Physical exercise, inflammatory process and adaptive condition: an overview <s> TIssUe TRAUmA AND INflAmmATORy ResPONse <s> Natural killer (NK) cells are highly influenced by physical exercise. The possible important mechanisms behind exercise-induced changes in NK cell function are cytokines, hyperthermia, and stress hormones, including catecholamines, growth hormone, cortisol, and beta-endorphins. Infusion studies mimicking stress hormone levels in blood during exercise indicate that increased plasma-adrenaline accounts for at least part of the exercise-induced modulation of NK cell function. During moderate as well as severe acute exercise, the NK cell activity is enhanced, but severe exercise is followed by immunodepression, at least in part caused by prostaglandins. Elite athletes have at rest elevated NK cell activity. However, due to frequent severe exercise the NK cell function is often temporarily severely depressed. It is suggested that during the time of immunodepression microorganisms, especially virus, invade the host, whereby infections can be established. However, in those who perform regular moderate exercise the immune system will often be temporarily enhanced and this will protect these from infections. <s> BIB001 </s> Physical exercise, inflammatory process and adaptive condition: an overview <s> TIssUe TRAUmA AND INflAmmATORy ResPONse <s> In the recovery phase after intense exercise is found suppressed blood concentration of lymphocytes, suppressed natural immunity of blood lymphocytes, decreased concentration of secretory IgA in mucosa, but increased blood concentration of neutrophils and increased levels in the blood of inflammatory cytokines. Thus, after intense long-term exercise, the immune system is characterized by concomitant inflammation and temporary suppression of the cellular immune system, the most pronounced findings being 2-4 h after the exercise. The underlying mechanisms are multifactorial and include neuroendocrinological and metabolic factors. High levels of cytokines, especially interleukin-6, are found in the recovery period after eccentric exercise, and it has been demonstrated that a close association exists between muscle damage and increased levels of interleukin-6. <s> BIB002 </s> Physical exercise, inflammatory process and adaptive condition: an overview <s> TIssUe TRAUmA AND INflAmmATORy ResPONse <s> PURPOSE ::: In recent years, health professionals have placed increased attention on the benefits of physical activity for maintaining health in the general population as well as regaining health in many disease states. Conversely, reports of apparent decreases in immune cell function after acute exercise are widespread in the literature. The purpose of this article is to evaluate critically the available data and currently employed methods, with the aim of establishing whether genuine or artefactual alterations of immune function are being reported. During and immediately after exercise, the total number of white blood cells in peripheral blood samples increases, such that the relative proportions of cell types within the leukocyte pool are altered. A number of important areas of discussion arise from these shifts in the number of circulating cells after exercise, not least of which is the artefactual effects they may have on currently employed assays of immune cell function. Recent advances in methodology are beginning to call into question the assumption that acute exercise has any genuine immunosuppressive effect. ::: ::: ::: CONCLUSION ::: At present, there is little evidence to suggest that the range of acute exercise intensities and durations recommended by ACSM has a major detrimental effect on the function of individual T- and B-lymphocytes, natural killer cells and neutrophils. Although individual cells may not be as adversely affected as previously supposed, it is unclear whether the numerical content of the circulating population is an important clinical consideration. <s> BIB003 </s> Physical exercise, inflammatory process and adaptive condition: an overview <s> TIssUe TRAUmA AND INflAmmATORy ResPONse <s> An athlete who trains intensely, yet consistently underperforms, ::: is considered to be suffering from overtraining syndrome ::: (OTS). OTS is a complex state that involves a large variety ::: of signs and symptoms. Symptoms include changes in mood ::: or behaviour, decreases or increases in concentration of different ::: blood molecules, and alterations in immune function. Although ::: several hypotheses have been proposed, each only explains a selective ::: aspect of OTS. Presently, the sole agreement is that OTS ::: is associated with excessive training and insufficient rest and ::: recovery. The hypothesis proposed in this paper suggests that ::: excessive training/competing causes repetitive tissue trauma, either ::: to muscle and/or connective tissue and/or to bony structures, ::: and that this results in chronic inflammation. It is further ::: proposed that traumatized tissue synthesizes a group of inflammatory ::: molecules, cytokines. Cytokines have been shown to coordinate ::: the different systems of the body to promote recovery. ::: Suggestions are made to detect, prevent, and rehabilitate the ::: overtrained athlete. <s> BIB004 </s> Physical exercise, inflammatory process and adaptive condition: an overview <s> TIssUe TRAUmA AND INflAmmATORy ResPONse <s> Modified muscle use or injury can produce a stereotypic inflammatory response in which neutrophils rapidly invade, followed by macrophages. This inflammatory response coincides with muscle repair, regeneration, and growth, which involve activation and proliferation of satellite cells, followed by their terminal differentiation. Recent investigations have begun to explore the relationship between inflammatory cell functions and skeletal muscle injury and repair by using genetically modified animal models, antibody depletions of specific inflammatory cell populations, or expression profiling of inflamed muscle after injury. These studies have contributed to a complex picture in which inflammatory cells promote both injury and repair, through the combined actions of free radicals, growth factors, and chemokines. In this review, recent discoveries concerning the interactions between skeletal muscle and inflammatory cells are presented. New findings clearly show a role for neutrophils in promoting muscle damage soon after muscle injury or modified use. No direct evidence is yet available to show that neutrophils play a beneficial role in muscle repair or regeneration. Macrophages have also been shown capable of promoting muscle damage in vivo and in vitro through the release of free radicals, although other findings indicate that they may also play a role in muscle repair and regeneration through growth factors and cytokine-mediated signaling. However, this role for macrophages in muscle regeneration is still not definitive; other cells present in muscle can also produce the potentially regenerative factors, and it remains to be proven whether macrophage-derived factors are essential for muscle repair or regeneration in vivo. New evidence also shows that muscle cells can release positive and negative regulators of inflammatory cell invasion, and thereby play an active role in modulating the inflammatory process. In particular, muscle-derived nitric oxide can inhibit inflammatory cell invasion of healthy muscle and protect muscle from lysis by inflammatory cells in vivo and in vitro. On the other hand, muscle-derived cytokines can signal for inflammatory cell invasion, at least in vitro. The immediate challenge for advancing our current understanding of the relationships between muscle and inflammatory cells during muscle injury and repair is to place what has been learned in vitro into the complex and dynamic in vivo environment. <s> BIB005 </s> Physical exercise, inflammatory process and adaptive condition: an overview <s> TIssUe TRAUmA AND INflAmmATORy ResPONse <s> Skeletal muscle is comprised of heterogeneous muscle fibers that differ in their physiological and metabolic parameters. It is this diversity that enables different muscle groups to provide a variety of functional properties. In response to environmental demands, skeletal muscle remodels by activating signaling pathways to reprogram gene expression to sustain muscle performance. Studies have been performed using exercise, electrical stimulation, transgenic animal models, disease states, and microgravity to show genetic alterations and transitions of muscle fibers in response to functional demands. Various components of calcium-dependent signaling pathways and multiple transcription factors, coactivators and corepressors have been shown to be involved in skeletal muscle remodeling. Understanding the mechanisms involved in modulating skeletal muscle phenotypes can potentiate the development of new therapeutic measures to ameliorate muscular diseases. <s> BIB006 </s> Physical exercise, inflammatory process and adaptive condition: an overview <s> TIssUe TRAUmA AND INflAmmATORy ResPONse <s> Muscle injury or modified muscle use can stimulate muscle invasion by leucocytes that have the potential to increase tissue damage or promote tissue growth and repair. In the present investigation, we examined the role of macrophages in muscle injury, repair and regeneration during modified muscle loading. Weight-bearing was removed from the hindlimbs of mice for 10 days followed by reloading through normal ambulation. During the unloading period, soleus muscle fibre cross-section decreased by 38%. Prior to the onset of reloading, mice received a series of intraperitoneal injections of anti-F4/80, which binds a mouse macrophage surface antigen. Although anti-F4/80 injections did not affect macrophage numbers in soleus muscles at 2 days of reloading, macrophages were reduced by 86% at 4 days of reloading. Muscle membrane lysis during the reloading period did not differ at 2 days of reloading between anti-F4/80-treated mice and mice that received isotype control antibody. However, control animals showed large decreases in the number of fibres with membrane lesions at 4 days of reloading, but this membrane repair did not occur in macrophage-depleted mice. Macrophage-depletion also reduced muscle regeneration (indicated by central nucleation) and satellite cell differentiation (indicated by reductions in MyoD-expressing satellite cells) and prevented growth of muscle fibres that normally occurred in control animals between days 2 and 4 of reloading. These findings collectively show that macrophages play a significant role in muscle fibre membrane repair, regeneration and growth during increased muscle use after a period of atrophy. <s> BIB007 </s> Physical exercise, inflammatory process and adaptive condition: an overview <s> TIssUe TRAUmA AND INflAmmATORy ResPONse <s> Thank you very much for reading immune function in sport and exercise. As you may know, people have look hundreds times for their chosen books like this immune function in sport and exercise, but end up in malicious downloads. Rather than reading a good book with a cup of tea in the afternoon, instead they are facing with some malicious virus inside their laptop. immune function in sport and exercise is available in our digital library an online access to it is set as public so you can get it instantly. Our books collection spans in multiple countries, allowing you to get the most less latency time to download any of our books like this one. Merely said, the immune function in sport and exercise is universally compatible with any devices to read. <s> BIB008
The damage repair mechanism is highly synchronized, and can be basically divided into three phases: a degenerative phase followed by a regenerative phase, and a third phase of remodeling of the injured tissue BIB004 . Tissue trauma is a complex condition in which inflammatory cells promote both injury and regeneration. This is achieved through the combined action of reactive oxygen species (ROS), enzymatic antioxidants of low molecular weight, growth factors, hormones and cytokines that maintain a balance between pro-and antioxidant and pro-and anti-inflammatory activities BIB008 BIB005 . The first phase of repair is triggered by the sarcolemma injury or damage. This injury favors the release of eicosanoids, particularly prostaglandins, prostacyclins, leukotrienes and thromboxanes BIB004 . These eicosanoids are derived from the arachidonic acid, a constituent of the phospholipids of cell membranes, especially of those of the immune system, playing a role in the vasodilation regulation, in the chemotactic activity and in the increase of the vascular endothelium permeability, which is inherent to tissue inflammation BIB004 BIB008 BIB005 . Together, these factors enable the influx of inflammatory cells into the injured site, which is a phenomenon known as diapedesis. Neutrophils are the first subpopulation of leukocytes to migrate into the tissue BIB005 . They show a peak after 60 minutes of exercise, which can last for up to 5 days. At the same time, there is an increase in the transport of neutrophils from bone marrow into the bloodstream, mediated by the action of cortisol and interleukin-6 BIB005 . The main function of neutrophils is the removal, by phagocytosis, of undesirable elements related to tissue injury. This action is the starting point for subsequent responses of tissue repair and growth BIB005 . For this, activated neutrophils release lysosomal proteases that degrade local proteins. They also form ROS as a result of the action of the NADPH oxidase enzyme through a process known as respiratory burst and also by activating the myeloperoxidase enzyme BIB005 . The response mediated by neutrophils should be acute and very well regulated in order to preserve the integrity of cells and tissue around the inflammatory event and to avoid the exacerbation of the injury by increasing the production of ROS BIB006 BIB005 . Monocytes form the second subpopulation of leucocytes to appear at the injured site. When these cells leave the circulation and migrate into the tissues begin to be called macrophages BIB005 . Recently, there is evidence that the role of macrophages that early invade the injured site (between 24-48h) is different from those that appear latter at this site (between 48-96h). The latter would have a more active role in muscle repair while the former would have the main function of removing the injured tissue BIB007 . In fact, in vitro and in vivo studies have confirmed that macrophages play an important role in growth and repair of injured tissue, probably by secreting pro-regenerative molecules BIB008 BIB007 . Among these, some hormones such as insulin-like growth factor (IGF) and cytokines regulators of cell growth such as fibroblast growth factor (FGF) and transforming growth factor (TGF-β) stand out  . These cytokines act in the recruitment and activation of fibroblasts that secrete collagen molecules, thus contributing to tissue regeneration. Moreover, they signal activation, proliferation and differentiation of muscle satellite cells, which are important for tissue recovery BIB002 . Macrophages also secrete several other molecules such as chemokines, prostaglandins, and ROS 8 . Lymphocytes are also important in the process of tissue regeneration after exercise, when they respond in a biphasic manner. They show an increase during and immediately after exercise, especially of Natural Killer cells (NK), followed by decrease, which can last for several hours (primarily of T lymphocytes and NK cells), inducing a loss of their functional capacity. Such changes may lead to the development of transient immunosuppression BIB008 . This immunosuppression seems to be related to increased susceptibility to upper respiratory tract infections in athletes, an acute effect of exhaustive and prolonged exercise BIB002 . Acute immunosuppression may also be associated with decreased activity of neutrophils and monocytes, reduced secretion of cytokines, attenuated respiratory burst, lower chemotactic capacity of neutrophils and lower expression of Toll-like receptors (TL) by monocytes, responsible for the recognition of injured tissues BIB008 BIB003 BIB001 . Cortisol appears to play a role in this immunosuppressant environment, known in literature as the "immunological window" or "open window" BIB004 . The phenomenon of open window seems to be related to the greater possibility of the development of post-exercise infectious conditions BIB008 BIB003 .