Journal of Exercise & Organ Cross Talk

Abstract The aim of this study was to considering the correlation between the muscle fibronectin type III domain-containing protein 5 (FNDC5), blood and heart level of Irisin in exercise-trained rats with Nano selenium supplementation after intraperitoneal injection of cigarette smoke extract induced chronic obstructive pulmonary disease (COPD). To this end, 49 male Wistar rats (8 weeks old) were divided into seven groups: control, SeNPs (2.5 mg/kg b.w by oral gavage, 3 days/week, 6 weeks), AIT (49 min/day, 5 days/week for 6 weeks, interval), SeNPs+AIT, CSE (150 µL by IP injection, 1 day/week for 6 weeks), CSE+AIT, and CSE+SeNPs+AIT. The results of the present study showed that CSE injection caused inflammation and damage to lung tissue, especially alveoli, compared to the healthy group. In other words, based on the histological examination of cigarette smoke extract, it was able to cause lung tissue damage similar to COPD, and doing exercise and taking nanoselenium antioxidant supplement could control these lung tissue damage. Pearson's correlation method was used to investigate the relationship between muscle FNDC5, serum and heart Irisin, and the results of this correlation were not significant in different groups (p>0.05). It seems that exercising and taking nanoselenium supplements can increase Irisin levels in serum and heart tissue by expanding muscle contraction and increasing muscle FNDC5. However, the relationship of this factor in muscle and heart crosstalk should be investigated more closely.

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 Dear Editor-in-Chief
Active lymphocytes under a burst during proliferation, biosynthesis, and secretory activity increase their metabolism. In order to achieve this dramatic increase in metabolism, they must obtain a metabolic substrate. Their insignificant nutrient stores force lymphocytes to have a significant increase in the consumption of the metabolic substrate around them. Although lymphocytes are able to utilize glucose, glutamine, ketones, and fatty acids, it has been confirmed that glucose and glutamine are the most important quantitative fuels for activated lymphocytes (Curi et al., 1999). The function of T cells is closely related to the metabolic program, meaning that a T cell fights antigens, invasive agents, and inhibits infection until the main fuels of this cell, glucose and glutamine, are consumed and metabolized in sufficient quantities. There are significant and growing techniques that target the metabolism of T cells for immunotherapy.
Degradation of lymphocyte metabolism and function has been observed in various inflammatory, metabolic and autoimmune diseases. Maximum activity and levels of HK, G6PDH, CS, GLUTase enzymes of lymphocytes are always reduced for patients with Graves (Werner et al., 1996). In vitro, it has been shown that thyroid hormone increases glucose and glutamine lymphocyte metabolism in these patients. Also, it has been reported to coexist with acute and chronic infection in several diseases such as cancer or asthma, and gradation of T1 and T2 metabolism (Zhao et al., 2012).
It has been suggested that a part of the safety effects of exercise is due to the ability of exercise to modulate lymphocyte cell metabolism, especially glucose and glutamine. It has also been observed that changes in lymphocyte function are associated with different effects of moderate exercise on T and B lymphocyte metabolism. In addition, T lymphocytes increase glutamine intake by altering the metabolism of this amino acid to the aerobic pathway. At the same time, these cells reduce glucose intake and lactate production levels. In contrast, B lymphocytes were shown to increase intake of both glucose and glutamine, while aerobic metabolism of glutamine increased (Navarro et al., 2013). All of these changes in lymphocytes are possible because key enzymes in glucose and glutamine metabolism are affected by chronic exercise. Thus, as the aerobic metabolism of glutamine increases, the maximum activity of GLUTase and CS in T lymphocytes increases in response to exercise. In addition to these two enzymes, maximal activity of HK and G6PDH increased in B lymphocytes in response to chronic exercise (Navarro et al., 2013). Most of these studies have examined the immune system and T lymphocyte response to exercise with moderate intensity. High intensity interval training (HIIT) usually consists of intermittent sets of exercise (Vo2max usually equal to or greater than 90%) accompanied by few minutes of active rest. Little is known about inflammatory and metabolic immune responses after HIIT.
Moderate-intensity exercise stimulates the immune system and increases resistance to infectious diseases. However, during prolonged and intense exercise or strenuous exercise and competition, an immune suppression often occurs during the recovery period. Immune responses after exercise are almost similar to those seen in infection and inflammation (e.g., neutrophilia and lymphocytopenia) (Tauler et al., 2006). Researchers have suggested that intense exercise induces these changes with oxidative stress, changes in neuroendocrine factors such as catecholamines, growth hormone, and cortisol (Fisher et al., 2011). Therefore, it is suggested that low-intensity, high-frequency, long-term exercise be effective in improving the lymphocyte metabolic crossover.

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.