Journal of Exercise & Organ Cross Talk

Abstract This study aimed to investigate the interactive effect of aloe vera intake and eight weeks’ aerobic exercise on serum BDNF, glucose, and insulin levels in women with type 2 diabetes. In this experimental study, 32 women with type 2 diabetes were selected and randomly divided into four groups of control, supplement, exercise, exercise + supplement. The exercise program was performed 3 sessions per week for 8 weeks (40 min of exercise with 50-60% of heart rate reserve in the first four weeks and 60 min of exercise with 60-80% of heart rate reserve in the second four weeks). The supplement taking groups received 400 mg/kg of oral aloe Vera 3 days per week for 8 weeks. The data were analyzed using analysis of covariance (ANCOVA). A significant increase was observed in BDNF levels, insulin sensitivity of patients in the supplement, exercise, and exercise + supplement groups (p=0.001). The glucose and insulin levels, insulin resistance, BMI, and body fat percentage significantly decreased in the supplement, exercise, and exercise + supplement groups (p=0.001). It seems aloe Vera intake and aerobic exercise to have protective effects against development of type 2 diabetes complications in women.

Abstract The current study aimed to compare the effect of hypertrophy-, strength-, and power-type resistance exercise in resistance-trained women with considering cortisol and androgen cross talk. After one-repetition maximum (1-RM) estimation, ten resistance-trained women (age: 26.30 ± 4.95 years; body mass index: 22.07 ± 2.02 kg/m2; body fat: 24.64 ± 4.98%) conducted hypertrophy- (70% of 1-RM), strength- (90% of 1-RM), and power-type (45% of 1-RM) resistance exercise for three consecutive weeks. The movements included lever leg extension, reverse-grip lat pull-down, horizontal leg press, standing biceps cable curl, lying leg curl, machines bench press, standing cable triceps extension, and seated calf raises. Fasting blood was taken before and immediately after each trial. Statistical analyses were performed at a significance level of P

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 The COVID-19 epidemic has caused lifestyle changes in people from all walks of life and has become a global threat to the health and well-being of all countries of the world. Considering changes caused by the prevalence of the disease and quarantine conditions, the increased likelihood of the prevalence of overweight and obesity in people is among these threats. On the other hand, patients with overweight and obesity, and consequently, non-alcoholic fatty liver disease (NAFLD) have a weaker immune system than other people with ideal weight, and as a result, are more likely to develop COVID-19. As there is currently no definitive treatment for COVID-19 and NAFLD, and because people with NAFLD are more likely to develop COVID-19 based on the research in this area, paying attention to this important issue is thus necessary. Considering a regular physical activity program and having a balanced diet are among the essential strategies and may help prevent NAFLD, and consequently, COVID-19. However, given the novelty of COVID-19 pathogen and the ambiguity of the exact cause of why people get NAFLD, further research is needed to be done on the type of effective diet, as well as the type, intensity, and volume of exercise for these people. This study aimed to summarize the available evidence on the pathology and epidemiology of NAFLDs and COVID-19, as well as the effect of NAFLD on COVID-19 in people. Given the existing risks, the nutrition and exercise strategies were investigated in this regard.
 

Abstract Dear Editor-in-Chief
Physical exercises decrement a network of diseases risk, and exercise may be suggested as medicine for lifestyle-related risk factors like insulin resistance, obesity, type 2 diabetes mellitus, dementia, cardiovascular diseases, and cancer. Recently, it has increasingly been approved that bone cooperates with several tissues and impacts several metabolic pathways in both animal and human models. The manner in which bone and muscle cross communicate and how they influence glucose homeostasis depends on osteocalcin (OCN)—an osteoblast-specific protein. OCN is a principally bone-derived hormone that exists in the circulation in carboxylated, undercarboxylated, and uncarboxylated forms. Because it was demonstrated that the un- or undercarboxylated forms (ucOCN) enhanced insulin sensitivity and secretion through direct impacts on the pancreatic beta-cell, it has been the center of most study (Kirk, Feehan, Lombardi, & Duque, 2020; Mohammad Rahimi, Bijeh, & Rashidlamir, 2020; Mohammad Rahimi, Niyazi, & Alaee, 2020).
Several clinical research has displayed that ucOCN rises following exercise training, and this has been connected to some metabolic effects with the overall effect of enhancing insulin secretion and sensitivity, and in glucose uptake (Kirk et al., 2020; Mohammad Rahimi, Niyazi, et al., 2020). Direct binding has never been seen; nevertheless, it has been suggested the G protein-coupled receptor family C group 6 member A (GPRC6A) as the putative receptor for ucOCN in both models and computational modelling. UcOCN, in muscle, results in an insulin-dependent enhance in glucose uptake after muscle contraction in animal models, with an alongside rising in GPRC6A. Moreover, from a more practical view, ucOCN has been involved in muscle hypertrophy and strength. In this regard, OCN-deficient mice have been shown to have lower muscle mass; inversely, improved muscle mass was found in older mice with ucOCN administrations. Recent data has figured out a novel mechanism of bone-muscle crosstalk in relation to OCN and IL6 signaling (Kirk et al., 2020).
After observing meaningful increments in both muscle-derived IL-6 and ucOCN following endurance training, it was observed that these alterations are dependent on one another. Mice with IL-6 deletions did not display the typical rise in OCN after exercise, showing that chemokine was needed for this crosstalk (Kirk et al., 2020). This influence was adjusted via the application of injected IL6, presenting strong evidence for the underlying mechanisms. As addressed above, it was demonstrated that the bone impacts of IL-6 happen through osteoblast signaling, with a resultant increment in receptor activator of nuclear factor kappa-Β ligand (RANKL) expression and osteoclastogenesis, and it seems that muscle performance advantages of IL-6 are mediated through the skeleton. While IL-6-deficient mice have been frequently demonstrated to have endangered muscle response to exercise training, mice lacking the IL-6R in myofibers did not suffer from the deficit. Alternatively, mice lacking IL-6R in osteoblasts mimicked the impact of total IL-6 deficiency, revealing that OCN was a mediator of the muscle response to the chemokine. Eventually, this mechanism was demonstrated to underpin the influences of OCN on muscle by enhancing glucose uptake and metabolism (Kirk et al., 2020).
Cross-sectional human investigations have suggested that resistance training leads to an increment in ucOCN, alongside a reduction in HbA1c, insulin resistance, and circulating glucose level as well as quadriceps strength (Levinger et al., 2014; Mohammad Rahimi, Niyazi, et al., 2020). This exercise-induced elevation in OCN has also been revealed to rely on IL6 secretion from muscle. The utilize of the IL6 antibody-drug tocilizumab resulted in an almost complete deletion of the exercise-mediated raise in OCN following an endurance training program, demonstrating that the associations found in rodent research also translate to human (Kirk et al., 2020). Notwithstanding these relationships, no interventional trials have presented causative evidence in vivo for the impacts of ucOCN on muscle metabolism or function.
It is acknowledged that when OCN is released to the circulation it becomes a mediator that stimulates pancreatic beta-cell proliferation and insulin secretion; on the other hand, it also increments the expression of peroxisome proliferator-activated receptor 𝛾 (PPAR-𝛾) and adiponectin in fat cells. The signaling cascade responsible for the influence on ucOCN is explained by crosstalk among cAMP–protein kinase A and extracellular signal-regulated kinase pathways through activation of Ras-proximate-1 (Rap1). The signaling of ucOCN in adipocytes in vivo leads to a reduction in the size of the adipocyte, which probably contributes to insulin sensitivity enhancement and glucose tolerance improvement via the up-regulation of the expression of adiponectin (Mohammad Rahimi, Niyazi, et al., 2020). Besides, ucOCN might has a direct role in enhancing skeletal muscle translocation of glucose transporters (GLUT-4) and has the capability to consume more glucose. Nevertheless, in order to examine these mechanisms, additional research is required. The metabolic impact of insulin may be bone-mediated via the release and decarboxylation of OCN. Taken together, these actions demonstrate a positive feedback mechanism between pancreatic beta-cells/adipose tissue/bone and the insulin increase of ucOCN production, which, in turn, increases insulin production and sensitivity (Ferron, Hinoi, Karsenty, & Ducy, 2008).

Abstract Dear Editor-in-Chief
Coronaviruses are a very large family of viruses that are phenotypically and genetically diverse and are common in humans and animals. The Prevalence of Coronavirus disease 2019 (COVID-19) began in Wuhan, China. As of 17 March 2020, extensive human-to-human transmission mainly occurs via the respiratory particles of the infected person.  Among COVID-19 cases, it seems that new pandemic complications are already well-defined in obese and overweight people with body mass indexes (BMI) over 25 kg/m2 or even higher that contribute to increased risk of SARS-CoV-2 infection. The higher BMI in COVID-19 patients, the higher risk of medical complications, hospitalization in the intensive care unit (ICU), and invasive mechanical ventilation (IMV) (Földi et al., 2020). However, BMI does not show the distribution of body fat, and therefore research results cannot show the effect of excess fat in different parts of the body on the severity of COVID-19. In confirmation of this finding, it can be said that although the ratio of total body fat in women is higher than men on average, the incidence of COVID-19 is higher in men (Simonnet et al., 2020).
The possible critical mechanism by which adipose tissue accumulation increases the risk of COVID-19 in patients is unknown. However, fatty tissue may serve as a reservoir for viral production that might contribute to the increased risk from COVID-19 for patients with obesity. It is suggested that fatty tissue is targeted by SARS-CoV-2. The mechanism by which SARS-CoV-2 enters cells is not fully elucidated. But apart from a direct fusion of the virus with the plasma membrane, it appears that various types of endocytosis might be involved in this process. These lipid membrane trafficking events include clathrin-mediated endocytosis, caveolin- mediated involved in muscle hypertrophy and strength. In this regard, OCN-deficient mice have been shown to have lower muscle mass; inversely, improved muscle mass was found in older mice with ucOCN administrations. Recent data has figured out a novel mechanism of bone-muscle crosstalk in relation to OCN and IL6 signaling (Kirk et al., 2020).
Endocytosis, macropinocytosis, and phagocytosis. Caveolin-mediated endocytosis is especially interesting to study as caveolae are abundant in fat cells, caveolins participate in fatty tissue function because caveolin was shown to interact with various viral proteins. In addition, the increased number of fat cells would increase the pool of infection susceptible cells. Fatty tissue contains not only fat cells but cells of stromal vascular fraction among which adipocyte precursors and macrophages. These cells also express ACE2 and display a potential target of SARS-Cov-2 infection and thus may contribute to increased inflammatory status (Dugail, Amri, & Vitale, 2020). Another possibility is that fatty tissue droplets could provide a platform for virus replication and production. Concerning the hypothesis that fatty tissue is an infection place for the SARS-CoV-2 virus, it has not yet been established if viral loads are proportional to fatty tissue mass in patients. The ACE2 activity leading to increased levels of angiotensin II and so increased inflammation and lung damage. It seems that fat cells play a substantial role in viral infection and the viral life cycle. Adipose tissue is directly involved in contact with the viral membrane of the host cell. For example, fats are critical to the formation and function of the viral replication complex and can provide some of the energy required for viral replication. In addition, specific fats are needed for the formation of double-membrane vesicles for viral genome amplification and the production of viral particles. Viral internalization can occur with endocytosis and viral release from cells. It is possible that fat availability and fats metabolism modifications occurring in an obese patient also contribute to improving several stages of the virus's life cycle and severity of the disease (Dugail et al., 2020).
In this regard, any approach should consider reducing the costs of intensive care units to reduce the mortality of patients. Especially with concerning increase their number and people at higher risk in obese people. Moderate-intensity exercise can directly boost the immune system, antioxidant defenses, and anti-inflammatory responses Adipose tissue molecular adaptation always was considered as one of the mechanisms for the anti-inflammatory effects of physical exercise. Aerobic exercise is a physical activity that is moderate-intensity and does not put much pressure on the body. Regular exercise has been shown to improve infection, antibacterial and antiviral immunity, reduce inflammation, and delay immune aging (Campbell & Turner, 2018). Following the moderate-intensity physical activity, an increase in the number of neutrophils and natural killer (NK) cells is detected, and salivary IgA concentrations increase (Brolinson & Elliott, 2007). During physical exercise, rapid and general mobilization of NK cells into the bloodstream is induced by adrenergic B signaling and catecholamines. It is suggested that mobilized NK cells are affected by muscle-derived myokines, exercise-related hyperthermia, and coronary arteries, which are affected by regulation, redistribution, and activation of mobilized NK cells (Brolinson & Elliott, 2007). Moreover, adipocytes play a critical role in NK cell activations. Adipose tissue may respond to the activation of NK cells during exercise in a cross-talk with the immune system.
Moderate exercise was exercise is one of the mechanisms in NK cell activation following physical exercise.  The results show a 20 to 30 percent reduction in upper respiratory tract infections in people who do moderate-intensity of physical activity in their daily lives (Brolinson & Elliott, 2007). Therefore, it can be said that moderate-intensity training can be an effective way to boosting the immune system. Possible cross-talk between fat and immune tissues was approved in some other studies. It is suggested that some exercise factors such as IL-6 and Hsp70 can be effective in the possible cross-talk between the immune system and fat tissue. Molecular and structural changes in adipose tissue following physical exercise can be effective in improving immune responses.
Fatty tissue is probably targeted by the SARS-CoV-2 virus, which causes adipose tissue dysfunction. Accumulation of fat tissue also serves as a platform for replication and production of virus. Based on the evidence, it seems that exercise activities, especially combined exercise training, reduce fat mass in obese or overweight people, reduce the risk of COVID-19, as well as the risk of severity and side effects in patients. Possible cross-talks between the immune system and adipose tissue could be one of the possible mechanisms in boosting immune responses against the virus.
 

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.