The aim of this study was to evaluate the effect of high intensity interval training on gene expressions of MST1andMAFbxin EDL muscles of aged C57bl/6 mice. 28 C57bl/6 mice (14 aged and 14 adults) were assigned to two groups of training and control. After one week of familiarization, training groups participated in 4 weeks of high intensity training program. 48 hours after the last training session, the mice were sacrificed, their EDL muscles were extracted. Then, gene expressions of MST1andMAFbxwere measured with Real Time PCR technique. The results showed that aging significantly increased gene expressions of MST1 andMAFbx(P=0.001 and P=0.028 respectively). On the other hand, 4 weeks of high intensity interval training significantly reduced MST1 gene expression (P≤0.05) and insignificantly reduced MAFbx(P≥0.05) in aged mice. Furthermore, decrease of these two genes in adult group was not significant. Also, a significant decrease was observed in EDL muscle weight in aged mice (P=0.032) although high intensity interval training could slow down the atrophy in the aged. In addition, aging and training had an interactive effect (P=0.001) but this interactive effect of these two factors was not observed on MAFbx (P=0.185). Thus, aging is associated with an increase in MST1 andMAFbx geneexpressions which could be possibly involved in muscle mass changes associated with aging. Since high intensity interval training decreases these gene expressions, it can be used to maintain muscle mass in the aged.

Inactivity may result in loss of muscle volume and subsequently reduce the power, by activating proteasome signaling pathways, which leads to a decrease in quality and expectations of life. The aim of this study was to evaluate the effect of high-intensity training and also detraining on the signaling pathways of FOXO3a, MAFbx, and MuRF1.
In this study, 32 2-month male Sprague-Dawley rats were used. At first, periodic exercise with intensity of 85-100% VO2max was performed for six weeks. Then, the groups (detrained for 48h, 7w, and 14w) were detrained and then soleus muscle was removed from hind limb. H&E staining and histochemical procedure were used to measure the amount and percentage of skeletal muscle fibers type. Also, RT-PCR method was used to examine gene changes.
The mean weight of the soleus muscle increased after exercise and decreased significantly after detraining (p=0.001).The fiber type conversion were happened from I to IIA (p=0.001). Hypertrophy was observed in fibers after training, whereas atrophy was seen after detraining in type II fibers (p=0.001). FOXO3a and MAFbx levels were significantly increased after training and decreased after detraining period (p=0.001).The MuRF1 expression shown an increase and a decrease after training and detraining, respectively (p=0.001).
The results of this study indicated that the exercise couldn’t prevent atrophy during the period of detraining. Also, the activation of pathway FOXO3a/MAFbx, not the FOXO3a/ MuRF1, is the atrophy inducer during detraining. In this regard, probably MuRF1 is an indirect target of FOXO3a and cannot always be an appropriate marker of atrophy. MuRF1 probably plays a more important role in pathological atrophy conditions.

Inactivity can ultimately lead to obesity and activation of the proteolysis messenger pathways, which decreases muscle mass and skeletal muscle contractile power. The aim of this study was to investigate the effect of resistance training during the period of muscular inactivity on the expressions of atrophy processes regulatory genes of soleus muscle in the trained rats. 18 male Sprague Dawley rats were divided into two groups: control (n = 6) and endurance training (n = 12). Endurance training rats ran on a treadmill for 6 weeks and 5 sessions per week. Then, their lower limbs were immobilized for 7 days by plaster cast method and they were divided into two groups: immobilization (n = 6) and resistance training (n = 6). Resistance training and immobilization groups performed 3 sessions of resistance training of ladder climbing with hands in 3 sets, 5 repetitions each set. At the end of 7 days of immobilization, soleus muscle was excised and gene expressions (FoxO3a, MuRF1 and MAFbx) were measured by Real Time-PCR. One-way ANOVA test was used to determine the differences and Tukey post hoc test was used to determine the significance level among the groups (P≤0.05). The results showed that resistance training significantly reduced FoxO3a (P=0.001), MuRF1 (P=0.013), MAFbx (P=0.008) compared with endurance immobilization group. Resistance training seems to prevent muscle atrophy in the immobilization period through reducing or not increasing gene expressions of FOXO, MuRF1, and MAFbx.  Resistance training is likely to be a suitable solution to reduce muscle atrophy caused by muscle immobility.

Diabetes is a metabolic disease that is associated with heart injury. It has been shown that exercise training and resveratrol can improve the cardiac structure and function of diabetic subjects. The aim of the present study was to examine the effect of aerobic training along with resveratrol on gene expression of AMPK and MAFbx on cardiac tissue of diabetic experimental model.

In this experimental study, 40 males Wistar rats were randomly were divided into 5 groups: control (CN), diabetes (DM), diabetes-Resveratrol (RDM), diabetes-aerobic exercise (TDM), diabetes-aerobic exercise-Resveratrol (RTDM).Training groups have performed a running program on the treadmill for 8 weeks. Resveratrol (20 mg/kg) was injected subcutaneously 8 weeks for RDM and TRDM groups. 48 hours after the last training session, rats were anesthetized. Changes in the expression of AMPK and MAFbx myocardial genes were quantified using real-time PCR methods.

The results of the present study showed a reduction in AMPK expression (P < 0.001) and an increase in MAFbx (P < 0.001) in cardiomyocytes in DM groups compared to CN group.
AMPK expression was significantly increased in TRDM group compared to DM (p=0.009), RDM (p=0.011) and TDM (p=0.043) groups. MAFbx expression of cardiomyocytes in RDM (p=0.012), TDM (p<0.001) and TRDM (p<0.001) groups had significantly reduction compared to DM group. Also, MAFbx expression was significantly reduction in TRDM groups compared to RDM (p=0.041) groups.

 Long-term aerobic exercise, with and without resveratrol consumption it may cause to reduce the genomic indicators of atrophy and increase myocardial hypertrophy in diabetic rats.

Neuromuscular dysfunction along with reduced physical activity has significant consequences on muscle function. Therefore, the aim of the present study was to investigate the effect of resistance and combined training on the MST1 and MAFbx genes expression in Plantaris muscle and behavioral tests in male Wistar rats before decreased physical activity in the form of spinal cord ligation (SNL).twenty four 8-week-old male rats with the mean weight of 250± 20 grams were randomly devided into 3 groups: 1) Sham-Spinal Nerve Ligation (Sham-SNL), 2) Resistance Training-Spinal Nerve Ligation (SNL-S), 3) Combined training-Spinal Nerve Ligation (SNL-CO). In all three groups, three branches of the sciatic nerve of rats were tightly tied after the end of training protocol. The duration of the SNL protocol was 4 weeks. At the end of the protocol, Plantaris muscle was extracted. Real-Time PCR method was used to measure the mRNA expression of the genes. MST1 and MAFbx gene expression in the Sham-SNL group was non-significantly higher than the training groups (P <0.05). On the other hand, the results of one-way ANOVA and Tukey’s tests showed that there is a significant difference in thermal hyperalgesia and mechanical allodynia test between Sham-SNL group and training groups (P <0.05). Considering the significant change of behavioral tests in the sham group compared to the training groups, it can be claimed that resistance and combination training can be useful for improving neuropathic pain.

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.

Reduction of muscle mass occurs in some models of muscle atrophy during mechanical unloading status and MST1 and MAFbx genes are believed to have a role. In the present study, the effect of reduced physical activity in the form of spinal nerve ligation (SNL) after a period of endurance training (ET) on the expression of MST1 and MAFbx genes were examined in the rat plantaris muscle.

In this experimental study, 16 rats were randomly divided into two groups: control-spinal nerve ligation (Sham+SNL) and endurance training-spinal nerve ligation (ET+SNL). Training program continued for six weeks, four sessions a week with moderate intensity (70-60% of VO2max). To create the SNL model, the rats were first anesthetized with pentobarbitol sodium and then their fifth lumbar spinal nerve was tightly tied. The duration of the SNL protocol was four weeks. After the last day of ligation, the plantaris muscle was extracted. Real-Time PCR was used to measure the mRNA expression of the MST1 and MAFbx.

The expression of MST1 gene showed no significant increase in ET+SNL group compared with Sham+SNL group (P>0.05). But, significant increase was seen in MAFbx gene expression in ET+SNL group compared with Sham+SNL group (P<0.05).

The study showed that reduced activity in the form of SNL after endurance training can lead to destructive effects on the muscular system and symptoms of muscle atrophy could be seen.

MAFbx and MuRF1 proteins are important factors in the ubiquitin pathway and are responsible for muscle atrophy. The purpose of this study was to investigate the effect of long-term high-intensity interval training (HIIT) on the intracellular content of MAFbx and MuRF1 proteins in the left ventricular of the heart of rats with type 2 diabetes.

In this experimental study, 18 rats 2-month-old male Sprague-Dawley rats with a mean weight of 270±20 g were selected. 12 rats became diabetic by intraperitoneal injection of Streptozotocin and nicotinamide solutions. These rats were randomly divided into 2 groups: diabetic training and diabetic control; A healthy control group was also considered. The training group practiced HIIT 4 days a week for 8 weeks. Data were analyzed using SPSS software version 23 and one-way ANOVA and Tukey post hoc tests.

MAFbx protein content showed a significant decrease after 8 weeks of HIIT (P=0.0001); Tukey post hoc test showed that this change was significant between pairs groups of diabetic training and diabetic control and also between pairs groups of diabetic control and healthy control (P=0.0001). MuRF1 protein content showed a significant decrease (P=0.0001); This was a significant difference between the pairs groups of diabetic training and diabetic control, diabetic training and healthy control groups, as well as diabetic control and healthy control groups (P=0.0001).

HIIT seems to can inhibit the process of atrophy and autophagy of cardiomyocytes by reducing the content of MAFbx and MuRF1 proteins in the hearts of diabetic subjects.

The Ubiquitin pathway is responsible for muscle atrophy; the Atrogin-1 or muscle atrophy F-box (MAFbx) and the muscle Ring-Finger protein-1 (MuRF1) are the important factors in this pathway. This study aimed to investigate the effect of endurance training on the intracellular content of proteins related to the Ubiquitin-Proteasome pathway in the left ventricular tissue of rats with type-2 diabetes. 

In this experimental study, 18 three-month-old male Sprague-Dawley rats with a mean weight of 270±20 grams were selected. Type-2 diabetes was induced in 12 rats by intraperitoneal injection of streptozotocin and nicotinamide solutions. These rats were randomly divided into two diabetic training and diabetic control groups. A healthy control group (six rats in each group) was also considered. The training group did endurance training four days a week according to the training program for eight weeks. Data were analyzed using one-way ANOVA and Tukey post hoc tests via SPSS software version 23.

MAFbx protein content showed a significant change after eight weeks of endurance training (P=0.0001); Tukey's post hoc test showed that this significant change was between pairs of the diabetic training compared with diabetic control (decrease) groups (P=0.0001)  and diabetic training compared with the healthy control (increase) groups (P=0.004). MuRF1 protein content showed a significant decrease (P=0.0001); This reduction was significant between pairs of diabetic training compared with diabetic control groups (P=0.0001).

Endurance training can prevent atrophy and lead to proper left ventricular function by reducing the content of MAFbx and MuRF1 proteins in the heart of diabetic rats.

Protein synthesis and degradation are dynamically regulated processes that to control the accretion or loss of muscle mass. However, the mechanisms responsible exercise-induced heart hypertrophy remains elusive. The aim of this study was to investigate the effect of aerobic training on expression of some indices of myocardial hypertrophy and atrophy in male rats.

In this experimental study, 16 Wistar male rats 10 weeks old with 299.74±19.32 g weight were randomly classified into control and training groups. Training group have performed an aerobic running program (at 10-18 m/min, 10-40 min/day, and 5 days/week) on a motor-driven treadmill for six weeks. At the end of six weeks heart tissue samples were collected and used for determination of gene expression (AMPK, FOXO3, MAFbx and MuRF1). Data were analyzed using Independent t test at p<0.05.

 Six weeks aerobic training significant increases heart AMPK in rats (p=0.014). Also heart FOXO3 (p=0.022), MAFbx (p=0.032) and MuRF1 (p=0.028) was significantly decrease than training group.

Aerobic exercise improves heart structure by improving the parameters that affect cardiac size, possibly improving cardiac function.