high-fat and high-energy diet for 4 weeks,then 30ms/kg of streptozotocin was injected intraperitoneally to create a model of type 2 diabetes.Thirty diabetic rats were then allocated at random into a diabetes control group,a low intensity exercise group and a moderate intensity exercise group with 10 in each group.The treadmill exercise was administered to the animals in the low and moderate exercise groups accordingly.Results Compared with the normal control group,plasma AGEs increased significantly in the diabetes control and moderate intensity exercise groups.Compared with the diabetes control group,AGEs in the lower intensity exercise group were significantly lower.Compared with the moderate intensity exercise group,plasma AGEs in the low intensity exercise group were somewhat lower,but not significantly.Conclusion Aerobic exercise can reduce plasma AGE levels in rats with a model of type 2 diabetes.The effect is probably related to decreasing excessive blood glncose and the exercise intensity. Key words: Aerobic exercise; Advanced glycation end products; Type 2 diabetes