reza gharakhanlou

Inflammasome complex causes maturation and expansion of caspase-1activity and pro-inflammatory  cytokines including IL-1β. It is also critical for inducing pyroptotic cell death in response to pathogens and endogenous danger signals. Therefore, the present study was conducted to investigate the effect of high-intensity interval training with high-fat food on the regulation of the inflammasome complex in the adipose tissue of male Wistar rats.

In the present experimental study; 24 male Wistar rats (age: six weeks); were divided into four groups: control (C), exercise (HIIT), high-fat diet (HFD), high-fat diet+exercise (HFD+HIIT). Diet and exercise interventions started at the same time and continued for 10 weeks. Weight, BMI, serum lipid profile, and also the expression of NLRP3 and IL-1β in visceral adipose tissue were measured. To determine changes between groups, one-way ANOVA and Tukey's post hoc test were used, and an independent t-test was used to determine the intensity of the effect size using SPSS27 software (P<0.05).

Significant weight reduction (P=0.009), NLRP3 expression (P=0.001), IL-1β (P=0.001), and LDL and cholesterol levels (P=0.001) in the HFD+HIIT group compared to HFD were seen. Also, a significant increase in HDL and HDL/LDL was observed in the HFD+HIIT group compared to the HFD group (P=0.001).

The exercise training protocol is used in the current study as an effective therapeutic strategy for improving metabolic disorders and inflammatory conditions, which leads to the reduction of inflammation. However, more research is needed to determine other cellular mechanisms of inflammation.

Physical activity is examined in various aspects, such as the structure of the muscular system. This study investigated the impact of a high-intensity interval training (HIIT) program combined with a high-fat diet on the expression of M1 and M2 macrophages in the gastrocnemius muscle of male Wistar rats.

24 healthy adult male Wistar rats with an average weight of 195±15 grams and age of 6 weeks were randomly divided into 4 groups: control, HIIT, high-fat diet, and HIIT with a high-fat diet. Interventions included 10 weeks of HIIT and a high-fat diet. Subsequently, samples were collected from the gastrocnemius muscle. The levels of M1 and M2 macrophages were measured using Real-Time-PCR. Data analysis was performed using one-way analysis of variance at a significance level of P<0.05.

Significant differences were observed between groups in the expression of M1 (P=0.0004) and M2 (P=0.0023) macrophages. M1 macrophage expression was significantly higher in the high-fat diet group compared to the HIIT group (P=0.0001). M1 macrophage expression was significantly lower in the HIIT with a high-fat diet group compared to the high-fat diet group (P=0.0001), but M2 macrophage expression was significantly higher in the HIIT with a high-fat diet group compared to the high-fat diet group (P=0.0003).

These findings suggest that HIIT can reduce M1 macrophage expression and increase M2 macrophage expression, mitigating the negative effects of a high-fat diet.

Fatigue is one of the most common symptoms among individuals with multiple sclerosis (MS). The imbalance of inflammatory cytokines in the brain causes mental fatigue. It is believed that aerobic exercise may moderate the level of inflammation of cytokines and thus reduce mental fatigue. This study was conducted to investigate the effect of swimming aerobic training on pro-inflammatory factors (interleukin 6) and anti-inflammatory factors (interleukin 10) to evaluate mental fatigue in the brains of female mice after EAE induction. In this research, 21 mice (8 weeks old, 18 to 20 grams) were divided into three groups: healthy control, EAE control, and EAE swimming aerobic exercise. The animals in the training group performed moderate-intensity swimming exercises for 4 weeks, with 5 sessions per week, each session lasting 30 minutes. The western blot method was used to analyze the research variables. The results showed no significant difference in the amount of IL-6 between the EAE group and the swimming training group, but the amount of IL-10 in the swimming training group showed a significant increase compared to the EAE group. The ratio of IL-10/IL-6 values between the swimming training group and the EAE group was also not significant. It seems that moderate-intensity swimming aerobic exercises, without changing the pro-inflammatory factor, along with increasing the anti-inflammatory factor IL-10, can lead to an improvement in the balance of the inflammatory index and a reduction in fatigue in the EAE group and the swimming exercise group.

The positive effects of exercise on spatial memory and learning have been demonstrated in research. The olfactory sensory neurons (OSNs) respond to mechanical stimulation induced by nasal airflow which is associated with airflow intensity. Accordingly, nasal breathing can modulate brain oscillations in nonolfactory areas, and respiration-entrained oscillations aid the improvement of cognitive abilities. Given that aerobic exercise increases the rate of respiration and intensity of nasal airflow, this study evaluates the role of OSNs in mediating the effects of aerobic exercise on memory. 

We examined spatial memory following exercise in animal models of olfactory sensory neuron impairment (methimazole injection 300 mg/kg/week).

Destroying OSNs significantly reduces olfactory bulb (OB) activity at delta and theta frequency bands as well as its coupling to respiration. More importantly, it abolished the positive effect of exercise on spatial memory (P<0.05). 

The OB activity is one of the probable mechanisms for improving spatial memory following exercise.

Nasal breathing has many health benefits, especially in exercise. Airflow through the nose stimulates the Olfactory Bulb (OB) during the breathing cycle, associated with the airflow intensity. This information reaches the OB and causes oscillations that transfer to other brain areas. Brain rhythms have been associated with different cognitive states and play functional roles in network computation, such as memory. Accordingly, this study investigates the effect of olfactory sensory neurons (OSNs) in improving working memory following aerobic exercise training in rats.

Methods and Materials: 

In this study, we used sixteen male Wistar rats (12-14 weeks, weighing 250-300 g). After implanting an electrode in the OB and HIP for Local field potentials recording, animals were divided into two exercises and two control groups. At the beginning of each week, one exercise group and one control group, to destroy the OSNs, received 300 mg/kg methimazole. After completing the exercise protocol (7 weeks/ 5 Days/week), we simultaneously recorded LFPs from rat Hip and OB during a Y-maze working memory task. Two-way variance analysis was used for statistical analysis.

Our results showed that destroying olfactory sensory neurons significantly reduces the working memory capacity (P=0.04). On the other hand, the power of the delta and theta frequency bands increased and working memory improved in exercise groups (P=0.01).

We propose that the non-invasive stimulation of OSNs during nasal breathing may be a mechanism for improving working memory through exercise.

To investigate the effect of Non-Local Muscle Fatigue (NLMF) in functional conditions on force and electromyographic activity of knee muscles in professional footballplayers.

Metodology: 

10 healthy male professional footballer players participated in this study voluntarily. After determining dominant leg,1- maximum repetition (1RM) of both legs calculated, then 1RM, the onset of electrical activity of the vastus medialis obliqus /vastus lateralis (VMO / VL) during jumping and the VMO / VL electrical activity, at the moment of contact with the ground on single leg, before and after the fatigue protocol with the dominant leg (3 sets of 3 minutes bend and open the knee with 25% 1RM and immediately after the third set, jump on one foot for 2 minutes with maximum effort) , Were compared in both legs and dependent t test or Wilcoxon were used to examine the changes.

After the fatigue protocol, 1RM of both legs decreased significantly (P = 0.00), while the onset of VMO / VL did not change significantly in both legs (P = 0.26, P = 0.49) and the ratio of VMO / VL electrical activity at the moment of contact with the ground, significantly decreased in the dominant (trained) leg (P = 0.005), but did not change significantly in the opposite leg (p = 0.22).

NLMF in functional conditions reduced 1RM in the nondominant leg while there is no intervention in the ratio of the onset of activity and the electrical activity of the muscles around the knee.

The effect of exercise in reducing fat tissue and fat cell size may be related to TGF-β1 signaling. This study aimed to investigate the effect of high-intensity interval training (HIIT) simultaneously with high-fat diet on TGF-β1 gene expression and cell size in the subcutaneous adipose tissue of rats.

In this study, 24 adult male rats were randomly divided into 4 groups: ND (normal diet), HFD (high fat diet), HIIT+ND and HIIT+HFT. HIIT consisted of eight bouts of intense activity at 90% of maximum running capacity (MRC) for 2.5 minutes, with active rest periods at 50% of maximum running capacity for 2.5 minutes for 10 weeks. 48 hours after the last training session, blood was taken and subcutaneous fat was removed. qRT-PCR method was used to measure TGF-β1 gene expression and the stereological method was used to determine the size of fat cells. Two-way ANOVA test with a significant level of P < 0.05 was used to analyze the data.

The interaction between HIIT and high-fat diet caused a significant decrease in TGF-β1 gene expression (F=24.99, P<0.001), but it had no significant effect on fat cell size (P=0.780, F=0.07). A positive and significant correlation was observed between TGF-β1 gene expression and fat cell size (r=0.896, P<0.001).

HIIT at the same time with consuming a high-fat diet prevents the increase of TGF-β1 in the subcutaneous fat tissue and may have a preventive effect on the increase in fat cell size.

The phenomena of fatigue of voluntary muscular effort is intricate and multidimensional in the field of sports sciences. The causes and effects of exercise-induced fatigue have been extensively studied, but the central nervous system's (CNS) involvement in this process is still unclear. In order to understand CNS fatigue after physical activity, the current review will examine changes in neurotransmitter function during exercise. Using primary sources such scientific journals and websites, a consensus and critical evaluation were carried out in order to accomplish this goal. For a number of neurotransmitters, including dopamine and serotonin (5-HT; 5-hydroxytryptamine), hypotheses have been established. The most well-known one is a rise in serotonin levels throughout the brain. Nutritional interventions intended to reduce brain serotonin synthesis during extended exercise enhance endurance performance, and there is strong evidence that increases and decreases in brain serotonin activity during prolonged exercise, respectively, accelerate and delay fatigue. There are several physiologically connected causes of fatigue. It is important to better understand how CNS effects affect fatigue in order to achieve maximum muscle performance in both daily life and athletics.

Exercise activities can act as an endogenous adjuvant, enhancing the efficiency of the host immune response after vaccination. However, the effect of repeated bouts of eccentric endurance exercise on cellular and humoral immune-related responses to the vaccine is unclear. The present study was performed to investigate the activation of type 1 and 2 (Th) helper lymphocytes following three bouts of endurance eccentric exercise as an adjuvant for DNA vaccination. Thirty-six female Balb-c mice (6-8 weeks, body mass mean=18g) were randomly divided into six groups: control, exercise, vaccine, PcDNA, exercise-vaccine and exercise-PcDNA (6 mice in each group). Different groups underwent DNA vaccine and PcDNA injection immediately after the last exercise, all stages of exercise and injections were repeated after 12 days according to the vaccine protocol, and 12 days after the second vaccine injection, spleen samples were collected. On-way variance analysis was used for statistical analysis and P<0.05 considered for significance. According to the results of the study, the ratio of Th1/Th2 after antigen stimulation was significantly different between the control group with vaccine and exercise-PcDNA (P <0.05). Also, the exercise-vaccine group was significantly different from all research groups (P <0.05). The results of the present study confirm the increase in the Th1/Th2 cell ratio following repeated bouts of eccentric endurance exercise. Stimulation of muscle damage through exercise before DNA vaccination may have been effective in invoking innate immune system cells and effectively stimulating acquired immunity.

To enhance knowledge about the role of regular physical activity on brain structure and function in multiple sclerosis, this study designed to investigate the effect of 6-month home-based exercise on the thalamic pathology and metabolites concentration using magnetic resonance imaging, diffusion and spectroscopy techniques. In this study, 56 people with multiple sclerosis (39 female and 13 male, age: 37.33±9.59 year) were randomly divided into two groups, home-based exercise and control. Intervention include aerobic (3-session per week, 50-75 % heart rate reserve) and resistance (2-session per week, rating of perceived exertion 5-8) exercise. Brain and thalamic volume using magnetic resonance imaging, thalamic metabolites using spectroscopy, and microstructure changes using diffusion technique were assessed before and after the intervention. Results showed that six months of home-based exercise did not have a significant effect on brain, thalamic volume and diffusion parameters including fractional anisotropy, mean penetration, axial penetration and radial penetration (p>0.05). Thalamic metabolites analysis showed that home-based exercise resulted in a significant increase in the ratio of N-acetylaspartate and N-acetylaspartylglutamate to creatine (p<0.007) and a significant decrease in the ratio of choline to creatine and inositol to creatine (p<0.22 and p<0.002, respectively). Overall, the results provided evidence about the beneficial effects of regular physical activity on thalamic metabolites associated with myelin loss and axonal function in the brain of people with MS using spectroscopy imaging. However, home-based exercise was not associated with change in diffusion parameters as indicators of changes in thalamic microstructures, which may indicate that longer-term intervention is needed.

Decreased physical activity due to sciatic nerve ligation (SNL) cause muscle atrophy. The purpose of the present study was to investigate the effect of decreased physical activity in the form of spinal nerve ligation (SNL) on the expression of muscle atrophy-related genes (TWEAK and Fn14) after resistance, endurance and combined exercises.

Thirty rats were randomly divided into four groups: 1- Control group-SNL (Sham+SNL) (N=7),2- Mixed training group-SNL (Mix+SNL) (N=7), 3- Endurance training group-SNL (TE+SNL) (N=8), and 4- Resistance training group-SNL (LA+SNL) (N=8). Mix+SNL, TE+SNL and LA+SNL groups participated in training program for six weeks. Decreased physical activity was implemented for four weeks. Real time-PCR technique was used to measure gene expression. To determine the difference between research variables, analysis of variance, Tukey's post hoc test were used at a significance level of 0.05.

The results showed that the gene expression of TWEAK and Fn14 increased by decreased activity. The expression of TWEAK in SNL+La and SNL+Mix groups was significantly lower than Sham+SNL group (P=0.001), and the expression of Fn14 was significantly lower only in the SNL+Mix group compared to the Sham+SNL group (P=0.003). However, there was no significant change in the expression of TWEAK and Fn14 genes in SNL+TE group compared to Sham+SNL group.

These findings show that performing six weeks of resistance or combined training compared to endurance training before reduced activity (SNL), prevents the increase in the gene expression of TWEAK and Fn14. Therefore, the animals that included resistance training in their training program are more resistant to muscle atrophy caused by reduced physical activity than the group that only did endurance training.

Understanding the involved mechanisms in muscle atrophy can help develop new treatment methods for atrophic conditions. Skeletal muscle atrophy via biochemical and transcriptional pathways can increase the expression of some muscle atrophy related genes. The present study aims to assess the effect of reduced physical activity by the spinal nerve ligation (SNL) after a period of resistance, endurance and combined exercises on the expression of MuRF-1 and Atrogin-1 genes in male rats.

In this experimental study, 30 male Wistar rats were randomly divided into four groups: Control+SNL, combined exercise+SNL, endurance exercise+SNL, and resistance training+SNL. The exercises were performed for six weeks. After this period, the protocol of reduced physical activity by the SNL was implemented for four weeks. At the end, soleus muscle was isolated and the expression levels of MuRF-1 and Atrogin-1 genes were measured by real-time polymerase chain reaction technique. To examine the gene expression differences between the groups, analysis of variance and Tukey’s post hoc test were used. The significant level was set at 0.05.

The results showed that the expression of MuRF-1 gene in the combined exercise+SNL and resistance training+SNL groups was significantly lower than in the control group (P<0.05). The Atrogin-1 gene expression was significantly reduced only in the combined exercise+SNL group compared to the control group (P<0.05).

It seems that the rats with resistance training are more resistant to SNL-induced atrophy than the group with endurance exercise.

Exercise, with beneficial effects on brain health and cognitive function reduces the destructive effects of some neurological diseases such as Alzheimerchr('39')s. The aim of this study was to evaluate the effect of four weeks of aerobic exercise on cognitive function and expression of Sirt1, CREB and BDNF genes in the hippocampus of male Wistar rats with Alzheimerchr('39')s disease.

The statistical population included 18 male Wistar rats from the Pasteur Institute. Rats were randomly divided into three groups including Alzheimerchr('39')s group, Alzheimerchr('39')s disease-exercise group and a healthy control group. Alzheimerchr('39')s disease group was induced by injecting Aβ42 into the hippocampus. Seven days after surgery, the rats performed the aerobic exercise for four weeks (five sessions per week at a speed of 10-15 m/min). They underwent behavioral tests 48 hours after the last training session. Twenty four hours later, rat hippocampal tissue was extracted. Sirt1, CREB and BDNF mRNAs were measured using Real time-PCR.

Learning and spatial memory performance decreased in rats of Alzheimerchr('39')s disease group compared to a healthy control group (p˂0.001). Decreased mRNA expression of Sirt1, CREB and BDNF genes was observed in the hippocampal tissue of Alzheimerchr('39')s disease group compared with the healthy control group (p˂0.001). Alzheimerchr('39')s rats with intermittent aerobic exercise had improved learning function, spatial memory and increased mRNA expression levels of Sirt1, CREB and BDNF genes in comparison with Alzheimerchr('39')s disease group (p˂0.001).

Periodic aerobic exercise in rats with Alzheimerchr('39')s disease can improve spatial learning and memory by positively regulating the Sirt1/ CREB/ BDNF signaling pathway in hippocampal tissue.

Alzheimer's disease (AD) is the most common form of dementia and amyloid peptides playing a central role in its pathogenesis. Recently, regular exercise has been considered as one of the most important non-pharmacological mechanisms to contrast with AD. The aim of this study was to investigate the effect of 4 weeks exercise on mRNA of GDNF in rat’s hippocampus with AD induced by Aβ1-42 injection.

56 male rats with mean±SD weight of 195±20 g were randomly divided Into four groups: training group, Aβ-42 induction + training group, Aβ-42 induction group and control group. injection of Aβ1-42 into the hippocampus was performed. Seven days after surgery, rats of each groups were either sacrificed or subjected to behavioral testing, randomly. Real-Time PCR were used for investigation of mRNA GDNF.

there is a significant difference between the groups. Gene expression level in training group was higher and in the Aβ-42 induction group was lower (p < 0.001). Moreover, spatial learning and memory were significantly better in the exercise + AD than AD group (p < 0.01).

It seems that 4 weeks of exercise could improve spatial memory and learning. Moreover, aerobic exercise could increase the level of neurotrophic factors gene expression specially GDNF in rat’s hippocampus.

One the major reason of the age-related muscular atrophy, Sarcopenia, is neurogenic atrophy. Despite this issue, the effects of some pathway which have probability effect, such as: kind of training methods, especially high interval intensive training, on the main factors of the neurogenic cascades is not yet clear. Therefore, the aim of this study was to investigate the effects of high interval intensive training period on the expression of the HDAC4, HDAC5, Dch2 and Myogenin gens in the plantaris muscle of the aged male Wistar rats. 28 male Wistar rats randomly assigned in to four groups (N=7, adult control, N=7, adult training, N=7, aged control, N=7, aged training). The training group performed HIT 5 times per week for 6 weeks. 48 hours after the end of the last session of training with control group were anesthetized and sacrificed. Then the plantaris muscle was removed. Real time PCR method was used to determine the gene expression levels of HDAC4, HDAC5, Dch2 and Myogenin. For the statical analyses two-way ANOVA and Tukey were used. The statical significant assumed P≤0.05. The results of this study have been shown that HDAC4, HDAC5 and Myogenin significantly decreased. The amount of the Dch2 increased significantly compared to young control group. According to the results of this study, it seems high interval intensive training suppress the neurogenic atrophy   in the orders adult.

Neuropathy is one of the complications of diabetes, probably due to the destruction of the extracellular matrix and the thickening of the peripheral nerve basement membrane. However, its mechanisms and the impact of exercise on these disorders has not fully understood. The purpose of the present study was to investigate the effect of aerobic exercise on collagen levels of type I and IV and collagen type I protein changes in the sciatic nerve of diabetic rats.

 Eighteen 10-week-old Wistar male rats weighing 250 ± 20 g were randomly divided into three groups of healthy control (n=6), diabetic (n=6) and diabetic + aerobic exercise (n=6). For this purpose, after introduction and adaptation of rats to new environment, diabetes was induced by single dose injection of dissolved streptozotocin in sodium citrate buffer at pH=4.5 at 45 mg/kg intraperitoneal. After confirming neuropathic conditions (with behavioral tests), diabetic+exercise rats underwent moderate-intensity aerobic exercise on the treadmill for 8 week. At the beginning and at the end of the period, blood glucose of all rats was measured by glucometer and the mean of each group was measured separately. Changes in collagen type I and IV gene expression, and collagen type I protein levels in sciatic nerve of rats were evaluated by real-time PCR technique and immunohistochemistry, respectively.

 Diabetes increased collagen type I and IV gene expression and collagen type I protein levels in the sciatic nerve samples of rats. However, exercise reduced blood sugar levels and expression of collagen type I and IV genes (p=0.05) and collagen type I protein significantly reduced in sciatic nerve (p=0.001).

 The results of the present study showed that aerobic exercise as a non-pharmacological strategy by negative regulating type I and IV collagen factors at the gene and protein level, was able to control and inhibit the effects of diabetes on extracellular matrix components in the sciatic nerve.

Diabetes causes nerve tissue damage and ultimately death of nerve cells, especially in important areas such as the hippocampus. It seems that exercise training and anti-inflammatory supplements can moderate this condition. Therefore, the aim of this study was to determine the effect of aerobic training exercise and L-carnitine consumption on the levels of hippocampus CNTF and CNTFR proteins in diabetic rat.

45 Wistar rats between 250 to 300 gr were randomly divided into six groups, including healthy control groups, sham, diabetic control, diabetes + aerobic exercise, diabetes + L-carnitine supplementation and diabetes + aerobic exercise + L-carnitine supplementation. L-carnitine supplements were divided. Diabetic groups underwent subcutaneous injection of 55 mg / kg STZ. supplementary groups received 100 mg of L-carnitine per day orally. The aerobic exercise program was performed for 6 weeks and 5 days a week. The research variables were measured 24 hours after the last training session by the ELISA technics in the hippocampal tissue. The statistical method of one-way analysis of variance and Toki post –hoc test were used to analyze the data.

The present study showed an significant increase in CNTF and CNTFR protein levels of hippocampal tissue after aerobic exercise and L-carnitine consumption (P = 0.001), which greater effect found in combination manner.

Due to the effect of aerobic exercise and L-carnitine supplementation alone and in interaction with each other on hippocampal tissue, the use of this method can be considered as maintaining neural tissue in diabetes.

Individuals ability are different for achieving to success in sports disciplines and most of this differences are related to genetic factors. Finding genetic structures that effect on athletic performance is an important step in developing methods related to talent identification. Judo athletes for being successes in this discipline need to high levels of strength and power. The previous investigations revealed the insulin-like growth factor (IGF2) is associated with body mass index, fat-free mass, hand grip strength and leg strength.

The aim of the present study was to evaluate the possible association between ApaI IGF2 and judo status. The athlete group includes 40 elite judo athletes who had medals in Asian and World championship and control group comprised of 120 health non-athletes men.

DNA was extracted from the peripheral blood using a non-enzymatic method and Genotyping was conducted by PCR method for identifying the IGF2 ApaI polymorphism. The distribution frequency of this polymorphism was determined by chi-square analysis.

There were no significant differences in genotype and allele frequency of the judo athletes compared with control.

The result of the present study revealed IGF2 ApaI polymorphism due to the influence of judo discipline from different factors and no relying completely on a single factor (such as strength or endurance) may have no effect in judo status in elite Iranian judo athletes.

Karate is considered as one of the most intense and challenging exercise due to its intensity and types of activities. In these activities, the body is inflicted by the number of injuries and its antioxidant capacity is disturbed. Therefore, the present study was aimed at assessing the responses of muscle damage markers, oxidative stress and plasma antioxidant enzymes to the simulated karate activities and supplementation of skullcap plant in the elite karate athletes. Twenty-four eligible elite karate athletes were randomly assigned to two groups, consisting of placebo-activity group (n=12) and skullcap-activity group (n=12). The considered activities were based on the World and European Karate Championships programs. First, blood samples were taken from research groups at the rest and then desired activities were performed by athletes. Next, the second blood sampling was taken, immediately after the activity and after that, the subjects in placebo and skullcap groups received 500 mg of placebo and skullcap capsules, respectively. The third blood samples were taken one hour after that and the fourth blood sampling was two hours after taking the supplement. Finally, plasma was removed from the blood and CK, LDH, MDA, GPx, TAC, and SOD indicators were measured.Results showed that the indicators of muscle damage and oxidative stress significantly increased (p < /em> < 0.001) immediately after simulated karate activates and decreased during the recovery period as well, while these changes were higher in supplement group (p < /em> < 0.05). Furthermore, antioxidant indicators have significantly increased after the activities, and this increase was at a higher level (p < /em> < 0.05) throughout the recovery period in the supplement group. The results of the present study showed that skullcap supplementation increased antioxidant indicators in the recovery period and decreased muscle and oxidative damage factors. Therefore, this plant can be recommended as a supplement to reduce damages, stress, and fatigue for karate athletes.

MicroRNAs (miRNAs) play a key role in the development of the heart. Recent studies have shown that miR1 and miR-133 are key regulators of cardiac hypertrophy. Therefore, we aimed to evaluate the effect of an endurance training (ET) program on the expressions of these miRNAs and their transcriptional network.

In this experimental study, cardiac hypertrophy was induced by 14 weeks of ET for 1 hour per day, 6 days per week at 75% VO2 max). The rats (221 ± 23 g) in the experimental (n=7) and control (n=7) groups were anesthetized to evaluate heart morphology changes by echocardiography. Next, we evaluated expressions of miR-1 and miR-133, and heart and neural crest derivatives express 2 (Hand2), Mef2c, histone deacetylase 4 (Hdac4) and serum response factor (Srf) gene expressions by real-time polymerase chain reaction (PCR). Finally, the collected data were evaluated by the independent t test to determine differences between the groups

The echocardiography result confirmed physiological hypertrophy in the experimental group that underwent ET as shown by the increased left ventricular weight/body surface area (LVW/BSA) (P=0.004), LVW/body weight (BW) (P=0.011), left ventricular diameter end-diastolic (LVDd) (P=0.003), and improvements in heart functional indexes such as fractional shortness (FS) (P=0.036) and stroke volume (SV) (P=0.002). There were significant increases in the expressions of miR-1 (P=0.001) and miR-133 (P=0.004). The expressions of Srf, Hdac4, and Hand2 genes significantly increased (P<0.001) in the experimental group Compared with the control group. The expression of Mef2c did not significantly change.

The expressions of miR-1 and miR-133 and their target genes appeared to be involved in physiological hypertrophy induced by ET in these rats.

The purpose of this study was to develop a strategic plan for monitoring the well-being and physical activity of Iranian students. This research is a mixed (qualitative-quantitative) research and has been conducted in the field. The statistical population of the study consisted of all governmental universities throughout the country and all other experts in the field of student sport and student well-being monitoring. In the quantitative section, the sample consisted of 39 elites and supervisors of university well-being and sport counseling centers. According to the findings, the mission of the student well-being and Physical Activity system is "policy making, planning and implementation of student health monitoring, providing sports counseling and training and improvement programs for well-being development." 'Physical health and quality of life of the country's students and the development of their knowledge and sensitivity to maintaining and promoting well-being' and the vision considered as 'Iranian student: healthy and vitality' and core values including well-being, vitality' Physical activity, fitness, employment and self-sufficiency were considered. In addition, 20 weaknesses, 11 strengths, 12 threats and 15 opportunities were identified. Six major objectives were formulated and five strategies and 21 operational plans were designed to achieve these goals. The program derived from this research can be implemented as an outline and guide framework for the development of the well-being and fitness of Iranian students.

L-carnitine is associated with an increase in antioxidant enzymes activities and reduction in oxidative damage. The aim of this study was to evaluate the effect of aerobic training and L-carnitine cconsumption on hippocampal oxidative stress and neurogenesis factors in diabetic rats.

In this experimental study, 45 male wistar rats were divided into six groups including sham (5 rats), healthy control (8 rats), diabetic control (8 rats), diabetic receiving L-carnitine (8 rats), diabetic receiving aerobic exercise (8 rats), diabetic receiving L-carnitine and aerobic exercise (8 rats). Rats with serum glucose level higher than 300 mg/dL were considered diabetic. L-carnitine supplemented dose was 100 mg per day. The aerobic exercise protocol including five sessions per week started at a speed of 10 for 20 min at a zero-degree grade in the first week and gradually reached a speed of 20 for 40 min at a grade of 5 in the sixth week. The Hippocampal tissues of the dependent variables (BDNF, MDA and GPX) were measured by ELISA 24 hours after the last session of the exercise program. One-way ANOVA and Tukey's post hoc test at P-value< 0.05 were used to analyze the data.

The results of the study revealed that aerobic exercise and L-carnitine consumption have a significant effect on BDNF (P-value= 001), MDA (P-value= 001) and GPX (P-value= 001) of the diabetic rats.

According to the results, it is suggested that diabetic patients use aerobic exercise and supplementation with carnitine with caution and physician advice.

Diabetic neuropathy can cause disorders in axon transmission, changes in the extracellular matrix, and peripheral nerve damages. However, its mechanism, along with the beneficial effects of exercise on these disorders is not entirely clear. The aim of the current study was to assess changes in fibronectin mRNA gene expression level of the sciatic nerve in rats with streptozotocin-induced diabetes after endurance training. Eighteen male Wistar rats (10 weeks old with 250±20 gr weight) were randomly assigned to three groups, including healthy, induced diabetes and induced diabetes plus endurance training. Induction of diabetes was conducted using an intraperitoneal injection of a single dose of streptozotocin (STZ). Neuropathy was confirmed using the behavioral tests. Rats in induced diabetes plus training group had 8 weeks of moderate and increasing intensity endurance training on the treadmill. The Fibronectin mRNA gene expression level of the sciatic nerve was assessed using Real-time-PCR. Changes in fibronectin protein and myelin thickness were measured by immunohistochemistry and luxol fast blue staining. The mean and standard deviation was used to report descriptive data. Data were entered into SPSS 22. Fibronectin mRNA gene expression level (1.90) of sciatic nerve fibronectin protein and myelin thickness reduced significantly due to diabetes (P<0.05). Eight weeks of endurance training increased fibronectin gene expression of sciatic nerve fibronectin protein and prevented further destruction of myelin, which was statistically significant. The results showed that diabetes leads to changes in the extracellular matrix and the reduction of the sciatic nerve myelin thickness. Endurance training as a non-drug strategy is effective in preventing these damages.

Diabetes is known as one of the diseases that has imposed many health, social and economic problems on human societies and has spread widely in recent decades (1). Glucose metabolism and related disorders for the central nervous system (CNS) and astrocytes, which are the most important glial cells of the central nervous system; It is important. Therefore, disorders of the hypothalamus, cerebral cortex and hippocampus, vascular disorders of the brain, etc. are among the complications of diabetes on the central nervous system (3). Among the brain regions, the hippocampus is one of the most sensitive areas that is vulnerable to harmful factors such as ischemia, stress and especially diabetes, during which it undergoes neurophysiological, structural and molecular changes such as decreased neurogenesis 3 and atrophy. Hippocampus (4), which leads to one of the significant changes caused by diabetes, namely neuronal death in the hippocampus (5).Due to the fact that insulin resistance and type 2 diabetes are characterized by hyperglycemia, hyperinsulinemia, increased plasma FFA levels, decreased fat oxidation ability and fat accumulation in body cells (6). And this increase in fat content has a high relationship with insulin resistance and the main cause of this accumulation of fat is mitochondrial dysfunction (7). Two mitochondrial enzymes that are important in the fat metabolism of cells in the body are Malonyl-CoA and CPT2. Malonyl-CoA, a coenzyme derived from malonic acid, plays an essential role in the transport of fatty acids into the mitochondria and in their synthesis. Are fatty acids (8). Accordingly, some evidence suggests that reducing the amount of malonyl coenzyme A reduces insulin resistance (10).In this regard, carnitine palmitol transferase 2 is a mitochondrial protein that is attached to the inner part of the mitochondrial membrane and plays a key role in the transport of fatty acids into the cell for beta oxidation (11). The regulation of CPT-2 activity by Malonyl-CoA or other metabolic mediators is not directly or indirectly known (12). One of the supplements that has been shown to facilitate beta oxidation of long chain fatty acids and participate in the metabolism of branched-chain amino acids and fix cell membranes is L-carnitine (14). Due to the fact that L-carnitine is able to transport the acetate group from the mitochondria to the cytoplasm, thereby reducing the ratio of acetyl coenzyme A to coenzyme A in the mitochondria, thereby increasing the activity of the enzyme pyruvate dihydrogenase and thus glucose catabolism. Give (15). Therefore, taking this supplement may be able to improve mitochondrial disorders caused by diabetes in various tissues, including nerve tissue.On the other hand, in addition to nutrition and various supplements, physical activity and exercise have been proposed as a way to control diabetes disorders (16). In confirmation of this, exercise activity in diabetic rats by reducing blood sugar levels, causes cell proliferation and increases the synaptic plasticity of neurons in the hippocampus of the brain (17). In fact, exercise creates endogenous neuroprotection by reducing endogenous neurons and protecting them against diabetic neuropathy, and ultimately reducing diabetic cognitive and motor disorders (18), thus increasing activity. Regular exercise can improve the malleability of the brain (19), the antioxidant system (20), and the upregulation of neurotrophins (21).Considering the above and considering the negative effects of diabetes on various body systems on the one hand and irreparable damage to society, researchers are always looking to discover the best way to prevent and treat this dangerous complication. Various studies have been performed on the effect of increased plasma L-carnitine on FFA intake or exercise endurance capacity following oral administration or intravenous injection; In this regard, some findings suggest that L-carnitine supplementation increases fat oxidation (25) decreases carbohydrate oxidation (26) improves exercise (27) and reduces recovery time following exercise (28) Leads. Given the above and differences in research results on the effect of aerobic exercise and L-carnitine on mitochondrial disorders on the one hand and the lack of research on the subject of research on the hippocampus on the other hand and discovering a way to minimize the negative effects of diabetes Specifically, the increase in cellular fat content in the hippocampus, the researcher seeks to answer the question of whether increased aerobic activity and consumption of L-carnitine have an effect on mitochondrial factors in the hippocampus of diabetic rats or not?

This research is of developmental type and its method is experimental. In which the ethical principles of working with laboratory animals, such as the availability of water and food, and proper storage conditions, and how to kill mice were observed.The statistical population of the present study consisted of male Wistar rats in the weight range of 250 to 300 g and 6 to 8 weeks of age that were bred at the Razi Serum Laboratory Animal Breeding Center. From the statistical population, 45 rats were randomly selected as a statistical sample and randomly divided into 6 groups. Groups include 1) sham injection group (5 rats), 2) healthy control (8 rats), 3) diabetic control group (8 rats), 4) diabetic group receiving L-carnitine (8 rats), 5) The diabetic group was aerobic exercise (8 rats) 6) The diabetic group was aerobic exercise and received L-carnitine (8 rats). In the diabetic group, animals became diabetic by injecting streptozotocin (STZ) at 55 mg / kg body weight. 48 hours after STZ injection, hyperglycemia was confirmed by glucose oxidase assay with biosystem kit. Thus, rats with serum glucose above 300 mg / dL were considered diabetic. In the diabetic and exercise groups, the animals ran on a treadmill for six weeks after induction of diabetes. Rats receiving L-carnitine received 100 mg of L-carnitine (29, 30) orally daily for 6 weeks. Aerobic exercise groups also performed a training program including aerobic exercise on a treadmill, 5 days a week, from 9 am to 11 am, for 6 weeks (31).

In the present study, the effect of aerobic exercise and consumption of L-carnitine on the mitochondrial CPT2 content of hippocampal tissue was observed (p= 0.008). However, there was no significant difference in the number of Malonyl-CoA mitochondria in the hippocampal tissue of diabetic rats as a result of aerobic exercise and L-carnitine administration (p= 0.227). The effect of aerobic exercise and alcarnitine consumption on Malonyl-CoA and CPT2 enzymes in the hippocampal tissue of diabetic rats was investigated. Based on the results of Tukey post hoc test, it was shown that diabetes is associated with a significant increase in Malonyl-CoA mitochondria of hippocampal tissue. Consistent with a study by Badiopada et al. (2006) that increased Malonyl-CoA levels and decreased fatty acid oxidation showed key abnormalities in insulin resistance in type 2 diabetic specimens (32).In general, exercise can stimulate lipid oxidation and inhibit lipid synthesis in the liver, a process that is mediated by activation of the AMPK pathway (33). However, as the results of the present study show, the response of Malonyl-CoA to exercise is different in hippocampal tissue, so it is possible that Malonyl-CoA levels in different tissues respond differently to exercise. The lack of significant change in Malonyl-CoA levels in the hippocampal tissue of diabetic specimens and the aerobic exercise program with L-carnitine can be attributed to changes in tissue insulin sensitivity and tissue oxidation. In the present study, the interaction between aerobic exercise and L-carnitine consumption had no effect on Malonyl-CoA hippocampus in rats. Although there are several mechanisms involved in supporting the effects of exercise on diabetes, the type of exercise and the dose of L-carnitine supplementation can also affect the results. Therefore, further studies are needed to discover the mechanism of Malonyl-CoA changes in the hippocampus, especially in diabetic specimens following L-carnitine exercise and consumption.The present study showed that diabetes was associated with a significant decrease in hippocampal tissue CPT2 index and the results showed that aerobic exercise and L-carnitine consumption had no effect on rat hippocampal CPT2. But the interaction of aerobic exercise and supplementation significantly increased CPT2 in the rat hippocampus. The palmitoyl carnitine transferase (CPT) system contains two enzymes, CPT I and CPT II, and are involved in the transport of long-chain fatty acids into the mitochondrial compartment. The enzymes are CPT I in the outer membrane and CPT II in the inner membrane of the mitochondria (11). The results of Aminizadeh et al. (2017) on the regulation of cellular energy homeostasis in the skeletal muscle of male rats after four weeks of endurance training showed that the expression of carnitine palmityl transferase 1 beta gene in the endurance training group was significantly higher than the control group (34). However, the exact mechanisms of the effect of exercise on CPT II regulation in hippocampal tissue are not well understood. Also, the physiological significance of the natural inhibition of CPT II by malonyl coa has not been determined. However, due to the high sensitivity of CPT II to Malonyl-CoA, it can be stated that changes in CPT II level are dependent on the level of Malonyl-CoA (35).

Due to the effect of aerobic exercise and L-carnitine supplement alone and in interaction, using them in consultation with a physician is recommended for diabetics.

Today, the sport of athletics and professional in the world is a major part of the sports industry. It is of a great impact on the development of countries economically, socially and culturally. Therefore, this research was conducted to designe the paradigmatic pattern of Iran's Athletics and Professional Sport Development. This study has a qualitative approach and we used the grounded theory as a research method. For gathering data, we studied high level documents and we interviewed with 19 experts who were aware of this subject. The validity of this research was examined and approved by the interviewers and then expert professors. The reliability of it is %82 which was obtained by using the methodology of the auditing result process. For data analysis, we used the continuous comparison method in three stages: open, axial and selective coding. Based on the results of the study of high handwritten document and in depth interviews, executive commitment factors, reform of government-oriented structural, commercialization, privatization, Professional foundation factors, Economic, technological, cultural and political factors, infrastructure upgrading and development of standard sport spaces, designing talent system and the establishment of a model for the development of athletics and professional sport were identified as nine effective components and extracted in the development of Iranian athletics and professional sport. The results of this study showed that it is undeniable necessity that the formation of a bargaining committee with the government, the parliament and the IRIB Organization as the most important component of the income generation of athletics and professional sports. It also seems that the management of the athletics and professional sport in Iran is very complex. It requires a comprehensive model that all factors such as economic and political factors (macro factor), infrastructure upgrading and the talent system (middle factor) and executive commitment (individual factor).