Journal of Exercise & Organ Cross Talk

Abstract This study examined the acute hormonal and myokine responses to traditional and circuit resistance training in young males with distinct BMI-based groups. Twenty sedentary men aged 20–30 years were classified as high-BMI (BMI >29.9) or low-BMI (BMI <18.5). Each participant completed both traditional resistance training (TRT) and circuit resistance training (CRT) protocols in a crossover design, with a one-week washout period. Sessions included multi-joint upper and lower body exercises at comparable intensities. Blood samples were taken immediately before and after each session. Serum levels of testosterone, cortisol, myostatin, and follistatin were assessed using ELISA kits. A repeated-measures ANOVA was used to compare within- and between-group changes across time and training modality. Baseline cortisol levels were significantly higher in low-BMI individuals (P=0.037), while testosterone levels showed no initial difference between groups (P>0.05). Post-TRT, testosterone levels increased significantly in high-BMI individuals compared to low-BMI individuals (P=0.017), with both training types elevating testosterone and cortisol across all participants (P<0.05). CRT led to a significant reduction in myostatin and increase in follistatin in high-BMI individuals (P<0.05), while only follistatin increased significantly in low-BMI individuals after TRT (P<0.05). These results suggest that CRT promotes superior anabolic signaling in high-BMI individuals, while TRT is more effective at enhancing testosterone response. Myokine and hormonal responses appear to be body-type-dependent and training-modality-specific. Practitioners designing hypertrophy-focused programs should tailor training protocols to the athlete’s BMI-based group to optimize muscle adaptation and endocrine outcomes. And also, trainers should individualize hypertrophy programs based on body composition to optimize both hormonal responses and muscle adaptation.

Abstract Skeletal muscle functions as an endocrine organ by releasing myokines—cytokines and peptides that mediate systemic physiological adaptations. This review synthesizes evidence establishing mechanical stretching (active/passive) as a potent mechanotransductive stimulus for myokine secretion. Key pathways include integrin-mediated signaling, stretch-activated ion channels (Piezo/TRP), and mechanosensitive transcriptional regulators (YAP/TAZ), which activate MAPK, calcium-dependent kinases, and other cascades to modulate myokine gene expression. We highlight stretch-responsive myokines (IL-6, irisin, myostatin, BDNF, SPARC) and their roles in metabolism, tissue repair, and inflammation. Clinical implications for aging, metabolic disease, and rehabilitation are discussed, emphasizing how targeted stretching protocols may harness myokine-mediated benefits in mobility-limited populations. Future research directions include optimizing stretch "dosing" and elucidating tissue-specific myokine actions.

Abstract The study aimed to compare the acute effects of low resistance exercises with partial and complete blood flow restriction (BFR) and heavy resistance exercise on growth hormone (GH), myostatin, testosterone, and cortisol in competitive wrestlers. Forty elite wrestlers were randomly divided into four groups (n=10); low resistance training with complete BFR (LRT+CBFR), low resistance training with partial BFR (LRT+PBFR), low resistance training (LRT), and heavy resistance training (HRT). Blood samples were collected before and after the intervention, and a specific ELISA kit measured variables. Analysis of covariance and paired t-test was performed to analyze the data. There were no significant differences in the variables between the four interventions. Intra-group results showed a significant decrease in myostatin levels in the HRT group (p=0.02), and a significant increase in GH in the LRT+CBFR (p=0.02) and LRT+PBFR (p=0.03), testosterone in the HRT group (p=0.04) and cortisol in the three groups LRT+CBFR (p=0.02), LRT+PBFR (p=0.01) and HRT (p=0.04). Despite the similarity of the changes in the four interventions, due to the percentage of changes, it seems that low resistance training with BFR could produce similar anabolic effects to high-intensity resistance training.

Abstract Dear Editor-in-Chief
Different types of exercise training with increasing muscle contraction can stimulate muscle secretome called myokines. Myokines are the main mediators of maintaining muscle structure and function in manner of autocrine and paracrine. These myokines can both affect distant tissues and have positive effects on muscle tissue itself (Chen, Wang, You, & Shan, 2021). In various diseases leading to muscle wasting, it seems that exercise and increased contraction can reduce the rate of muscle wasting and muscle atrophy by regulating myokines. Myostatin is a myokine that negatively regulates skeletal muscle development. In animal models, myostatin degradation has been shown to increase muscle mass and inhibit myostatin signals which can control the loss of muscle mass due to cancer cachexia (X. Zhou et al., 2010). Zhou et al. (2021) showed that exercise training (strength or balance in combination with endurance training) seems to be effective in preventing sarcopenia and maintaining muscle mass in non-dialysis-dependent patients with chronic kidney disease (CKD) with inhibition of myostatin signaling (Y. Zhou, Hellberg, Hellmark, Höglund, & Clyne, 2021).
Apelin is another myokine that decreases in age-dependent manner (Vinel et al., 2018). Apelin signaling in aging helps to increase muscle function by stimulating mitochondrial biogenesis and anti-inflammatory pathways in myofibers and improving regenerative capacity by targeting muscle stem cells (Vinel et al., 2018). It has been shown that exercise can positively regulate the Apelin and improve muscle growth. Apelin, an exerkine, is elevated due to maternal exercise, and maternal apelin administration mirrors the effect of maternal exercise on mitochondrial biogenesis in fetal muscle (Son et al., 2020). In other words, Apelin inhibits skeletal muscle dysfunction.
Leukemia inhibitory factor (LIF) is primarily expressed at low levels in type 1 muscle fibers. LIF has been shown to affect the growth and regeneration of skeletal muscle. For example, the expression of LIF protein in rat plantaris muscle is increased by mechanical load (Sakuma et al., 1998). Furthermore, LIF stimulates the hypertrophic response to increased load in the animal model, and in this respect LIF has been shown to be an important factor in skeletal muscle hypertrophy. In addition, LIF mRNA increases in human skeletal muscle following muscle damage leading to better repair. Therefore, this factor secreted by skeletal muscle can increase in various injuries and diseases with exercise and controls muscle wasting. Irisin is one of the most important muscle myokines that is secreted from muscle tissue through exercise and has auto and paracrine effects. It was shown that the injection of irisin induced muscle hypertrophy, improved muscle strength and reduced necrosis and development of connective tissue in a murine model (Reza et al., 2017). Therefore, increasing this factor with exercise can counteract cachexia and atrophy.
Musclin is an exercise-responsive myokine associated with plasma atrial NP (ANP) and cyclic guanosine monophosphate (cGMP) and the expression of the peroxisome proliferator-activated receptor γ coactivator 1-α (PGC1-α) expression in skeletal muscle after exercise training (Subbotina et al., 2015). Musclin helps increase exercise capacity by increasing mitochondrial biogenesis in mice (Subbotina et al., 2015). In addition to its role in exercise, Musclin reduces muscle tissue damage during the development of cachexia-induced tumors and has beneficial effects on cancer patients at risk for cachexia (Re Cecconi et al., 2019). C - X - C motif chemokine ligand 12 (CXCL12) is another type of myokine that is involved in the growth of skeletal muscle. CXCL12 helps proliferate myogenic and angiogenic somite progenitor cells and controls myotoma formation (Abduelmula et al., 2016). Moreover, it has been shown that the concentration of plasma CXCL12 is enhanced in response to training on a bicycle ergometer (Wang, Lee, Lien, & Weng, 2014). Overall, muscle - muscle crosstalk with several myokines mediates the beneficial effects of exercise training, including regulating muscle growth, preventing muscle loss, and increasing muscle function and regeneration, and these factors can decrease muscle wasting diseases.