Omega-3 Fatty Acid Supplementation on Post-Exercise Inflammation, Muscle Damage, Oxidative Response, and Sports Performance in Physically Healthy Adults-A Systematic Review of Randomized Controlled Trials.

Omega-3 is a family of n-3 polyunsaturated fatty acids (PUFAs), which have been used to treat a wide variety of chronic diseases, due mainly to their antioxidant and anti-inflammatory properties, among others. In this context, omega-3 could be post-exercise recovery agent and sports supplement that could improve performance by preserving and promoting skeletal muscle mass and strength. No conclusive evidence, however, exists about the potential effects of omega-3 on post-exercise biomarkers and sports performance in physically healthy adults. Based on the PRISMA in Exercise, Rehabilitation, Sports Medicine, and Sports Science (PERSiST) guidelines, we systematically reviewed studies indexed in Web of Science, Scopus, and Medline to assess the effects of omega-3 on post-exercise inflammation, muscle damage, oxidant response, and sports performance in physically healthy adults. The search was performed on original articles published in the last 10 years up to 5 May 2024, with a controlled trial design in which omega-3 supplementation was compared with a control group. Among 14,971 records identified in the search, 13 studies met the selection criteria. The duration of the interventions ranged from 1 day to 26 weeks of supplementation and the doses used were heterogeneous. Creatine kinase (CK) and lactate dehydrogenase (LDH) were significantly higher (p < 0.05) in the control group in 3 of the 4 studies where these markers were analyzed. C-reactive protein (CRP) was significantly higher (p < 0.05) in the control group of 2 of the 13 studies where this marker was analyzed. The delayed onset muscle soreness (DOMS) gave mixed results. Interleukin 6 (IL-6) showed improvements with supplementation, but tumor necrosis factor-α (TNF-α) displayed no differences. The consumption of n-3 PUFAs improved some indicators of oxidative stress such as reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio. Additional evidence is needed to establish clear recommendations regarding the dose and length of n-3 PUFA supplements. These may benefit the post-exercise inflammatory response, mitigate muscle damage, and decrease oxidative stress caused by exercise. However, studies did not evaluate omega-3 status at baseline or following supplementation and therefore the observations must be treated with caution.

Voluntary wheel running from early adolescence reduces disease progression, and anxiety- and depression-related symptoms in an adult male mouse model of rheumatoid arthritis.

Rheumatoid arthritis (RA) is a multifactorial autoimmune disease that progressively destroys synovial joints and leads to chronic systemic inflammation. This autoimmune disorder is associated with increased anxiety- and depression-related symptoms, which reduces quality of life. Clinical and experimental evidence suggests that higher physical activity from early adolescence may prevent chronic diseases and reduce the risk of mental health problems in adulthood. This study aimed to assess whether voluntary wheel running from early adolescence can decrease clinical symptoms, anxiety- and depression-related behaviors in adult mice with rheumatoid arthritis. Adolescent male mice were exposed to voluntary wheel running until adulthood and got collagen-induced arthritis. We measured body weight, the thickness of the hind paw and knee joint (clinical signs), anxiety- and depression-related behaviors, serum testosterone, and cytokines (IFN-γ IL-1ß, IL-6, TNF-α, IL-10). The findings showed that collagen-induced arthritis resulted in anxious-like behavior, increased anhedonia, elevated IL-6, IL-1ß, TNF-α, and IFN-γ, and decreased testosterone levels in the serum of mice. However, no change was observed in behavioral despair. We found that higher physical activity from early adolescence significantly reduced the severity of clinical signs, anxiety- and anhedonia-like behaviors, and decreased behavioral despair in RA-induced mice. In addition, the running wheel exposure normalized RA-induced abnormalities in testosterone and inflammatory cytokines in mice. Altogether, this study suggests that higher physical activity from early adolescence may make mice less vulnerable or resistant to RA-induced clinical symptoms and anxiety- and depression-related behaviors by changing testosterone and inflammatory cytokines productions in adulthood.

Aerobic exercise training reduces deep-frying oil-induced apoptosis of hippocampal tissue by reducing oxidative stress in male rats.

Deep-frying oil (DFO) contains high amounts of free radicals, and consuming foods prepared with this method causes damage to nervous tissue due to oxidative stress (OS). Since moderate-intensity aerobic exercise training (AT) reduces OS, the current search investigated the effects of AT on OS, apoptosis, and neurogenesis markers in the hippocampal tissue of DFO-fed rats. Eighteen Wistar male rats (200-280 gr) were randomly allocated to a control group fed with normal food (Con-ND), a control group receiving DFO (Con-DFO), and a group receiving DFO-aerobic exercise (EX-DFO) (n = 6 in each). DFO was gavaged for four weeks, five days a week, with a dose of 2 ml. AT included running on a treadmill for four weeks and five sessions per week (40 min per session). The expression of genes B-cell lymphoma 2 (BCL-2), Protein X associated with Bcl-2 (BAX), Caspase-3 (Casp-3), and Caspase-9 (Casp-9) was measured by PCR method. The ELISA method was used to calculate levels of Superoxide dismutase (SOD) and Catalase (CAT) activity, malondialdehyde (MDA), and Brain-Derived Neurotrophic Factor (BDNF). Also, the expression of the proteins Cannabinoid receptor type 1(CB1), Cannabinoid receptor type2 (CB2), Glial fibrillary acidic protein (GFAP), Neuronal nuclei (NeuN), and DNA fragmentation was evaluated by Immunohistochemical and TUNEL staining. DFO feeding led to a significant increase in apoptotic markers, such as BAX, Casp-3, and Casp-9 gene expression, and DNA fragmentation (p ≤ 0.05) while decreasing BDNF concentration SOD activity (p ≤ 0.05). AT significantly reduced the BAX, Casp-3, Casp-9, MDA, CB1, GFAP, and DNA fragmentation (p ≤ 0.05). In conclusion, AT can reduce the harmful effects of feeding with DFO on the hippocampal tissue.

Physical activity in a swimming pool attenuates memory impairment by reducing glutamate and inflammatory cytokines and increasing BDNF in the brain of mice with type 2 diabetes.

Type 2 diabetes is a risk factor for the development of cognitive impairment. Increasing evidence suggests that regular exercise is beneficial for the treatment of clinical symptoms in diabetic patients. The current study aimed to evaluate whether increasing physical activity through swimming training can reduce memory impairment in an animal model of type 2 diabetes. Diabetes and non-diabetes mice underwent swimming training for four weeks, and then working, spatial, and recognition memory were evaluated using three behavioral tests. Body weight, glucose, and insulin resistance were monitored. We also measured inflammatory cytokines (interleukin (IL)- 6, IL-1ß, and tumor-necrosis-factor (TNF)-α), an anti-inflammatory cytokine (IL-10), and brain-derived-neurotrophic-factor (BDNF), and glutamate levels in the hippocampus or prefrontal cortex of mice. The findings showed that diabetes increased body weight, glucose, and insulin resistance, impaired working, spatial and recognition memory, increased levels of IL-6, IL-1ß, TNF-α, and glutamate levels, and decreased BDNF in the hippocampus of diabetic mice. While higher physical activity was associated with reduced body weight, glucose, and insulin resistance, attenuated memory impairment, IL-6, IL-1ß, TNF-α, and glutamate, and increased BDNF levels in the hippocampus and prefrontal cortex of diabetic mice. This study shows that swimming training can normalize body weight and glucose-insulin axis and reduce inflammation and glutamate in the hippocampus and enhance the neurotrophic system in both the hippocampus and prefrontal cortex of diabetic mice. This study also suggests that higher physical activity through swimming training can improve cognitive impairment in a mouse model of type 2 diabetes.

Diazepam and exercise training combination synergistically reduces lipopolysaccharide-induced anxiety-like behavior and oxidative stress in the prefrontal cortex of mice.

Anxiety-related disorders are among the most important risks for global health, especially in recent years due to the COVID-19 pandemic. Benzodiazepines like diazepam are generally used to treat anxiety disorders, but the overall outcome is not always satisfactory. This is why psychiatrists encourage patients with anxiety to change their lifestyle habits to decrease the risk of anxiety recurrence. However, the effect of diazepam and exercise in combination is unknown. This study aimed to investigate the effect of diazepam alone or in combination with swimming exercise on lipopolysaccharide (LPS)-induced anxiety-like behavior and oxidative stress in the hippocampus and prefrontal cortex of mice. Mice were exposed to diazepam and swimming exercise alone or in combination with each other and then received LPS. We assessed anxiety-like behavior using open field and light-dark box and measured oxidative markers including glutathione (GSH), malondialdehyde (MDA), and glutathione disulfide (GSSG) in the hippocampus and prefrontal cortex. The findings showed that LPS increased anxiety-related symptoms and oxidative stress by decreasing GSH and increasing MDA and GSSG levels in the prefrontal cortex but not in the hippocampus. Although diazepam alone did not reduce anxiety-like behavior and oxidative stress, it in combination with exercise significantly decreased anxiety-like behavior and oxidative stress in the prefrontal cortex of LPS-treated mice. This drug and exercise combination also displayed a more effective effect in comparison with exercise alone. Overall, this study suggests that diazepam in combination with swimming exercise has higher efficacy on anxiety-like behavior and oxidative stress than when they are used alone.

Effect of resistance training with and without vitamin D calcium chitosan nanoparticle supplements on apoptosis markers in ovariectomized rats: An experimental study.

Background: Hormone therapy is one of the most effective treatments for menopausal disorders, but it may increase the risk of breast cancer, coronary heart disease, and pulmonary embolism. Objective: The present study investigated the effect of resistance training with and without vitamin D calcium(Ca + + ) chitosan nanoparticles on apoptosis markers in ovariectomized rats. Materials and Methods: 42 female Wistar rats were divided into 7 groups (n = 6/each). One group was assigned as the healthy controls to show the induction of menopause. The other 6 groups comprised ovariectomized (OVX) animals including: 1) vitamin D + calcium + chitosan + resistance training, 2) saline + estrogen + resistance training, 3) saline + resistance training, 4) vitamin D + calcium + chitosan, 5) saline + estrogen, and 6) OVX + control. 48 hr after the last intervention, the hippocampus tissue was extracted to measure the BCL-2-associated X (BAX), B-cell lymphoma 2 (BCL-2), and caspase-3 gene expression as well as the percentage of dead cells. Results: OVX rats demonstrated increased BAX gene expression, ratio of BAX gene expression to BCL-2, caspase-3 gene expression, and percentage of dead cells of hippocampal tissue, but decreased BCL-2 gene expression. Resistance training and vitamin D Ca + + chitosan nanoparticle supplements seemed to reverse these changes. Conclusion: The combination of resistance training and vitamin D Ca + + chitosan nanoparticle supplements may be considered a non-pharmacological treatment for OVX-induced apoptosis.

The effects of aerobic exercise training with octopamine supplementation on cardiomyocyte apoptosis induced by deep-frying oil: The role of caspase and procaspase 3.

BACKGROUND AND AIM: Clinicians who understand how the body responds to exercise, how aerobic training enhances cardiovascular fitness and the benefits and essentials of prescribing aerobic exercise can effectively encourage patients to be active. Deep-frying is a standard cooking method accompanied by the production of carcinogenesis substances such as acrolein. Acrolein is a toxic byproduct of lipid peroxidation involved in the development of pulmonary, cardiac, and neurodegenerative diseases. This study aimed to explore the effect of aerobic exercise (E.X.E.), and octopamine (OCT) on caspase three expression levels in the heart tissue of rats were fed deep-frying oil (D.F.O.). METHODS: 30 male Wistar rats were divided into 5 groups (n = 6 in each) including (1) control (CO), (2) deep-frying oil (DFO), (3) deep-frying oil + exercise (DFO + EXE), (4) deep-frying oil + octopamine (DFO + OCT), and (5) deep-frying oil + exercise + octopamine (DFO + EXE + OCT). The apoptotic effects of D.F.O. in heart tissue were examined by TUNEL assay. Masson's trichrome stain was used to study cardiomyocytic fibers. Moreover, caspase three gene expression in all groups was evaluated using quantitative real-time PCR and the Western blot method. RESULTS: Data showed a significant increase in apoptotic cells in the D.F.O. group (P < 0.05). In Masson's Trichrome stain analysis, more cardiomyocytic fibers degradation and lymphocytic aggregation cells in the DFO + EXE + OCT group significantly improve this degradation. Also, the expression level of caspase 3 was significantly decreased in the DFO + EXE + OCT group (P < 0.05). CONCLUSION: According to the result of the current study, it can be assumed that D.F.O. can lead to programmed cell death via the activation of caspases in heart tissue. However, it seems that aerobic exercise with octopamine supplementation improves heart tissue function by inhibiting the expression of caspase 3 and pro-caspase 3, leading to a significantly decreased apoptosis in cardiomyocytes of DFO-treated models.

Elastic resistance training is more effective than vitamin D3 supplementation in reducing oxidative stress and strengthen antioxidant enzymes in healthy men.

OBJECTIVE: Today, reducing oxidative stress and improving the antioxidant system with antioxidant supplements along with exercise training has received a lot of attention. Vitamin D plays a very important role in general health and reducing oxidative stress. The aim of this study was to examine the effect of vitamin D3 supplements during elastic-band resistance training (EBT) on oxidative stress and antioxidant indices in healthy men. METHODS: Forty healthy men (Serum: 20 ≤ 25 (OH) D ≤ 25 ng/mL) voluntarily participated in the current study and randomly were assigned to EBT-vitamin D3 (ED, n = 10), EBT-placebo (EP, n = 10), vitamin D3 (VD, n = 10), and control (Con, n = 10). EBT was performed three times per week on non-consecutive days for eight weeks, in seven exercises. The subjects in the ED, VD, and EP consumed 50,000 IU vitamin D3 or placebo once every 2 weeks. Ten ccs blood samples were collected before and after exercise training and the total antioxidant capacity (TAC), superoxide dismutase (SOD), glutathione peroxidase (GPX), and creatine kinase (CK) activities were measured in the plasma. Malondialdehyde (MDA), as the lipid peroxidation index, and 25(OH) D were measured in the plasma. RESULTS: We found that there was a significant difference between ED with VD (p = 0.011) and Con (p = 0.022) for MDA. A significant difference was also seen for SOD in ED with VD (p = 0.024) and Con (p = 0.038) and TAC in ED with VD (p = 0.020) and Con (p = 0.030), and GPX in ED with VD (p = 0.040) and Con (p = 0.010). While there were no significant differences between ED and EP in all mentioned variables (p > 0.05). CONCLUSION: Finally, it can be said that elastic resistance training improved antioxidant defence. However, vitamin D3 supplementation during resistance elastic training has no synergistic effect on attenuating oxidative stress indices.

Swimming exercise decreases depression-like behaviour and inflammatory cytokines in a mouse model of type 2 diabetes.

NEW FINDINGS: What is the central question of this study? Can swimming exercise decrease depression-like behaviour and inflammation in type 2 diabetic mice? What is the main finding and its importance? Swimming exercise decreased depression-like behaviour by reducing inflammation in type 2 diabetic mice. Swimming exercise might be useful for the treatment of depression-related disorders in patients with type 2 diabetes. ABSTRACT: Clinical and experimental studies have shown that type 2 diabetes is associated with depression-related disorders. Inflammation has been identified as a common mechanism in both type 2 diabetes and depression. Several studies have suggested that swimming exercise might be able to reduce depression-related symptoms. The present study aimed to explore whether swimming exercise can decrease depression-like behaviour in type 2 diabetic mice. To induce type 2 diabetes, male C57BL6 mice were treated with a high-fat diet and streptozocin. Type 2 diabetic animals were subjected to swimming exercise for 4 weeks. Then, depression-like behaviours were evaluated by sucrose preference, novelty-suppressed feeding, social interaction and tail suspension tests. We also measured levels of glucose, insulin and pro-inflammatory cytokines such as interleukin-1ß and tumour necrosis factor-α in the serum of animals. The results indicated that type 2 diabetes significantly increased anhedonia- and depression-like behaviours in mice. We also found significant increases in glucose, insulin and inflammatory cytokines in diabetic mice. Moreover, swimming exercise reduced anhedonia- and depression-like behaviour in type 2 diabetic mice. Swimming exercise also decreased glucose and inflammatory cytokines in the serum of mice with type 2 diabetes. Collectively, this study demonstrates that swimming exercise decreased depression-like behaviour by reducing inflammation in type 2 diabetic mice. Further clinical studies are needed to validate these findings in patients with type 2 diabetes.

Swimming exercise attenuates anxiety-like behavior by reducing brain oxidative stress in type 2 diabetic mice.

Anxiety-related behaviors are among the most prevalent psychiatric disorders in patients with type 2 diabetes (T2D). The protective effect of exercise on neuropsychiatric disorders has been documented. However, there are no studies that examined whether swimming exercise can decrease anxiety-like symptoms in type 2 diabetes. We investigated the effects of swimming exercise on body weight, anxiety-like behavior, glucose and insulin levels, and brain oxidative stress in male C57BL/6 mice. T2D-induced mice were subjected to swimming exercise, then anxiety-like behaviors were measured by the open field, light-dark box, and elevated plus-maze tests. Glucose and insulin levels were measure in serum, and antioxidant/oxidative markers including glutathione (GSH), malondialdehyde (MDA), and glutathione disulfide (GSSG) were measured in the brain. Our findings showed that T2D increased body weight, anxiety-like symptoms, glucose and insulin resistance, and oxidative stress by increasing MDA and GSSG levels in the brain of mice. Interestingly, swimming exercise reversed these parameters in diabetic mice. Our findings clearly indicate that there is a protective impact of swimming exercise on anxiety-like behavior by reducing insulin resistance and brain oxidative stress in mice with type 2 diabetes. Further studies are needed to validate these findings in humans.

Combination effect of exercise training and eugenol supplementation on the hippocampus apoptosis induced by chlorpyrifos.

The aim of this study was to investigate the combination effect of exercise training and eugenol supplementation on the hippocampus apoptosis induced by CPF. 64 adult male albino rats were randomly selected and devided into eight groups of eight including: control, exercise (EXE), chlorpyrifos (CPF), Control + Oil (Co + Oil), Control + DMSO (Co + DMSO), chlorpyrifos + eugenol (CPF + Sup), chlorpyrifos + exercise (CPF + Exe) and, chlorpyrifos + exercise + eugenol (CPF + Exe + Eu). Four experimental groups received intraperitoneal injection (5 days a week) of 3.0 mg/kg body weight CPF in DMSO for 6 consecutive weeks. The exercise groups performed aerobic 5 days per week over 4 weeks. Eugenol were administered by gavage. Finally, the animals were sacrificed using CO2 gas (a half of the rats were anesthetized with ketamine and xylazine and then perfused) to evaluate hippocampus histology and parameters. The results of this study showed that CPF injection significantly decreased BDNF, AChE and ATP in CA1 area of the hippocampus (p ˂ 0.05). Also, CA1 apoptosis by tunnel assay, it was found that CPF receiving groups with different dosage, showed a significant increase compared to other groups, which was confirmed by increasing cytochrome C and procaspase-3 in CPF groups (p ˂ 0.05). The result of this study show that 4 weeks of exercise training and eugenol supplementation does not improve the destructive effects of CPF in CA1 area of the hippocampus. As a result, it is recommended that future studies longer periods for treatment with exercise and eugenol supplementation.

Long-term exercise from adolescence to adulthood reduces anxiety- and depression-like behaviors following maternal immune activation in offspring.

Maternal immune activation is an environmental risk factor for the development of neuropsychiatric disorders such as anxiety and depression later in life. There is an urgent need to develop therapeutic strategies for treating or preventing psychiatric disorders with developmental origins. There is important information that physical exercise is a therapeutic strategy for treating anxiety and depression-related disorders. This study set out to determine the long-term effects of exercise on anxiety and depression-like behaviors following maternal immune activation in adult offspring. Pregnant mice were treated with lipopolysaccharides (LPS) or vehicle. Then offspring were subjected to a combination of different exercise protocols including voluntary running wheel, swimming, and treadmill exercises from adolescence to adulthood. Anxiety and depression-related symptoms in adult offspring were evaluated using open field, elevated plus maze, sucrose preference test, and forced swim test. The hypothalamic-pituitary-adrenal (HPA) axis reactivity was assessed by measuring corticosterone in serum. We also measured oxytocin, malondialdehyde, tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, and IL-10 in the brain of adult offspring. Our findings indicated that long-term exercise significantly decreased anxiety- and depression-like behaviors in offspring prenatally exposed to maternal immune activation. The exercise also decreased corticosterone levels in the serum, and increased oxytocin and IL-10 levels in the brain of these offspring; whereas no significant alterations in TNF-α, IL-1ß, IL-6 were found. Taken together, this study suggests that exercise might be a therapeutic strategy for the treatment of anxiety and depression-related behaviors following maternal immune activation in offspring.

Combined therapies with exercise, ozone and mesenchymal stem cells improve the expression of HIF1 and SOX9 in the cartilage tissue of rats with knee osteoarthritis.

PURPOSE: Knee osteoarthritis (OA) is a common type of degenerative joint disease which decreases the quality of life. Sex-determining region Y box 9 (SOX9) and hypoxia-inducible factor-1 (HIF1) are considered as the key regulators of OA. We investigated the effect of combined therapies with mesenchymal stem cells (MSCs), ozone (O3) and exercise training on SOX9 and HIF1 expression in the cartilage of rats with knee OA. METHODS: Knee OA was induced by surgical method. OA rats were divided into model, MSCs, ozone, exercise, MSCs + ozone, MSCs + exercise, ozone + exercise and MSCs + ozone + exercise groups. Rats in the MSCs group received intraarticular injection of 1 × 106 cells/kg. Rats in the ozone group received O3 at the concentration of 20 µg/mL, once weekly for 3 weeks. Rats in the exercise group were trained on rodent treadmill three times per week. 48 hours after the programs, cartilage tissues were isolated and the expression of SOX9 and HIF1 was determined using Real-Time PCR. RESULTS: Significant differences were found in the expression of SOX9 and HIF1 between groups (P < 0.0001). Although combined therapies with exercise, MSCs and O3 significantly increased the expression of SOX9 and HIF1 in the cartilage tissue of rats with knee OA, combination of exercise with O3 was significantly more effective compared to the other combined therapies (P < 0.001). CONCLUSIONS: Combined therapy with exercise, MSCs and O3 significantly increased the expression of SOX9 and HIF1 genes in the cartilage of rats with knee OA; however, exercise + O3 was significantly more effective.

The Therapeutic Effect of Exercise on Anxiety and Bowel Oxidative Stress in the Maternal Separation Animal Model.

INTRODUCTION: According to evidence, Early-Life Stress (ELS), mood disorders, and medical comorbidities, i.e. Irritable Bowel Syndrome (IBS), are correlated; however, the direct contribution of ELS to IBS manifestations is less understood. The current study aimed at evaluating the effect of voluntary exercise on the mitochondrial dysfunction of the bowel fibroblasts, following the confirmation of anxiety behavior. METHODS: In this study, Postnatal Day (PND) rats underwent Maternal Separation (MS), as a valid animal model of the brain-gut axis dysfunction, in the days 2-14; three hours daily. On day 21, the study animals were divided into 4 groups, as follows: control, Running Wheel (RW) exercise, MS, and MS+RW groups. The study groups were housed in separate cages (4 rats per cage) until the onset of intervention. On day 60, the elevated plusmaze was used to assess anxiety-like behaviors; the level of oxidative stress biomarkers, i.e. Reactive Oxygen Species (ROS), Glutathione (GSH), as well as Adenosine Triphosphate (ATP) was measured to determine the gut mitochondrial function. RESULTS: Findings revealed that ELS affected the gut energy metabolism in the studied rats; the negative effects of MS on anxiety and the gut mitochondrial dysfunction decreased via RW exercise during adolescence. CONCLUSION: Overall, anxiety behaviors and ROS production, leading to increased GSH and ATP levels, improved after RW exercise; this significantly impacts the function of colon secretory mitochondria. According to the positive effects of RW exercise on mitochondrial dysfunction in an ELS animal model, a potential relationship was found between the brain and gut in the study rats.

Synergic effects of exercise training and octopamine on peroxisome proliferator-activated receptor-gamma coactivator -1a and uncoupling protein 1 mRNA in heart tissue of rat treated with deep frying oil.

Octopamine (OCT) have an adverse effect on heart function. One of the positive effects of exercise training is improving cardiac function and cardiomyocytes signaling, which along with herbal supplements can have better effects on the heart tissue. Therefore, the aim of this study was to evaluate the effects of exercise training and OCT on changes of PGC1α and UCP1 expression in heart tissue of rat treated with deep frying oil (DFO). In this study, 45 male wistar rats were divided into 5 groups (n = 9 in each): I) control (Co), II) DFO, III) DFO + exercise, IV) DFO + OCT, and V) DFO + OCT + exercise. The quantification of apoptotic effects of DFO in heart tissue was assessed by TUNEL assay. Masson's trichrome stain applied to study cardiomyocytic fibers. Moreover, PGC1α and UCP1 genes and proteins expression in all groups were investigated using quantitative real-time PCR and immunohistochemical method. A significant increase in apoptotic cells was observed in the DFO-treated group (p < 0.05). In Masson's Trichrome stain study, more cardiomyocytic fibers were observed and some lymphocytic cells were present in some fibers. Also, the expression of PGC1α and UCP1 was significantly increase in DFO + exercise group, DFO + OCT group, and DFO + OCT + exercise group compare to DFO group (p < 0.05). Based on these findings, exercise and octopamine can be considered as factors affecting the expression of PGC1α genes and UCP1 as well as drug poisoning.

Role or Synergistic Interaction of Adenosine and Vitamin D3 Alongside High-Intensity Interval Training and Isocaloric Moderate Intensity Training on Metabolic Parameters: Protocol for an Experimental Study.

BACKGROUND: Obesity is known as one of the major causes of epidemiologic diseases worldwide; therefore, the introduction of treatment strategies by medical professionals, such as the use of various medicines and exercise programs to reduce fat or prevent obesity, is on the rise. Recently, researchers have shown special interest in assessing the effect of lipolytic adenosine and vitamin D deficiency, as well as the effect of exercise, on decreasing body fat percentage. OBJECTIVE: This study has been designed to examine the effect of adenosine and vitamin D3 injections, in conjunction with high-intensity interval training and isocaloric moderate-intensity training, on the metabolic parameters of obesity induced by a high-fat diet. METHODS: This is an experimental study using 92 Wistar rats. At 6 weeks of age, the rats' weights will be recorded, after which they will have 1 week to adapt to their new environment before being divided into 12 groups. The rats will participate in a 2-stage experimental intervention, including a 13-week fattening diet phase followed by a 12-week exercise training phase consisting of an exercise program and the injection of adenosine and vitamin D3. Groups 1 and 2 will have a normal diet, and the other groups will have a diet of 40% fat, with free access to food and water up to the second half of the second stage of the study (end of the sixth week of training). After termination of the interventions, tissue collection and molecular assessments (blood for biochemical, tissues for gene expression analyses, and anthropometrical indexes) will be performed. RESULTS: The project was initiated in April 2017 and completed in December 2017. Data analysis is under way, and the first results are expected to be submitted for publication in November 2018. CONCLUSIONS: We hypothesize that weight loss-induced molecular changes and upregulation will be observed in line with an increase in lipolysis and beta oxidation in muscle and fat tissue as a result of performing isocaloric training in drug-receiving rats and groups on a high-fat diet. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): RR1-10.2196/10753.

Changes in Knee Laxity and Relaxin Receptor Isoforms Expression (RXFP1/RXFP2) in the Knee throughout Estrous Cycle Phases in Rodents.

The changes in knee laxity and relaxin receptor expression at different phases of rodent estrous cycle are not known. Here, changes in the parameter were investigated in rats at different phases of the estrous cycle. Estrous cycle phases of intact female rats were determined by cytological examination of the vaginal smear. Following phase identification, blood was collected for serum hormone analyses. Knee passive range of motion (ROM) was determined by using a digital miniature goniometer. The animals were then sacrificed and patellar tendon, collateral ligaments and hamstring muscles were harvested for relaxin/insulin-like family peptide receptor 1 and 2 (RXFP1/RXFP2) analyses. Knee passive ROM was the highest at proestrus followed by diestrus and the lowest at estrus. Estrogen level was the highest at proestrus while progesterone and relaxin levels were the highest at diestrus. A strong correlation was observed between relaxin and progesterone levels. At proestrus, expression of RXFP1 and RXFP2 proteins and mRNAs were the highest at proestrus followed by diestrus and estrus. The finding shows that higher level of progesterone and relaxin in diestrus might be responsible for higher laxity of knee joint in rats.

Effect of moderate and high resistance training intensity on indices of inflammatory and oxidative stress.

This study was designed to examine the effect of moderate (MR) and high resistance (HR) training on systemic inflammation and circulating enzymatic antioxidant activity. Thirty males were assigned to HR (n = 10), MR (n = 10), or control (C; n = 10) groups. Resistance training was performed for eight weeks. Activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), creatine kinase (CK), and concentrations of malondialdehyde (MDA), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were measured before and after training in plasma. The results show increased SOD activity in MR (p = 0.026) and HR (p = 0.044) groups. GPX activity in HR (p = 0.012) and MR (p = 0.037) increased significantly more than in C. Whilst a significant reduction in MDA in MR (p = 0.013) and HR (p = 0.023) was observed compared with C, no significant difference in IL-6, TNF-α and CK occurred between groups. We conclude that changes in enzymatic antioxidant defense and inflammatory markers following resistance training are independent of training intensity.

Protective effect of Ferula gummosa hydroalcoholic extract against nitric oxide deficiency-induced oxidative stress and inflammation in rats renal tissues.

Nitric oxide (NO) synthase inhibition increases hypertension and causes renal injury. Ferula gummosa is used in Iranian traditional medicine for treatment of several diseases and has been reported to exert a potent anti-inflammatory and antioxidant action. The aim of this investigation was to evaluate the renoprotective effects of hydroalcoholic extract of Ferula gummosa (HEG) on Nω-nitro-L-arginine methyl ester (L-NAME)-induced oxidative stress and inflammation and explore the mechanisms that link NO deficiency with altered renal heat shock protein (HSP70). Rats were injected intraperitoneally with L-NAME (10 mg/kg) to induce renal injury. Simultaneously, HEG (90 mg/kg) was administered by gastric gavage to L-NAME-treated rats for 6 days/week during an 8-week period. Renal thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), HSP70, plasma NO and total antioxidant capacity (TAC) were evaluated. The administration of L-NAME significantly increased renal TBARS, TNF-α, IL-6, HSP70 levels and decreased renal SOD activity, that these changes were accompanied by the reduced plasma NO and TAC levels. HEG administration decreased TBARS, HSP70, TNF-α and IL-6 levels and increased SOD activity in the kidney tissues of L-NAME treated rats (p<0.05). Also, plasma TAC level and NO bioavailability have been elevated after administration of HEG (p<0.05). These findings support that NO deficiency induces renal stress oxidative and inflammation, which markedly increased renal HSP70 and HEG could protect kidney against these damaging effects via its anti-oxidative, anti-inflammatory action and modulate renal HSP70.