جستجوی مقالات مرتبط با کلیدواژه « بی تمرینی » در نشریات گروه « پزشکی »

The corona epidemic and the closure of the clubs led to the forced non-training of athletes and as a result increased abdominal fat and obesity and caused the spread of liver diseases. Therefore, the purpose of the present study was to investigate the effect of a strength training session on alpha phytoprotein, gamma glutamyl transferase and alkaline phosphatase in men with regular training and forced non-training due to covid-19.

The current research was a semi-experimental study. According to the current quarantine conditions due to the spread of the coronavirus, 18 male athletes were selected in a targeted manner from among the available male athletes in Zanjan city. The second included 9 people who had not exercised in the past 6 months. On the day of the test, after consuming a standard breakfast by the subjects, the first blood sample was taken in the amount of 5 ml while sitting, then a training program with weights, consisting of 10 movements with 60% of a maximum repetition with supervision Three referees were conducted. Then, the second blood sample was taken one hour after the end of the training under the same conditions. To adjust the plasma volume, the Dale and Castile formula was used and AFP was measured with the Architect 2000 device. Correspondingly, the GGT level was measured with the Prestige autoanalyzer and ALP was also measured using the fully automatic biolis50i autoanalyzer. Data were analyzed using independent sample T-test, paired-sample-T-test, and Covariance using SPSS software.

A session of resistance training had no significant effect on the levels of alpha phytoprotein (AFP), gamma glutamyl transferase (GGT) and alkaline phosphatase (ALP) in the plasma of trained and untrained men(P>0.05). Also, after a session of resistance training, the level of gammaglutamyl transferase, alkaline phosphatase and alpha-phytoprotein in the plasma of the untrained group did not change significantly(P>0.05), but the level of alpha-phytoprotein in the trained group decreased significantly(P<0.05).

Considering the lack of effect of a strength training session on AFP, GGT and ALP serum levels of untrained and trained men, it can be said that the effect of a strength training session on changes in liver enzymes of trained and untrained men is the same. However, the reduction of alpha-phytoprotein as a cancer parameter and a predictor of acute liver problems in the exercised group may indicate the effect of regular exercise in reducing risk factors in response to an acute activity session.

Diabetes mellitus is one of the most common chronic diseases in the world (1). Diabetes and hyperglycemia caused by diabetes lead to disorders in various organs such as lungs, heart, muscles, kidneys, etc. (9, 10). One of the main complications of diabetes is diabetic cardiomyopathy; Diabetic cardiomyopathy is the result of diabetes-induced changes in the structure and function of the heart. Diabetic cardiomyopathy occurs as a result of impaired glucose and lipid metabolism associated with diabetes, which leads to increased oxidative stress and activation of multiple inflammatory pathways that mediate cellular and extracellular damage, pathological remodeling of the heart, and diastolic and systolic dysfunction. Preclinical studies in animal models of diabetes have identified several intracellular pathways involved in the pathogenesis of diabetic cardiomyopathy and potential cardioprotective strategies for disease prevention and treatment, including anti-fibrotic agents, anti-inflammatory agents, and antioxidants (11). Cellular energy homeostasis is a fundamental process that governs the overall health of the cell and is critical for cell survival. Central to this is the control of ATP production and utilization, which is regulated by a myriad of enzymatic reactions controlling cellular metabolism (12). Adenosine monophosphate-activated protein kinase (AMPK) is an energy sensor with aberrant expression in various diseases, including diabetes (12). There is considerable evidence that AMPK is reduced in cardiac tissues of animals and humans with type 2 diabetes or metabolic syndrome compared with non-diabetic controls, and that AMPK stimulation (physiological or pharmacological) can ameliorate diabetes-related cardiovascular complications (14). Considering the role of AMPK in energy metabolism in the heart, as well as the effects of diabetes and exercise on the gene and protein expression of this energy sensor, measuring the changes of this gene can improve our knowledge about the effect of different adaptations caused by different exercises, as well as the effect of lack of exercise. With the aim of investigating the effect of maintaining these adaptations after training (22, 23). However, so far, no research has been done that specifically compares the effect of two common training methods, continuous and intermittent training, followed by no training on cardiac AMPK gene expression in diabetic rats, which shows the necessity of the current research. According to the mentioned information, the present study was conducted with the aim of comparing the effect of a detraining period followed by aerobic and HIIT exercises on cardiac AMPK gene expression in alloxan-treated diabetic rats.

In this experimental research, 48 male Wistar rats (age: 10-weeks; weigh: 220±20 grams) were randomly divided into six groups (n=8). One group was considered as a healthy control and the rest of the rats were made diabetic using a single dose of 90 mg/kg of alloxan. One group was considered as diabetic control; and the rats were divided into two groups of high-intensity interval training (HIIT) and continuous moderate aerobic training (MICT). After 12 weeks of training, half of the rats in each group were sacrificed; and the rats were sacrificed after 2 weeks of no training. MICT program was performed for 5 sessions per week with a gradual increase in speed (18-26 m/min) and time (10-55 minutes). HIIT program also included 5 30-minute sessions per week in the form of running on a treadmill with one-minute repetitions and 2-minute active rest between each interval. For statistical analysis, one-way analysis of variance and Tukey's post hoc test were used and the significance level (P ≤ 0.05) was considered.

The results showed that the induction of diabetes decreased the cardiac AMPK gene expression compared to the healthy control group (P < 0.001), also the results showed that after 12 weeks of training, there was a significant increase in the cardiac AMPK gene expression in the training groups compared to the control group. Diabetes control was observed (P < 0.001), but no significant difference was observed between the two exercise groups (P > 0.05). Also, the results showed that after 2 weeks of non-training, there was a slight decrease in cardiac AMPK gene expression compared to the training groups, and these changes were not significant (P > 0.05).
Conclution: The results of the present study showed that induction of diabetes with alloxan decreased cardiac AMPK gene expression, which was related to hyperglycemia caused by induction of diabetes with alloxan injection. Previous research has also shown that a single dose of alloxan injection with 90 mg/kg body weight of rats induces diabetes (24-26). According to the findings of the present study, 12 weeks of continuous aerobic exercise and HIIT both significantly increased cardiac AMPK gene expression in diabetic rats, but no significant difference was observed between the two types of exercise. Based on the research conducted in animal models, exercise increases cardiac AMPK values, which are consistent with the results of the present study (30, 31). However, comparing the effects of continuous and HIIT exercises, the results of these two studies were different from our findings; In their research comparing the effect of moderate intensity continuous training and HIIT training on AMPK of skeletal and cardiac muscle, Wen et al. reported that the effects of HIIT training on increasing oxidative capacity and AMPK are more obvious (30); The results of Su et al.'s research showed better effects of continuous training on AMPK and PGC-1α gene expression in the HIIT group than continuous aerobic training (30). As shown in various animal models and patient studies, physical exercise is known to be cardioprotective and can partially compensate for cardiac damage. At the cellular level, exercise counteracts heart disease-related changes in these cellular pathways and can improve heart function (32). AMPK activation leads to the regulation of metabolism, protein transport, transcription factors and/or activators, kinases, and other enzymes and non-enzymatic proteins. AMPK increases substrate uptake and utilization in the heart, enhances mitochondrial biogenesis, and modulates the activity of specific proteins and transcription factors to exert cardioprotective functions (33). Therefore, exercise training can moderate the effects of diabetes on the heart by increasing cardiac AMPK. AMPK also plays an important role in reducing oxidative stress, regulating autophagy and anti-apoptosis of cardiomyocytes (29, 34). Exercise activates signaling molecules and transcriptional networks to promote physiological adaptations such as mitochondrial biogenesis (35). It has been reported that after swimming exercises in rats, the levels of activated AMPK showed a decrease in cardiac fibrosis due to the inhibition of NADPH oxidase (36). This finding has been confirmed as decreased AMPK activity by beta-adrenergic activation exacerbates cardiac fibrosis (37). These changes are important because exercise activates AMPK and thus may be able to inhibit pathological hypertrophy and cardiac fibrosis (38). Other findings of our research showed that 2 weeks of detraining after exercise decreased AMPK in both exercise groups, but this decrease was not statistically significant. In line with the findings of the current research, Cao et al also reported in their research that after the training period, a significant increase in AMPK level was observed, but after stopping training for 10 days, the AMPK level started to decrease, but the changes were not significant 40). Based on the results, it can be said that any two methods of continuous aerobic exercise and HIIT increase the expression of the AMPK gene; Also, after two weeks ofdetraining, cardiac AMPK gene expression is still high in diabetic rats. However, more research is needed to investigate the longer-term effects of non-exercise on AMPK gene expression and mechanisms related to non-exercise on diabetic cardiomyopathy.

 Detraining may affect cardiovascular adaptations. The present study aimed to investigate the effect of a detraining period followed by resistance training on immunohistochemical expression of ATP-sensitive potassium channels and mitochondrial biogenesis of heart tissue in male rats.

The present study was experimental. Thirty male Wistar rats were randomly divided into four groups (control, control-detraining, resistance training, and resistance-detraining training). The control group was sacrificed at the beginning of the study, and the control-detraining group did not exercise for 11 weeks. The resistance training group performed eight weeks of training. The resistance-detraining group did not train for three weeks after training. One-way analysis of variance and Tukey’s post hoc test were used for statistical analysis.

 The expression of KIR6.2, SUR2a, PGC1α, and TFAM in the heart tissue of the control-detraining group was significantly lower than those in the resistance training group (P=0.001). Also, they were significantly higher in the resistance training group compared to those in the resistance-detraining group (P=0.001). PGC1α expression in the resistance-detraining group was higher than in the control-detraining group (P=0.001).

 Resistance training increases PGC1α and TFAM in the heart tissue of rats by increasing the expression of KIR6.2 and SUR2a. But lack of exercise reduces the expression of potassium channels and factors that increase mitochondrial biogenesis.

The purpose of this study was to investigate the effect of a period of detraining following two types of concurrent training on glycosylated hemoglobin and exercise performance in women with type 2 diabetes.

Twenty-three women with type II diabetes mellitus in Shiraz, randomly were divided into three groups: control group that performed one day endurance training and one day resistance training (Different Day), and a group that performed endurance and resistance exercises in one day (Same Day). Before and after 8 weeks of concurrent training and after four weeks of detraining, glycosylated hemoglobin (Hb A1c) measured after 12 hours of fasting. Maximum oxygen consumption (VO2max) and Time to Exhaustion (TTE) was also calculated through the implementation of the Balkan test on the treadmill.

Two months of concurrent training in both groups of training significantly decreased Hb A1c, a significantly increased in VO2max and TTE in women with type II diabetes (p≤0.05). One month after the concurrent training in SD group resulted in a significant decrease in VO2max and TTE (p ≥0.05), but this decrease was not statistically significant in the DD group. Increase in Hb A1c after detraining was not statistically significant in both training groups (p ≥0.05).

The findings indicate that concurrent training improves glycemic control and increases exercise performance (VO2max and TTE) in women with type II diabetes, but doing DD concurrent training results to keep longer outcomes of training in the detraining periods.

The aim of this study was to investigate the effect of aerobic exercise with detraining in different phases of prevention on Bcl-2 gene expression and protein.

For this purpose, 32 female BALB-c mice (18-20 g) were purchased and randomly assigned to four groups of primordial prevention (A), primary prevention (B), secondary prevention (C), and control (D). Group A performed aerobic exercise for 4 weeks, followed by injection of 4T1 cells and 8 weeks of detraining after the injection. Group B performed aerobic exercise for 4 weeks immediately after the injection of 4T1 cells and then detrained for 4 weeks. Group C received a 4T1 cell injection and maintained a sedentary life for 4 weeks, followed by 4 weeks of aerobic exercise. The subjects were killed 48 hours after the last training session and detraining courses and tumor tissues were removed. Real-time polymerase chain reaction was used to measure gene expression and western blotting was used to measure protein content.The one-way ANOVA test was used to analyze the data.

The mean gene expression due to aerobic exercise was significantly (P<0.001) lower in groups A (0.481), B (0.323), and C (0.035) compared with group D (1.711). Also, aerobic exercise caused a significant decrease in Bcl-2 (P=0.005) protein expression in groups A (0.692), B (0.821), and C (0.670) compared with group D (1.000). It should be noted that tumor growth in experimental groups was not significantly different from the control group (P=0.092).

Exercise may be able to reduce anti-apoptotic agents in tumor cells, leading to apoptosis of tumor cells and reduced tumor growth.

The Akt / FoxO3a pathways is an important player in skeletal and cardiac muscle atrophy. In this study, the expression of Akt / FoxO3a / MAFbx / MuRF1 genes in soleus and heart muscle following exercise and detraining was investigated.

Male mice were randomly assigned to the control and exercise group after familiarization. HIIT training group was randomly divided into three groups of eight after six weeks of intermittent training. After a six-week training period, tissue removal was performed for the 1st, 2nd, and 3rd groups respectively after 48 hours, seven days, and 14 days of inactivity. The RT-PCR method was used to investigate gene expresion changes.

Exercise significantly increased the weight of the heart and soleus muscle relative to body weight. However, it decreased after seven and 14 days of inactivity [15% and 22% in the heart muscle (p=0.002) and 9% and 16% in the soleus muscle (p=0.001), respectively]. AKT expression increased in both the heart and the soleus muscles after exercise, while FoxO3a decreased. During exercise, increased FoxO3a activity lead to activation of MAFbx and MuRF1 in the heart muscle and only MAFbx in the soleus muscle.

In cardiomyocytes, like skeletal muscle, FoxO3a activates MAFbx transcroption, which slows or prevents hypertrophy. But changes in MuRF1 showed that the FoxO3a / MuRF1 pathway in the heart and skeletal muscles may have different regulatory mechanisms and react differently.

Cardiovascular disease is one of the most common causes of mortality in advanced countries today. Fibrinogen and resistin are two important markers of inflammation that predict atherosclerosis. The aim of this study was to investigate the effect of eight-week aerobic training and two weeks of detraining on the levels of resistin and fibrinogen in elderly men. 

22 inactive elderly men were selected from nursing homes and randomly divided into experimental and control groups of 11. The experimental group performed an aerobic exercise with 55% to 70% of maximum heart rate for 8 weeks, 3 sessions per week and 30-45 minutes in each session. Then they stopped their training for two weeks. In the entire study period, the control group performed their daily activities only. Blood samples were taken before, after the eighth and tenth weeks. The Kolmogorov-Smirnov test, repeated ANOVA and Bonferron's post hoc test were used to analyze of the data (p≤0.05). 

There was no significant difference in the level of resistin (p = 0.40) and fibrinogen (p = 0.95) changes in the control group in the first, eighth and tenth weeks. However, the levels of resistin (p = 0.01) and fibrinogen (p = 0.001) in the experimental group were significantly lower in the 8th weeks than in the control group. Fibrinogen levels in the 10th weeks were significantly higher than the eighth weeks (p = 0.001). 

It appears that eight weeks of aerobic training led to a significant reduction in the resistin and fibrinogen in older men. However, after two weeks of detraining, the levels of reduced fibrinogen increased again.

The aim of this study was to investigate changes in serum levels of TNF-α after 12 weeks endurance training and GnRH agonist in girl with central precocious puberty.

Twenty-five girls (age 6-8 years) with precocious puberty were randomly divided into three groups (medication, training, medication + training).  Ten healthy girls (with no precocious puberty) were also included as control group. At the beginning of the study, blood samples were taken from all subjects and serum level of TNF-α were measured by ELISA technique. The experimental groups then did an aerobic exercise program 3 days/week with 20-75 min per day with 45-75% of maximum heart rate for 12 weeks. The medication groups were also received GnRH agonist during the study, once monthly (1 ml every four weeks) by subcutaneously. TNF-α serum level were measured again at 24 hours after completing the training program and also after 4 weeks of detraining.

The Analysis of Variance (ANOVA) with repeated measures analyses showed no significant difference in serum level of TNF-α in medication group before and after treatment (p = 0.203). However, in training and training+medication groups a significant decrease in TNF-α level was observed after aerobic exercise (p  =  0.001). The detraining led to return of TNF-α level to the levels of before training (p = 0.001). Further comparison of groups by ANOVA showed a significant difference only between training and medication groups.

GnRH alone does not affect TNF-α serum level in girls with precocious puberty. However, aerobic training and also the combination of aerobic training with GnRH decrease TNF-α serum level. The subsequent detraining returns TNF-α serum level to the level of before training. A long time regular and moderate exercise can decrease inflammation indices in girl with precocious puberty.