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 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.