The immune system is comprised of two major components, the innate immune system and the adaptive immune system. The components of the innate system includes surface barriers such as skin and mucosal membranes, non specific immune cells such as neutrophil, macrophages, natural killer (NK) cells and lymphokine activated killer (LAK) and non specific non cellular agents such as acute phase proteins and complement. The adaptive immune system is comprised of antigen specific immune cells such as T and B lymphocytes. The innate immune response is a primitive defence mechanism use to prevent invasion of common pathogen. The adaptive immune response is a more advance defence mechanism that is able to recognise new pathogens. It also has the potential to memorize previous encounter pathogen and prevent future infections. The functions of these two systems are is essential for maintaining good health
It has long been suggested that stress-inducing exercise can implement temporary changes in the immune system. Many different types of exercise varying in intensity or dynamics may induce different alterations to the immune response.
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1. Immunology response relationships
a) Innate Components Affected By Exercise
Cytokines & Mechanical Barriers
Many studies performed in the 80s to 90s suggest that exercise often induced a cytokine response. Cannon, Evans, Hughes, Meredith & Din-Arello reported an increased in serum IL-1 in response to exercise. Whereas studies performed by Northoff & Berg (1991) were unable to detect IL-1Î² from individuals who had completed a marathon run, however an increase in serum IL-6 was observed. Mix results were obtained from many individual studies of TNF-Î± and exercise with some studies reported the increase of TNF-Î± after exercise, while others reported undetectable levels of TNF-Î±. The variation of results is possibly due to the different types of exercise used to induce physical stress. Another possible reason for mix results could be due to the low specificity and sensitivity of the bioassay used to access thymocyte activity (Pedersen & Hoffman-Goetz, 2000).
Pedersen & Hoffman-Goetz (2000) suggested that the relationship between cytokine levels and exercise may not be a direct one. The mechanical barrier of the gut wall prevents the entry of endotoxin to the circulation. However if there is a breach in the mucosal wall caused by exercise trauma, then endotoxin can cross this barrier can stimulate the production of cytokines such as TNF-Î±, IL-1Î² and IL-6. More supporting evidence that suggest that the increase cytokine produced during exercise maybe used to support protein catabolism and the inflammatory response.
The appearance of muscle pain with elevated prostaglandin serum concentration and increased macrophage numbers 24hrs after eccentric exercising has suggested a possible relationship between the three. Dejana et al (1988) investigated the in-vitro effects of IL-1 to endothelial cells, smooth muscle cells and skeletal muscle cells. They were able to stimulate the production of PGE2 from endothelial cells and various muscle cells by administrating cytokine IL-1Î±, IL-1Î² and TNF-Î±.
Ostroeski, Rohde, ASP, Sschjerling & Pedersen (1999) reported an increase in cytokine inhibitor IL-1ra and TNF-R after exercise. An increase in the anti-inflammatory cytokine IL-10 was also detected. These cytokine inhibitory may restrict the magnitude and duration of the inflammatory response during exercising.
The many studies reviewed by Pedersen & Hoffman-Goetz (2000) has led them to conclude that strenuous exercise can stimulate moderate production of pro-inflammatory cytokine such as TNF-Î± & IL-1Î² and initiate mass production of IL-6. The cytokine profile observed during exercise resembles the cytokine profile observed in patients with trauma. The inflammatory & cytokine response observed during eccentric exercising is generally localised and not systemic. These findings suggest that cytokine production may be a response to be tissue damage. Cytokines have the potential to stimulate prostaglandin production. However, the causation or the role of increased cytokine production is still not clear. The increase in pro-inflammatory cytokine is usually balance by the release of cytokine inhibitors and cytokine receptors, which act as a control to counter the unwanted effects of increase cytokine release during exercise.
Non-Cytokine Acute Phase Reactants
Non-Cytokine acute phase reactants such as Haptoglobulin, ceruloplasmin, transferring, amyloid A, Î±2-macroglobulin and C-reactive protein are essential components of the innate immune system.
The effects of exercise on non-cytokine acute phase reactant have not been well documented.
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Exercise may alter the functions of the immune system by changing its activity or the composition of the lymphocyte population. The composition of the lymphocyte population is an important factor to consider when assessing the functionality of the immune system. Depending on the composition of the lymphocyte population, certain attribute of the immune system may be reduced or enhanced. For example, if the lymphocyte counts decrease after exercise, then one would expect a reduced response to phytohemagglutinin or to any other lymphocyte mitogen. If the monocyte counts increase after exercise, then one would expect an increase response to endotoxin (Pedersen & Hoffman-Goetz, 2000).
Thomsen et al (1992) suggests that immune-complex-induced complement activation does not occur during concentrix exercise. This is because the concentration of immune complexes, C3c & C3d do not increase during exercise. The complement receptors type one on erythrocytesÂ
C5a is an anaphylatoxin release during the complement cascade. Myeloperoxidase is a hemoprotein release during inflammation. Camus et al (1994) measured the C5a production and myeloperoxidase level during acute sub maximal exercise and found that maybe a possible relationship between the two. Complement activation may contribute to post-exercise neutrocytosis.
b) Cellular Components Affected By Exercise
Viral infections and malignant tumour cells can spread throughout the body before the adaptive immune system have a chance to recognise it and respond to it. NK cells act as the first line of defence against viral infections and the spread of tumour cells. NK operate by mediating non-MHC mediated cytotoxicity to viral infected cells and cytolysis of tumour cells. In-vitro assays have been used to assess the activity of NK cells during exercise. The NK cell activity appears to increase with exercise, however this may be due to the fact that more NK are recruited during exercise (MacKinnon, Chick, Vanas & Tomasi, 1994). Pedersen et al (1988) was able to demonstrate that NK cells that were highly responsive to IL-2 were recruited to the vascular system during exercise. The NK cell activity was increased during and after short periods of moderate to intense exercise. The NK concentrate and activity falls below pre-exercise levels with prolonged exercise of intense levels and continue to do 2-4 hours after exercise (Pedersen & Hoffman-Goetz, 2000).
Neutrophils are one of the major cellular components of the innate immune system. They constitute of more than half of the circulating leucocytes in the blood. They are the primary effector cells of acute inflammation. Neutrophil's functional contribution to the immune system is highly dependent on its ability to travel to the site of infection or inflammation via cellular adhesion and chemotaxis. Upon arrival, neutrophil must be able to eliminate pathogen or debris either by phagocytosis (Roitt, Brostoff & Male, 2001).
Many reports reviewed by Pedersen & Hoffman-Goetz (2000) suggest that the amount and intensity of exercising can influence cellular expression of neutrophils. Moderate exercising can increase neutrophil functions by enhancing chemotaxis, phagocytosis and oxidative potential. However extreme exercising can impair neutrophil function by reducing phagocytosis, the oxidative potential and cellular adhesion.
Gabriel, Schmitt, Urhausen & Kindermann (1993) recorded an increase of cells with the CD45R0+ marker (a marker for memory cells) after prolonged exercise despite the decrease in total lymphocytes. This suggests that memory cells are recruited to the vascular system during vigorous exercise, possible in response to physical stress.
In order for the adaptive immunity system to function effectively, rare antigen specific lymphocytes must first proliferate to a significant number before differentiating into effector cells. Therefore the ability of lymphocytes to proliferate will affect the responsiveness of the immune system. In earlier studies, it was believed that the proliferation of T cells was suppressed due to vigorous exercise. T cell mitogens were use in the Human studies perform by Nielsen & Pedersen (1997) to demonstrate the effects exercise have on lymphocyte proliferation. Results show that the effects of T cell mitogen decline during exercise and also for up to several hours after vigorous exercise. It is important to note that during exercise there is a relative decrease of CD4+ cells in the circulation. Therefore the decline in the responsiveness to T cell mitogen is most likely due to the reduction of CD4+ cells rather than a decline in the proliferation function of the T cells (Pedersen & Hoffman-Goetz, 2000).
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Lymphocyte migration is an essential process in the immune response. During an infection, antigen presenting cells indentify the pathogen and release chemokines to attract lymphocytes to the location of the infection. The pathogen specific lymphocytes are then activated to undergo proliferation and differentiation. Lymphocytes must also be able to freely migrate into any tissue in the body from the circulation to monitor and protect the body from pathogens (Rotti, Brostoff & Male, 2001).
Bruunsgaard et al (1997) evaluated the effects of prolonged exercise of intense levels to cellular immunity. Skin test response to recall antigen was used to assess the level of cellular immunity. Triathletes that have just completed a triathlon race were compared with other triathletes & untrained individuals who did not participate in a triathlon. The skin test response of those who completed the triathlon was significantly lower than those that did not participate
Immunoglobulin A (IgA) is the predominant class of immunoglobulin found in mucosal secretions. About 10-15% of the immunoglobulin in serum is class IgA. IgA mucosal secretion act as the first line of defence against pathogenic microbe in the upper respiratory tract. MacKinnon, Chick, Vanas & Tomasi (1994) recorded a 70% decrease in salivary IgA after prolonged exercise of intensive level. This reduction of salivary IgA was evident for several hours after the exercise. McDowell el al (1992) also observed the effects of exhaustive exercise on salivary IgA. It also came to their attention that reduction of salivary IgA only occurred after exhaustive exercising and had little or effect with light or exercise. With respect to the decrease level of IgA with intensive exercising, the proportion of B cell to blood mononuclear cell did not change despite the increase of lymphocyte during exercising (Pedersen & Hoffman-Goetz, 2000). Tvede, Heilmann, Halkjaer Kristensen, Galbo & Pedersen (1993) were able to demonstrated that activation of post-exercise B cells was not permanently impaired and that the temporary suppression effect could be partially reversed by the addition of indomethacin with IL-2 stimulation.
c) Exercise Trauma and the Stress Response
Exercise is viewed by Hoffman-Goetz & Pedersen (1994) as a quantifiable and reproducible stressor that can alter the function of the immune system. Many studies have demonstrated that the body can release "stress hormones" such as catecholamines, cortisol, Î²-endorphin and sex steroids during intense or prolonged exercise. The association between these hormones and exercise is quite evident, although in-vivo studies and in-vitro studies often give conflicting results. Many Factors such as the functional activity of the cells, numbers of total cells, numbers of cells at site of infection and the mobility of the cells, can each contribute to the function of the immune system. Stress hormones may help the body cope to better with stress by increasing cellular activity and trafficking during the period of stress. Whether or not these stress hormones are the cause of immune suppression or immune enhancement or simply are the by product of the stress mechanism, it is truly evident that under moderate to extreme physical stress, the body will release these hormones.
Epinephrine and norepinephrine are catecholamines that are released by the nervous system during exercise. These catechoamines can bind to Î²-adenoreceptors which are present on T & B lymphocyte, macrophages, neutrophils and NK cells. NK cells have high expression of Î²-adenoreceptor and are generally more responsive to exercise than the other blood mononuclear cells (Hoffman-Goestz L & Pedersen BK, 1994). The relationship between plasma epinephrine concentration and the duration of exercise has prompted researchers to investigate more into its function.
Tvedes et al (1994) were able to mimic the exercise-induce effect on blood mononuclear cells by administrating epinephrine to achieve a serum epinephrine concentration close to the level that would be obtained during prolonged exercising. The activity of NK cells and LAK cells increased along with lymphocyte proliferation. Other studies (Klokker et al, 1997) reports that exercise-induced effects such as lymphocytosis and the increase number of NK cells can be neglected by the administration of Î² receptor blockers. These receptor blockers can prevent epinephrine from binding to Î²-adenoreceptors. From these findings, Pedersen & Hoffman-Goetz (2000) suggest that epinephrine may have a role in the recruitment of NK cells to the vascular circulation during exercise.
Cortisol is a steroid hormone and sometimes considered as a stress hormone. It is produced and released by the adrenal gland in response to stress. Cortisol release can implement many effects to body. One of its primary functions is to suppress the immune system by inhibiting T helper 1 cytokine production and inducing the production of TGFÎ². It is believe that Lewis rats are more susceptible autoimmune conditions due to its low plasma cortisol (Rotti, Brostoff & Male, 2001).
Galbo H (1983) measured plasma cortisol concentration of individuals subjected to exercise of long duration (greater than 1 hr) and found that plasma cortisol was elevated after exercise. Only minor changes in plasma cortisol was observed in acute exercising. This finding suggests that cortisol maybe only involved with prolonged exercising. Repressed production of blood mononuclear cells was observed after the intravenous administration of corticosteroids (Rabin, Moyna, Kusnecov, Zhou & Shurin, 1996). It took approximately 4 hours for cortisol administration to take its maximal effect. This finding suggests that the role of cortisol maybe not be an immediate one and that it play a long term role in stress management of the body.
Hoffman-Goetz & Zajchowski (1999) demonstrated the in-vitro effects of corticosteroids by incubating thymocytes and splenocytes with corticosteroid at level which would be observed in the body during near maximal exercise. In-vitro apoptosis and necrosis of lymphocyte was the result after 24 hours of exposure. The lymphocytopenia, monocytopenia, eosinopenia and neutrophilia observed maybe due to the fact that corticosteroid can induce apoptosis and necrosis to thymocytes and splenocytes, thus reducing immunity.
The plasma concentration of Î²-Endorphin under normal (non-stress) conditions is generally very low (around 1-100 Pico Moles). Physical stress however can induce a 3-10 times increase. The increase is only evident in prolonged exercising of medium to high intensity (Maisel, Harris, Rearden & Michel, 1990). Infusion studies reviewed by Pedersen & Hoffman-Goetz (2000) suggest that Î²-Endorphin may act as an immune suppressant by inhibiting T cell proliferation and antibody production.
Studies performed in relation to NK cell activity and Î²-Endorphin has been inconclusive, with in-vitro experiment being non reproducible in vivo. NK cells are recruited to the circulation almost immediately after the initiation of exercise and also during low intensity exercise. However Î²-Endorphin serum concentration only increases during high intensity exercise. Pedersen & Hoffman-Goetz (2000) suggest that Î²-Endorphin's role maybe involved with increasing NK activity rather than with the recruitment of NK cells.
It is long been known that testosterone can alter the functions of the cellular and humoral components of the immune system. Elevation of serum testosterone has been observed in acute exercise of high intensity as well as moderate exercising. However a reduction of testosterone has been observed with prolonged exercising (Pedersen & Hoffman-Goetz, 2000)
Araneo, Dowell, Diegel & Daynes (1991) administrated dihydrotestosterone in-vitro to activated murine T cells. They notice that interleukin-4 (IL-4), IL-5 and gamma-interferon production was all reduced after testosterone administration. IL-2 production however was not affected. IL-4 is involved with the initiating T helper differentiation as well as stimulating activated B & T cells to proliferate. IL-5 is involved with stimulating B cell proliferation and antibody production (Rotti, Brostoff & Male, 2001). One would expect that a reduction of IL-4 & IL-5 would result in a depressed humoral response.
Kanda N, Tsuchida T & Tamaki K (1996) performed in-vitro studies on the effects of testosterone in human blood mononuclear cells with immunoglobulin production. Results show that administration of testosterone can inhibit IgM and IgG production as well as IL-6 production from monocytes.
2. Environment and Biological Influences on Immune Process
As discussed above, exercise can alter the immune system by recruiting immunocompetent cells to the circulation. The proportional distribution of the lymphocyte population may also change with exercise. The release of the pro-inflammatory cytokine or immune suppressant can further alter the functions of the immune system. These alterations to the immune system may be critical in determining the host's resistance or susceptible to certain infections (Pedersen & Hoffman-Goetz, 2000).
Poliomyelitis is an acute viral infection of the spinal cord. The causative agent is poliovirus. Around 90% of polio infections are asymptomatic. Infection is evident only when the virus may enter the blood circulation and infect the central nervous system. Poliovirus can destroy motor neurons, cause muscle weakness and paralysis (Ryan & Ray, 2004).
Early reports in the 1930s-40s by Limper, Thelander & Shaw (1931) suggested that exercising during the early stages of a polio infection can worsen the infection. This suggestion was well supported by studies performed a decade later. Epidemiological studies and animal experimental studies performed by Horstmann (1950) found that those who suffered poliomyelitis had an increased risk of severe paralysis if they performed physical activity of any kind during the paralytic stages of the infection.
Myocarditis is the inflammation of heart muscles. It is generally cause by common viruses such as parvovirus but sometimes can be due to an autoimmune response. Molecular mimicry between streptococcal M protein and Coxsackie B virus antigen to cardiac myosin can stimulate the production of antibody that is reactive to cardiac muscle (Leslie & Cooper, 2009). Chlamydia pneumonia is a common pathogen implicated in upper respiratory tract infections. However it is generally relatively harmless to healthy individuals. Pedersen & Hoffman-Goetz (2000) suggest that transient immunosuppression induced by exercise may render the host susceptible to opportunistic microorganisms such as Coxsackie B virus and C. pneumoniae.
Gatmaitan, Chanson & Lerner (1970) exposed mice to murine Cox-Sackie B3 virus and then subjected them to swimming exercises during the acute phase of the infection. An increased mortality from 5.5 to 50% was observed in mice were subjected to exercise. The acute exercise had cause an increase in viral replication along with inflammation and necrosis in the myocardium. Autopsy shows that majority of the mice died from congestive heart failure during the swimming exercises. Myocardial fiber damage was seen in nearly all of the mice that were subjected to exercise, in comparison to 25-50% observed in the non-exercised controls. Gatmaitan, Chanson & Lerner (1970) also emphasized on the influence exercise may have on viral replication and to severity of the disease. They inoculated mice with the murine Cox-sackie B3 virus and then subjected them to swimming exercises 9 days after virus inoculation. This experiment was aimed to reduce the possible influence exercise may have on viral replication. Only a small increase in the mortality rate was observed with mice that were subjected to exercise 9 days after virus inoculation in comparison with that were not subjected to exercise. This suggest that the mortality of the disease may be linked to viral replication and that viral replication must be a disease contributing factor that is strongly enhance by exercise
The human immunodeficiency virus (HIV) is the causative agent of acquire immunodeficiency syndrome (AIDS). HIV primarily infects CD4+ T cells but can also infect antigen presenting cells such as macrophages and dendritic cells. Individuals suffering from AIDS have an impaired immune system due to the reduction of T helper cells. The concentration of CD4+ is often used as a prognostic value to the development of AIDS. The impairment of the immune system will allow opportunistic micro-organism that otherwise would be controlled in healthy individuals, to cause disease (Roitt, Brostoff & Male, 2001).
Ullum et al (1994) wanted to investigate the effects of acute exercise on the immune response in individuals that were suffering from HIV. The subjects were asked to cycle at 75% of VO2max for one hour. They recorded many different parameters of the immune system such as lymphocyte subsets, NK cells activity, LAK cell activity, the proliferation response and also cytokines production in those that were infected with HIV and compared it with HIV-serology negative controls. They found that the percentage of CD4+, CD4+ 45RO+ (memory) & CD4+ 45RA+ (mature) did not change in response to exercising but the CD4+ concentration doubled during exercise. The recruitment of neutrophils during exercise was impaired along with NK cell activity in HIV infected subjects. LAK activity increased in response to exercise in HIV-serology negative controls but did not increase in HIV infected subjects.
There is more than one factor contributing to the recruitment of immunocompetent cells to the circulation during exercise. Factors such as the stress response, receptor expression and total cell reservoir can all affect cell recruitment. Doweiko (1993) suggested the stress response in HIV infected individuals may be lower. Î²-receptors on NK cell are the recipient of the stress response and that a reduced expression of Î²-receptors in HIV-infect individual could be the cause of a reduced response. The reservoir of immune competent cells in a HIV-infected individual could be severity depleted depending on the stage of the disease. Cell recruitment would have little or no effect if the reservoir is severely depleted.
Laperriere et al (1991) recorded an insignificant increase in CD4+ t cells of HIV infected patients that that exercise regularly. However the increase is not significant enough to conclude that exercising can be considered as a form of treatment to counter the effects of declining CD4+ cells.
The effects of chronic exercise on the immune system in HIV infected subjects were further investigated by many different independent studies. Majority of researchers have concluded that chronic exercising did not have any significant effects on CD4+ cell or other lymphocyte subpopulations. However the dropout rates in some of these studies were quite high. Clinical deterioration is a likely cause of the dropout rates and that clinical deterioration is likely to be related to the decline of CD4+ cells and other lymphocyte subpopulations (Pederson & Goetz, 2000).
Several comprehensive studies have demonstrate the effects of exercise on host's resistance to infections. Experiments conducted by Nicholls & Spaeth (1922) show that sedentary guinea pig had 80% fatality rate after exposure to type I pneumoccus in comparison to a 20% fatality rate observed in guinea pigs that were subjected to acute exercise before pneumoccus inoculation. This finding supports the idea that exercise can induce the recruitment of immunecompetent cells to the circulation, which may offer the host a temporary increase resistance to pathogens.
Cannon & Kluger (1984) experimented on mice that were trained on running wheels before inoculation with Salmonella typhimurium. They found that trained mice had a significant higher survival rate that of sedentary control mice. This increased survival rate may be due to the elevated levels of serum IL-1 measured in trained mice.
Studies performed by Chao, Strgar, Tsang & Peterson (1992) show that swimming exercise induce on mice during incubation period of Toxoplasma gondii infection did not significant change the outcome of the disease.
Pederson & Goetz (2000) suggests that the beneficial effects of exercise to the outcome of the disease is dependent on the type of exercise perform as well as the timing of the exercise. Quite often in the studies that used swimming as the form of exercise, no beneficial effects to the outcome of disease was observed. This may be due to the intensity level of swimming exercises as we know from previous discussion that intensity of the exercise is the determine attribute to the activation of the stress response. Exercise performed before infection tends to have either no effect or decrease morbidity and mortality. Whereas exercise performed during infection tend to have either no effect or an increase in severity of the disease.
The findings based on epidemiological studies on exercise and upper respiratory tract infection hints that moderate training may reduce the severity of disease and that strenuous exercise may increase the severity. However with many of these studies, the result is based on self-reported symptoms rather than clinical diagnosis of the disease.
As mention earlier, exercise induced alterations of the immune system may occur via many different mechanisms and that many factors can contribute the observed effects of exercise. Furthermore, many of these mechanisms require the metabolism of neuroendocrinlogical factors such as stress hormones. Depletion of resources may affect the ability to generate an adequate stress response and may also affect lymphocyte function. Therefore diet intake may be a limiting factor to exercise associated immune function.
Glutamine is the most abundant naturally occurring amino acid in the human body. Skeletal muscles are the main producers of glutamine. It is believe that skeletal muscles may also play a role in glutamine utilization in immune cells. The main consumers of glutamine are cells of the intestines but immune cell such as macrophages and lymphocyte can also utilize glutamine for energy. Newsholme (1994) suggest that even in quiescent state, the consumption of glutamine can be quite high. Therefore the supply of glutamine maybe essential for lymphocyte functions. The glutamine hypotheses suggest during high intensity exercise, the demand of glutamine may exceed the production of glutamine from skeletal and that the lymphoid system may be forced into a glutamine debt.
Many studies reviewed by Pederson & Goetz (2000) have similar findings all suggesting the decline of serum glutamine concentrate with high intensity long term exercising. However glutamine supplementation after exercise often restored serum glutamine concentration but did not removing the suppressing effects of post exercise immune impairment (Rohde, MacLean & Pedersen, 1998).
Energy is essential for the normal function of cells. The lack of energy may contribute to the stress induce by physical exercising. Applying the same concept as the glutamine hypotheses, insufficient glucose due to high demands from muscle may affect the function of immune cells. Mitchell el al (1998) investigated the effects of carbohydrate supplement to immune functions before and after endurance exercise. Serum glucose level rose after carbohydrate supplementation. A Reduction of serum cortisol and growth hormone was recorded. As mention earlier, cortisol reduce immunity by induce apoptosis and necrosis to thymocytes and growth hormones such as testosterone can inhibit antibody production. However, reductions in monocyte phagocytosis, oxidative burst activity, cytokine response and blood immune cell count was also observed and that carbohydrate supplement did not remove post-exercise immune impairment.
There are two main types of essential fatty acids, omega-3 (n-3) and omega-6 (n-6). Dietary n-6 and n-3 fatty acids are important regulators of bone metabolism (Weiler & Fitzpatrick-Wong, 2002). The (n-6):(n-3) ratio determines the fatty acid status of the individual. It is believed that shifting the balance in favour of n-6 fatty acid can increase prostaglandin production and induce immune suppression. One would expect that increasing n-3 fatty acid would restore balance and counter the effects of exercise induced immune suppression. Johnson, Griswold & Muakkass (1993) were able to demonstrate that pre n-3 fatty acid supplementation (fish oil) was able to reduce stress response in animals stimulated by endotoxin administration.
Benquet, Krzystyniak, Savard & Guertin (1994) wanted to know the effects of polyunsaturated fatty acid on post-exercise immune suppression. Mice that were fed on a diet rich in linseed oil (source of n-3) was compared with mice that were fed on normal diet consisting of various oils. They found that the post-exercise immunosuppression of IgM plaque-forming cell response was absent in mice that were fed on a rich linseed oil diet. A possible explanation for this phenomenon is that a n-3 rich diet may inhibit the production of prostaglandin and hence inhibit exercise induced immune suppression.
Antioxidants are reducing agent capable of inhibiting oxidation of other molecules and prevent the release of free radicals (Sies, 1997). In a double-blind placebo study performed by Peters, Cambell & Pawley (1992), they found that vitamin A supplementation did not improve the resistance of upper respiratory tract infection in marathon runners. However, in a study performed by Peters, Goetzsche, Grobbelaar & Noakes (1993) a year later shows that vitamin C supplementation reduced the number of self reported symptoms of upper respiratory tract infection. Nieman et al (1997) found that vitamin C supplementation did not have any effect on lymphocyte function or on the stress response. The mechanism of improved resistant offered by vitamin C maybe an indirect one.
The effects of exercise on immune functions are highly dependent on the type of activity, the intensity and the duration of the exercise. When considering the function of the immune system, activity is just as important as composition of the lymphocyte population. NK activity seems to increase during and after acute & moderate exercise but decrease with prolonged exercise of intense levels. Moderate exercising also seems to increase neutrophil functions and extreme exercising can impair neutrophil functions. Reduction of CD4+ cells, salivary IgA and cellular immunity has been observed after prolonged exercise of intense levels.
Under moderate to extreme physical stress, the body will reproduce stress hormones. The release of particular stress hormone can be dependent on the type and intensity of the exercise. Stress hormone such as epinephrine may have a role in NK cell recruitment to the circulation. Some stress hormone such as cortisol can suppress the immune system. Î²-Endorphin may increase NK activity.
The release of stress hormone can change during exercising. A good example is testosterone.
Currently there are many studies that support the theory that exercising during an infection can increase the severity of the infection. Exercising may enhance viral replication. The transient immunosuppression induced by exercise may render the host susceptible to opportunistic infections
However, several comprehensive animal studies have shown that exercising can increase host's resistance to infection. Exercise performed before infection tends to have either beneficial effect to the disease whereas exercise performed after infection tend to increase the severity of the disease
Nutritional supplement may also have a role to play a role in determining the effects of post-exercise induced immunosuppression. Depletion of resources may affect the ability to generate an adequate stress response and may also affect lymphocyte function. The observed decline of nutrient with exercise induced alteration of immune system is not often removed with nutrient supplementation.