Journal of Exercise & Organ Cross Talk

Abstract Aging is associated with mitochondrial dysfunction, which leads to decreased cellular function and the development of age-related diseases. Exercise training is considered one of the most effective strategies for improving muscle cell function. The aim of the present study was to investigate the effect of six-week combined exercise on mitochondrial dynamics and biogenesis markers (MFN1, DRP1) as well as oxidative stress markers (MDA and SOD) in fast- and slow-twitch muscles of aged rats. In this study, 16 male Wistar rats (463.2 ± 9.3 g) were randomly divided into two groups (n=8 per group): control and resistance-endurance training. The training group underwent combined resistance-endurance training, 6 days a week for 6 weeks (3 resistance days, 3 endurance days). Forty-eight hours after the last training session, animals were sacrificed and fast-twitch (gastrocnemius) and slow-twitch (soleus) muscle tissues were collected. Gene expression levels of mitofusin 1 (MFN1), dynamin-related protein 1 (DRP1) were measured by real-time PCR (RT-PCR). In slow-twitch muscle, exercise training significantly increased mRNA expression levels of SOD genes, and significantly decreased mRNA expression of DRP1 and the concentration of MDA compared to the control group (p<0.05). Similarly, in fast-twitch muscle, six weeks of combined training significantly increased SOD gene expressions and decreased DRP1 mRNA and MDA levels compared to controls (p<0.05). Combined exercise training positively modulates mitochondrial biogenesis and dynamics markers (decreased DRP1 mRNA) and enhances antioxidant capacity (increased SOD gene expression and enzyme activity, decreased MDA levels) in both fast- and slow-twitch muscles of aged rats, highlighting its significant role in mitigating age-associated mitochondrial dysfunction. These findings reflect improvements in markers of mitochondrial quality control and oxidative stress rather than direct measurements of mitochondrial function.

Abstract We investigate the effect of exercise training in different stages of growth on protein synthesis (4E-BP1) and proliferation of heart cells (S6K1) in male rats. 30 male Wistar rats were prepared in three age groups of 2 weeks, 8 weeks, and 90 weeks (10 in each group), and each age group was divided into two control and training groups (5 in each group). In the exercise training group, the animals performed the resistance and aerobic training program every day (interval). The amount of overload for the resistance-training program was determined based on the body weight of the animals. For the aerobic training group, the training intensity increased from 50% of maximum speed in the first week to 80% in the last week. The results showed that there is no significant difference between the control and training groups in each age, as well as between the training groups in the three age (p>0.05). In contrast, the 2-week exercise groups (p=0.022) showed a significant increase and the 90 weeks control group (p=0.002) showed a significant decrease in S6K1 protein in cardiac tissue compared to the 2-week control groups. In the analysis of gene expression, it was also found that the 2-week training group showed a significant increase in S6K1 gene expression compared to the 2-week control group (p=0.018). It seems that doing combined exercise at different ages, especially childhood, has a greater effect on the proliferation index of heart cells (S6K1). However, studies with longer training durations should also be considered.

Abstract The purpose of this study was to determining the range of aerobic exercise on a treadmill for male Wistar rats at different ages. Twelve male Wistar rats were divide in three groups of immature, adults, and old (n= 4 in each). At first session, the rats began to run at a rate of 2 m/min to perform the fatigue test, and the treadmill speed was increased by 2 m/min every 2 minutes. This process of acceleration continued until the rats were no longer able to continue moving on the treadmill and became exhausted. Then, blood lactate of each subject measured immediately and their maximum speed was recorded. After 48 hours of recovery, animal performed maximum recorded speed on a treadmill in three 10-minute steps of 25%, 50% and 75%, respectively. Immediately after each percent blood lactate were measured and recorded. Immature rats at an average speed of 18 m/min were reached to their maximum speed with an average lactate concentration of 8±1.8 mmol/l. Adults rats at an average speed of 36 m/min were reached to their maximum speed with an average lactate concentration of 6.8±0.4 mmol/l. The old rats reached their maximum velocity with an average of 30 m/min with an average lactate concentration of 6.95±0.9 mmol/l. Therefore, it recommended that aerobic exercise in untrained rats start at a light speed, i.e. 25% of their maximum speed, which is lower than the lactate threshold, and gradually continue up to 50% of their maximum speed.

Abstract Puberty with interactive growth in tissues is a sensitive period in life that can be more affected by obesity. Also the increase of leptin and insulin resistant independent of obesity have been seen in puberty. The aim of our study was to investigate the role of puberty on changes in leptin, testosterone, and insulin resistance in sedentary obese boy with considering possible crosstalk between leptin and insulin resistance. 58 sedentary obese boys (14.10 + 1.37 years) participated in this study. Tanner stage scales were used to measure puberty by self-reporting. Initially anthropometric characteristics and then, fasting serum’s glucose, insulin, leptin and testosterone, were measured. With increasing mature from TS2 to TS5, the increasing of testosterone, body mass and lean body mass and the reduction of body fat percentage were significantly (p≤0.05). but the changes in leptin and HOMA-IR were not significant. However, the decreased leptin after adjusting for BMI between TS3 and TS4 were significant (p≤0.05). During puberty, rapid growth in muscle tissue were associated with decreased body fat percent, serum leptin and insulin resistance. Among the possible reasons is a 15-fold increase in serum testosterone from TS2 to TS5. These changes reflect the cross talk between muscle and adipose tissue by hormonal mediators.