Sarcopenic obesity is defined as a multifactorial disease in aging with decreased body muscle, decreased muscle strength, decreased independence, increased fat mass, due to decreased physical activity, changes in adipokines and myokines, and decreased satellite cells. People with sarcopenic obesity cause harmful changes in myokines and adipokines. These changes are due to a decrease interleukin-10 (IL-10), interleukin-15 (IL-15), insulin-like growth factor hormone (IGF-1), irisin, leukemia inhibitory factor (LIF), fibroblast growth factor-21 (FGF-21), adiponectin, and apelin. While factors such as myostatin, leptin, interleukin-6 (IL-6), interleukin-8 (IL-8), and resistin increase. The consequences of these changes are an increase in inflammatory factors, increased degradation of muscle proteins, increased fat mass, and decreased muscle tissue, which exacerbates sarcopenia obesity. In contrast, exercise, especially strength training, reverses this process, which includes increasing muscle protein synthesis, increasing myogenesis, increasing mitochondrial biogenesis, increasing brown fat, reducing white fat, reducing inflammatory factors, and reducing muscle atrophy. Since some people with chronic diseases are not able to do high-intensity strength training, exercises with blood flow restriction (BFR) are newly recommended. Numerous studies have shown that low-intensity BFR training produces the same increase in hypertrophy and muscle strength such as high-intensity strength training. Therefore, it seems that exercise interventions with BFR can be an effective way to prevent the exacerbation of sarcopenia obesity. However, due to limited studies on adipokines and exercises with BFR in people with sarcopenic obesity, more research is needed.

Cardiovascular diseases are the most common cause of death in the world. One of the major causes of cardiac death is excessive apoptosis. However, multiple pathways through moderate exercise can reduce myocardial apoptosis. After moderate exercise, the expression of anti-apoptotic proteins such as IGF-1, IGF-1R, p-PI3K, p-Akt, ERK-1/2, SIRT3, PGC-1α, and Bcl-2 increases in the heart. While apoptotic proteins such as PTEN, PHLPP-1, GSK-3, JNK, P38MAPK, and FOXO are reduced in the heart. Exercise-induced mechanical stress activates the β and α5 integrins and subsequently, focal adhesion kinase phosphorylation activates the Akt/mTORC1 and ERK-1/2 pathways, leading to an anti-apoptotic response. One of the reasons for the decrease in exercise-induced apoptosis is the decrease in Fas-ligand protein, Fas-death receptor, TNF-α receptor, Fas-associated death domain (FADD), caspase-8, and caspase-3. In addition, after exercise mitochondrial-dependent apoptotic factors such as Bid, t-Bid, Bad, p-Bad, Bak, cytochrome c, and caspase-9 are reduced. These changes lead to a reduction in oxidative damage, a reduction in infarct size, a reduction in cardiac apoptosis, and an increase in myocardial function. After exercising in the heart, the levels of RhoA, ROCK1, Rac1, and ROCK2 decrease, while the levels of PKCε, PKCδ, and PKCɑ are activated to regulate calcium and prevent mPTP perforation. Exercise has an anti-apoptotic effect on heart failure by increasing the PKA-Akt-eNOS and FSTL1-USP10-Notch1 pathways, reducing the negative effects of CaMKIIδ, and increasing the calcineurin/NFAT pathway. Exercise plays a protective role in the heart by increasing HSP20, HSP27, HSP40, HSP70, HSP72, and HSP90 along with increasing JAK2 and STAT3 phosphorylation. However, research on exercise and factors such as Pim-1, Notch, and FAK in cardiac apoptosis is scarce, so further research is needed. Future research is recommended to discover more anti-apoptotic pathways. It is also recommended to study the synergistic effect of exercise with gene therapy, dietary supplements, and cell therapy for future research.

Sarcopenia is a severe loss of muscle mass and functional decline during aging that can lead to reduced quality of life, limited patient independence, and increased risk of falls. The causes of sarcopenia include inactivity, oxidant production, reduction of antioxidant defense, disruption of mitochondrial activity, disruption of mitophagy, and change in mitochondrial biogenesis. There is evidence that mitochondrial dysfunction is an important cause of sarcopenia. Oxidative stress and reduction of antioxidant defenses in mitochondria form a vicious cycle that leads to the intensification of mitochondrial separation, suppression of mitochondrial fusion/fission, inhibition of electron transport chain, reduction of ATP production, an increase of mitochondrial DNA damage, and mitochondrial biogenesis disorder. On the other hand, exercise adds to the healthy mitochondrial network by increasing markers of mitochondrial fusion and fission, and transforms defective mitochondria into efficient mitochondria. Sarcopenia also leads to a decrease in mitochondrial dynamics, mitophagy markers, and mitochondrial network efficiency by increasing the level of ROS and apoptosis. In contrast, exercise increases mitochondrial biogenesis by activating genes affected by PGC1-ɑ (such as CaMK, AMPK, MAPKs) and altering cellular calcium, ATP-AMP ratio, and cellular stress. Activation of PGC1-ɑ also regulates transcription factors (such as TFAM, MEFs, and NRFs) and leads to the formation of new mitochondrial networks. Hence, moderate-intensity exercise can be used as a non-invasive treatment for sarcopenia by activating pathways that regulate the mitochondrial network in skeletal muscle.

Background:The present research aims to examine the effect of anaerobic exercise with melatonin consumption on the expression of Bax and Bcl-2 markers in rat myocardium after ischemic-reperfusion by isoprenaline.Methods: In the present experimental study, 28 male Wistar rats weighing approximately 200-250 g with two to three months old were divided into five groups: pilot (n=14), control (n=4), melatonin (n=4), anaerobic (n=4) and melatonin anaerobic (n=4). Pilot group were divided into two groups, isoperalin (n=7) and normal (n=7): isoperalin group injected isoprenaline with dose of 150 and 125 mg/kg BW with 24 hours in two consecutive days; and normal group has no injection. Then more fibros level was confirmed in isopernalin into normal groups used Massontrichrom tanique. In the following Rats in melatonin group were gavaged every day for one month using a dose of 10 mg/kg BW. Meanwhile, rats in anaerobic group and melatonin anaerobic group were exposed training course with frequency of three times weekly for one month. But control group were injected only with isopernalin in the end of one month. Finally, rats were sacrificed after confirmation of infarct and expressions of bax and bcl2 gene were studied by real-time method.Results: Melatonin treatment and anaerobic training have negligible effect on Bax and Bcl-2 gene expression. In the other hand, anaerobic exercise with consuming melatonin can decrease and increase Bax and Bcl-2 gene expression respectively and show significant effect, compared to treatment with melatonin alone. Conclusion:The anaerobic exercise with consuming melatonin into consuming melatonin alone can reduce inactive induced-Infarction level.

The present research aims to examine The Effect of aerobic and anaerobic training with melatonin consumption on the expression of apoptotic genes BAX and BCL2 myocardial in rats after ischemic reperfusion. In this study, Wistar rats (n = 38) were used weighing approximately 200-250 g with two to three months old. The study was conducted using Stroke (n = 7) and healthy (n = 7) rats to determine the stroke of isoprenaline injection; and left ventricular stroke was confirmed after the isoprenaline injection with the Terry Chromasone technique. Then, the rats were divided into 6 groups of aerobic (n = 4), anaerobic (n = 4), aerobic with melatonin (n = 4), anaerobic with melatonin (n = 4), Melatonin (n = 4) and control group (n = 4). The research group rats were familiar running on treadmill for a week, and One-month aerobic and anaerobic training was performed with three sessions per week. Also, melatonin gavage (10 mg / kg) was applied to melatonin treatment groups. After two rest days, all rats were injected with isoprenaline at 24 hours intervals. However, control group rats were only injected with isoprenaline. Data was analyzed using independent T, one way ANOVA and 2-∆∆ct formula. The results of this study showed that aerobic and anaerobic training and melatonin alone had a negligible effect on BAX and BCL2 genes expression, However, aerobic and anaerobic training combined with melatonin was able to reduce and increase the expression of the BAX and BCL2 genes, respectively. Of course, these changes had a significant effect on melatonin alone. Therefore, it seems that this intensity and duration of training with melatonin intake into melatonin alone can provide the

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Introduction Autophagy, apoptosis, and atrophy pathways are responsible for controlling cardiac cell homeostasis. This study aims to investigate the effect of high-intensity interval training (HIIT) on the expression of proteins involved in autophagy, apoptosis, and atrophy pathways in the myocardium of type 2 diabetic rats. Methods In this experimental study, 18 male Sprague-Dawley rats (2 months old, weighing 280 ± 20 g) were selected. 12 rats were made diabetic through intraperitoneal injection of STZ and nicotinamide solutions. These rats were randomly divided into 2 groups, HIIT + diabetes (HIIT + D), and diabetic (6 rats in each group). A control group (6 rats) was also considered. The HIIT + D group did HIIT protocol 4 days a week for 8 weeks. To analyze the data, one-way ANOVA and Tukey's post hoc tests were used. Results It was shown that HIIT leads to a significant increase in AKT and mTOR protein content between the HIIT + D and diabetic groups in the left ventricle. But there is no significant change in the content of AMPK proteins. The content of FOXO3a, Beclin1, P53, myostatin, and SMAD2/3 proteins showed a significant decrease in the HIIT + D group. The protein content of caspase-3 in the activated form did not show a significant change, but there was a significant decrease in the content of the initial form (Pro). Conclusion HIIT along with increasing regulation of AKT and mTOR proteins can disable autophagy, apoptosis, and atrophy pathways. Therefore, the process of apoptosis and atrophy of heart cells is reduced in type 2 diabetic rats.

ARTICLE INFO ABSTRACTThe present research aims to examine the effect of aerobic and anaerobic exercise on Bax and Bcl-2 markers after the induced reperfusion ischemia by isoprenaline. In this study, there were used 26 male Wistar rats weighing approximately 200-250 g with two to three months old. The rats in pilot group were divided into two subgroups of reperfusion ischemia (n= 7) and healthy (n= 7) for study of heart-failure byisoprenaline. The rats in research group were divided into three subgroups ofaerobic (n= 4), anaerobic (n= 4) and control (n= 4) for study of gene expression. In rats of reperfusion ischemia group were confirmed heart-failure after injection isoprenaline by Trichromation staining technique. However, the rats in research group were familiar running on treadmill after one week, then they were exposed for one month training with frequency of three times weekly. After one month, all rats were rest for two consecutive days. Then within 24 hours, there were injected isoprenaline with dose of 150 and 125 mg per kg of their body weight. Data was analyzed using independent T, one way ANOVA and2 -ct formula. The research results showed that aerobic and anaerobic exercise can reduce and increase Bax and Bcl-2 gene expression respectively, but these changes were not significant. However, it seems that one month training can't decrease amount of myocardial apoptosis. Therefore, study of effect increase of period physical activity is essential for decrease amount of heart-failure.