Journal of Exercise & Organ Cross Talk

Abstract Skeletal muscle functions as an endocrine organ, secreting myokines that mediate crosstalk with organs like the brain, liver, adipose tissue, and vascular system, influencing metabolism, inflammation, and disease progression. Advances in artificial intelligence (AI) are revolutionizing our ability to decode these complex interactions by predicting novel myokines, modeling signaling networks, and identifying therapeutic targets. Exercise training plays a pivotal role in modulating myokine expression, with both aerobic and resistance exercise inducing small to large increases in circulating myokines immediately to 60 minutes post-exercise, though levels typically return to baseline within hours. Different exercise modalities (resistance, aerobic, concurrent, high intensity interval training) stimulate distinct myokine profiles. These exercise-induced myokines contribute to improved metabolic regulation, muscle regeneration, and systemic health benefits, underscoring the therapeutic potential of tailored exercise interventions mediated through myokine signaling networks. This review explores how machine learning and network analysis tools bridge gaps in understanding myokine dynamics, particularly in exercise-induced contexts and pathologies such as obesity, cancer, and neurodegeneration. By integrating multi-omics data, AI-driven approaches offer unprecedented insights into myokine-mediated organ communication and their potential as biomarkers or treatments.

Abstract Air pollution is one of the most important problems of recent decades, which has serious toxic effects on human health and the environment. Sources of pollution vary from small units of cigarettes and natural sources such as volcanic activity to large volumes of emissions from car engines and industrial activities or even radioactive ones. Today, there are various pollutants around the world that negatively affect human health. Walking and being in a polluted environment can increase the penetration of pollutants such as lead in the body. Increasing physical activity such as long-term running, which is widely used in some jobs such as military jobs, can increase the activity of muscle tissue, and as a result, the cardiovascular system becomes more active and helps absorb more pollutants. Lead acetate is a possible carcinogen in humans, which is absorbed into the human body by pollutants. There is evidence that lead compounds can cause lung, brain, stomach, and kidney cancer in humans. However, pollution does not include air pollution only, and noise pollution can endanger human health as well. Since some occupations such as those of military experience various types of noise, as well as chemical and radioactive pollution and the point that having high physical fitness is essential for these people, this study examined the impact of various pollutants on the military personnel and also sought to see whether exercising and having high physical fitness of military personnel can reduce the stress caused by the pollution.

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 Dear Editor-in-Chief
The chemokines are a superfamily of small, secreted proteins that regulate leukocyte migration. Several of these chemokines have been associated with various diseases. Some chemokines have been reported to be expressed in the lung, including interleukin (IL)-8/CXCL8, eotaxin/CCL11, macrophage-inflammatory protein (MIP)-3α/CCL20, and DC-CK1/pulmonary- and activation-related chemokine (PARC)/alternative macrophage activation-associated CC-chemokine (AMAC)-1/CCL18 (Homey et al., 2000). It is interesting that there is even one reported chemokine that is specifically expressed in the lung, lungkine/CXCL15 (Rossi et al., 1999). Lungkine is an important mediator of neutrophil migration from the lung parenchyma into the airspace.
Chemokine CXCL15, which absorbs neutrophils during pulmonary inflammation, is also known as lungkine because of its reported exclusive expression in the lung. CXCL15, previously reported as the only lung-specific chemokine, is also highly expressed in other mucosal organs and endocrine glands of mice. The functional role of CXCL15 is unclear with precise exercise training, and little research has addressed this issue. Files et al. (2015) evaluated the effects of therapeutic exercise on lung disease and also measured CXCL15 levels (Files et al., 2015). In this study, although CXCL15 was down regulated in response to exercise therapy, they stated that exercise therapy improved both alveolar neutrophil lung damage and skeletal muscle atrophy in the animal model of ARDS. They stated that more studies are needed to identified mechanisms underlying exercise and its benefits in the lungs, which may indicate new molecular targets for the treatment of ARDS.
Clinical and experimental studies have shown that regular aerobic exercise can prevent or even eliminate a number of diseases, especially in patients in the intensive care unit. This beneficial effect of exercise is associated with anti-inflammatory and antioxidant protection. Despite the apparent benefits, the dose of exercise intensity is still unknown. Balducci et al. (Balducci et al., 2010), showed that people with type 2 diabetes who performed intense exercise had a significant improvement in their inflammatory status. High-intensity exercise reduced pneumonia and improved oxidative status in experimental models of allergic pneumonia and exposure to contaminants (Ávila et al., 2015). Due to the mechanism involved in changes in epithelial pathogenesis, strenuous exercise with hyperventilation can affect the airway epithelium by altering the viscosity, elastic force, or amount of airway fluid. In an animal model trained with an intense exercise protocol, an increase in the infiltration of leukocytes into the bronchial wall was observed (Chimenti et al., 2007). Therefore, it is believed that performing intense exercise may cause inflammatory cells to invade the airways, epithelial changes, and defective remodeling. However, studies in this area are also contradictory. In a study high-intensity swimming showed a protective effect on ALI, decreasing inflammatory processes and preventing disturbances in antioxidant defenses into the lungs (Cardoso et al., 2018). However, little is known about the possible protective effects of HIIT on lungkine CXCL15 and its mechanisms of action.

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.

Abstract COPD is an inflammatory disorder caused by prolonged inhalation of harmful substances such as cigarette smoke that leads to an irreversible respiratory disorder. Airway obstruction usually has a progressive period characterized by chronic cough, sputum production, and dyspnea, resulting in decreased physical activity. Two hypotheses have been proposed for the pathogenesis of lung diseases, especially COPD, including the oxidant-antioxidant imbalance hypothesis and the protease-antioxidant imbalance hypothesis. Oxidants can cause irreversible damage to lung cells. Oxidants activate inflammatory gene expression primarily through NFκB signaling. Increase inflammation promotes apoptosis in the epithelial cells, endothelial cells, and airways, that resulting Emphysema. This pathological period causes progress the disease. Recently, has been shown that decreased physical activity is associated with COPD injuries, and the level of physical activity is most associated with COPD mortality. Therefore, the tendency to maintain and improve the physical activity of pulmonary patients, especially COPD was increased. In lung diseases, muscle mass usually decreases and severe atrophy occurs. Most studies suggest increased mobility and exercise to enhance cardiorespiratory endurance and decrease atrophy. However, the exact biological mechanism for the recovery of patients with COPD after a physical activity has not been explained. Exercise can produce Irisin and Semaphorin-3A by stimulating muscle and nerve cell, which have positive effects on other tissues, including the lungs. Limited studies have examined the role of these factors in lung tissue. Therefore, in this mini-review, the lung muscle cross-talk is examined by evaluating the role of Irisin and Semaphorin-3A.

Abstract PH stress can be caused by menopause, poor nutrition, high protein intake, old age, prolonged strenuous and anaerobic exercise, anemia, diabetes, AIDS, and respiratory diseases. High calcium enters the bloodstream from the bones during the proton buffering due to metabolic acidosis, which the renal system excretes a significant amount of this calcium to eliminate the acidosis condition and regulate body pH. At the bone surface, this increase in hydrogen ions due to metabolic acidosis can destroy osteoblastic and strengthen osteoclast activity, which negative bone turnover and increases the amount of excreted calcium, thus accelerating the progress of osteoporosis. Due to the widespread prevalence of osteoporosis in postmenopausal women and the provision of various therapies such as medication, estrogen therapy, and proper diet, in recent studies, special attention has been paid to the role of endurance and resistance exercise to decrease osteoporosis or prevent the development of this disease. Also exercise training increases irisin secretion from muscle tissue, which this myokine has beneficial effects on other tissues especially on bone. Irisin increases osteocytic survival and production of sclerostin in bone tissue, which is associated with bone remodeling. However, exercise training in some intensity through metabolic mechanisms can increase pH stress and acidosis and may contribute to the development of osteoporosis in postmenopausal women.  As a result, the hypothesis of different intensities of exercise and their induced acidosis stimuli in postmenopausal women should be considered.