altIntensive training, frequent competition, and resuming exercise too quickly after a winter lay-up can all have a negative impact on the horse’s ability to fight disease and infection. Proper nutrition is critical for maintaining the immune system. This session will discuss key nutrients, including fatty acids, amino acids, minerals and vitamins, that have potential to enhance immunity in performance horses.

Author - Dr. Lori Warren

Dr. Lori Warren is an equine nutritionist and Assistant Professor in the Department of Animal Sciences at the University of Florida. Prior to joining the faculty in Florida, Dr. Warren served as the Equine Extension Specialist at Colorado State University and as the Provincial Horse Specialist in Alberta. She is currently serving on an NRC committee to evaluate the safety of dietary supplements for horses. Dr. Warren received an MS and PhD in equine nutrition and exercise physiology from the University of Kentucky.

Chicken Soup for the Horse?
When you have a cold, your mom forces you to eat a bowl of chicken noodle soup. Cough drops now contain added Vitamin C or Zinc. What’s the common theme here? Nutrition! Just like all other systems in the body, the immune system requires specific nutrients to do its job. When illness or infection sets in, more nutrients are needed to support the immune system as it works overtime to eliminate pathogens and repair damaged tissue. In addition to helping fight infection once it’s established, some nutrients are useful for strengthening the immune system so it can respond quicker, reducing the severity or duration of the illness.

 

Can we improve the horse’s immune system through his feed bucket? The short answer is: we don’t know; the research hasn’t been done yet. The field of nutritional immunology (also known as “immunonutrition”) in humans is a relatively young science—in horses, it’s just beginning. But information learned from studies in humans and other animals suggests there is potential for the things we feed the horse to improve (or in some cases, harm) their immune response.

For this article, I have chosen to focus on the performance horse. Not only does exercise itself affect immune function, these horses are usually exposed to lots of different pathogens as they travel from one competition to the next. Many performance horses also undergo long hours in the trailer getting to the show, and the stress associated with transport is a known suppressor of the immune system. While the research is not yet in place to make concrete feeding recommendations for performance horses, we will take a look at some of the nutrients that have shown potential for aiding the immune response in human athletes.

The Immune System
When asked about the immune system, most people think of antibodies. While antibodies are certainly an important component of the immune system, they are not the only players. The immune system is actually quite complex, with lots of overlapping roles and “checks and balances.” This redundancy is important so that if one component fails, there is another to back it up. Without such road blocks, pathogens such as bacteria and viruses would hijack the body.

The immune system has two functional divisions: 1) the innate system (also termed non-specific) and, 2) the adaptive system (also termed specific or acquired). Both divisions of immunity involve several different kinds of white blood cells (leukocytes), as well as other physical and chemical barriers. These components act in a coordinated fashion to eliminate infectious agents (bacteria, viruses, fungi, parasites) and tumor cells, as well as respond to injury and trauma. Some of the major cells (the “players”) and their roles in the immune response are provided in Table 1.

Innate immunity is the first line of defense against infectious agents. An innate immune response will occur regardless if the body has seen the infectious agent before (ie, it is automatic, it has no memory, and is not specific for a particular antigen). It functions to prevent entry of infectious agents into the body and if they do enter, it rapidly eliminates them. The innate immune system includes physical barriers (eg, skin, stomach acid, mucus membranes in the nose, tears, etc), phagocytic cells (“the Kamikazes”) and natural killer cells (“the Exterminators”) (See Table 1). The innate immune system is particularly important during the early phases of an infection or injury—in fact, the inflammatory response is an innate immune response.

Adaptive immunity primarily involves T and B cells, with varying roles and responsibilities (see “Commanding Generals,” “Sentinels,” “Bomb Factories,” and “Reconnaissance Team” in Table 1). In contrast to non-specific innate immunity, adaptive immunity is highly specific, meaning each cell targets a specific antigen. Also unlike innate immunity (which is immediate), there is a lag time between exposure to pathogens and the maximal response of the adaptive immune system. Whereas the innate response would be maximal within an hour, the adaptive response becomes active over several days after pathogen exposure. However, the adaptive response also persists for some time after removal of the antigen. This persistence gives rise to immunological memory, which is the basis for a stronger, more effective immune response when the body is re-exposed to the same antigen. Some of this memory comes from the proliferation of certain lines of cells that, now that they know what they are looking for, will monitor the body for specific antigens. Memory also comes from antibodies to specific antigens, which attach to the pathogen when it reappears, thus marking them for destruction by cells of the innate immune system (ie, the “Kamikazes”). The practice of administering vaccinations takes advantage of this immunological memory—the vaccination provides initial exposure to the pathogen, creating a memory in the form of antibodies. When the vaccinated horse is exposed to the real disease, the immune system will be ready to fight that specific pathogen more effectively.

As you can see from the discussion above, the innate and adaptive immune systems work together. No one component is any more important than the others, but a more effective immune response requires that all the “players” do their jobs. When one component fails or does its job too well (ie, an exaggerated response), the illness can be prolonged or compounded by additional pathogens, or the inflammation can do more harm than good. Heaves (or asthma) is an example of an exaggerated inflammatory/immune response. Severe combined immunodeficiency (SCID) in Arabian foals is an example of failure of the adaptive immune system to mount and coordinate a defense.

Communication among cells is important for a coordinated and effective immune response. Communication within the adaptive immune system and between the innate and adaptive systems is brought about by direct cell-to-cell contact and by the production of chemical messengers. Chief among these chemical messengers are proteins called cytokines. Cytokines bind to immune cells and induce changes in growth, development, or activity of the cell. In this capacity, cytokines are important in directing local immune responses, as well as coordinating whole body responses to infection or injury.

Over 100 cytokines that are produced by a variety of immune and tissue cells have been identified. Three of them are particularly important in organizing immune responses. They include tumor necrosis factor-alpha (TNF), interleukin 1-beta (IL-1), and interleukin 6 (IL-6). These cytokines activate neutrophils, monocytes and macrophages (the “Kamikazes”) to initiate bacterial or tumor cell killing, stimulate an increase in the number of T- and B-cells, and initiate the production of other pro-inflammatory cytokines. Thus, these cytokines are mediators of both innate and adaptive immunity and are an important link between them. In addition, these cytokines mediate the systemic effects of inflammation, such as fever, weight loss, and acute-phase protein synthesis in the liver. Production of appropriate amounts of TNF, IL-1, and IL-6 is an important response to infection; however, inappropriate production or overproduction can be dangerous. In fact, these cytokines (particularly TNF) are implicated in causing some of the pathological responses that occur in acute/chronic inflammatory conditions (Calder et al., 2002).

Impact of Exercise on the Immune System
The effects exercise on the immune system varies depending on the duration and intensity of exercise, as well as the current level of fitness. In general, regular moderate intensity exercise is associated with beneficial effects on host defense mechanisms. In contrast, acute bouts of high intensity activity or prolonged exercise can suppress immune function, which can increase risk of infection (see Figure 1).

A study conducted in horses by Raidal et al. (2000) is a great illustration of this phenomenon. Untrained horses undergoing moderate intensity exercise (30-40% of maximal effort) exhibited improved neutrophil phagocytosis and oxidative burst activity (“the Kamikazes” of the innate immune system) compared to sedentary horses. However, when the untrained horses were exercised at high intensity (sprint to fatigue) they experienced a decrease in neutrophil function that lasted about 6 hours after exercise. After the horses underwent a 10-week endurance training program, the suppressive effects of high intensity exercise on innate immunity were eliminated. In contrast, after a further 6 weeks of training at higher intensity, neutrophil function was again suppressed in response to a sprint to fatigue.

Many components of the immune system are altered after heavy exertion (either sprinting activities, or prolonged endurance activities). Many of these changes reduce the function of immune cells and increase risk of infection. Some of the key changes include:
• An increase in the number of circulating neutrophils and monocytes (the “Kamikazes”), and a decrease in the number of B-cells, T-cells and Natural killer cells (the “Sentinels,” “Commander Generals,” “Exterminators,” and “Reconnaissance Team.”) These changes are induced by high levels of stress hormones (ie, adrenaline, cortisol, growth hormone).
• An increase in macrophage phagocytic activity and activation markers (reflecting an inflammatory response and repair of injured muscle cells). But a decrease in neutrophil phagocytosis and neutrophil/macrophage oxidative burst activity. The duties performed by these “Kamikazes,” particularly neutrophils, are critical in the early control of invading pathogens.
• Blunted major histocompatibility complex II expression and antigen presentation in macrophages. As a “Sentinel,” a decrease in the ability of macrophages to present antigens to T-cells (the “Commander Generals”) means that the T-cells will not know they need to respond to a challenge by viruses.
• A decrease in Natural killer cell (an “Exterminator”) cytotoxic activity, which is normally an important antiviral measure.
• A decrease in T-cell response (ie, proliferation) to antigens. Loss of such “Exterminators” and “Commander Generals” means less effective elimination of virus-infected cells and a slower coordination of other immune cells and components needed to mount an effective defense.
• A large increase in the anti-inflammatory cytokine IL-6, most of which is produced by the muscles themselves. This is thought to be beneficial, because it suppresses the ability of the immune system to induce tissue damage and inflammation. However, it also negatively affects certain populations of T-helper cells (Th1), which are important in coordinating protection against viruses.

The alterations in immune function described above generally last between 3 and 72 hours following heavy exertion. During this “open window” of altered immunity, viruses and bacteria may gain a foothold, increasing the risk of infection.

It is important to recognize that although several aspects of immunity are depressed during chronic heavy training and/or competition, the horses are not clinically immuno-deficient. In other words, exercise-induced immune dysfunction does not necessarily put the performance horse in danger of serious illness, but it could be sufficient to increase the risk of contracting common infections. And when combined with environmental stressors that typically accompany a heavily campaigned performance horse (eg, frequent transport over long distances, concentrated housing and close contact with other horses at show and racetrack facilities), exposure to airborne pathogens and disease susceptibility can be further elevated.

Even minor infections can result in a drop in exercise performance and the ability to sustain heavy training. Therefore, strategies to mitigate risk of contracting an infection would be of great use to most performance horses. The use of nutrition as an immunomodulator is one such strategy.

Immunonutrition for the Performance Horse
Nutrition plays a supportive role in immunity and host defense. Table 2 summarizes some of the key nutrients involved in immune function. For example, various amino acids (i.e., glutamine, arginine, methionine and cysteine) and minerals (i.e., zinc and selenium) are critical to the formation, proliferation and functional activity of immune cells and other components of the immune system. Vitamin A (as well as lycopene and lutein) and vitamins E and C are also important in immune cell function, as well as mitigation of reactive oxygen species generated by the highly metabolic immune cells participating in host defense. In addition, polyunsaturated fatty acids, acting via their conversion to eicosanoids, are responsible for directing many activities associated with inflammation and immune response. Deficiencies or imbalances of these nutrients generally result in compromised immune function and decreased disease resistance. Therefore, a balanced diet is critical to mount an appropriate immune response to infection or trauma.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Based on the role of nutrition in immunity, it has been proposed that the transient immuno-suppression seen in response to intensive training may be alleviated with strategic nutrient supplementation (Pedersen and Hoffman-Goetz 2000; Gleeson 2007). This area of study has not yet received a lot of attention in the performance horse, but has been gaining momentum in the human athlete. Therefore, the remainder of this paper will highlight nutrients that have shown the most promise in modifying immune response in human athletes, and which could potentially be investigated further in the horse.

Although the mechanisms underlying exercise-associated immune changes are multifactorial, there are four key areas where exercise may directly contribute to altered immune function: 1) Reductions in plasma glutamine concentrations; 2) decreased plasma glucose concentrations; 3) increased production of free radicals and other reactive oxygen species; and 4) increased production of pro-inflammatory prostaglandins (Pedersen and Hoffman-Goetz 2000). Thus, nutritional supplementation of the athlete with glutamine, carbohydrate, antioxidants, or prostaglandin inhibitors may, in principle, provide a means of minimizing exercise-induced immunosuppression.
Glutamine Supplementation
Together with glucose, glutamine (a non-essential amino acid) is an important energy source for T-cells, B-cells and monocytes (Table 2). Plasma glutamine concentration has been shown to decline in response to various stressors, including prolonged strenuous exercise (Rohde et al., 1998 ; Kryzwkowski et al., 2001a,b). Furthermore, low glutamine levels have been described in athletes with “overtraining syndrome” (Castell, 2003). It has been hypothesized that during intense physical exercise, the demand on muscle and other organs for glutamine is such that the immune system may be forced into a glutamine “debt,” which temporarily affects its function (Castell, 2003). However, results on the ability of glutamine supplementation to ameliorate post-exercise immunosuppression have been variable. In a series of placebo-controlled field studies conducted in marathon runners, glutamine supplementation after competition resulted in faster restoration of circulating immune cells and a lower incidence of self-reported infections (Castell, 2003). Glutamine supplementation following a marathon (Rohde et al., 1998) or repeated bouts of bicycle ergometer exercise (Rohde et al., 1998b; Kryzwkowski et al., 2001a,b) abolished the post-exercise decline in plasma glutamine, but did not influence the post-exercise impairment in specific measures of immune function.

Plasma glutamine has also been shown to be reduced in horses following exercise that simulated the road and tracks phase of a three-day event, as well as after sustained high intensity (115% VO2MAX) exercise to fatigue (Routledge et al., 1999). Harris et al. (2006) demonstrated that plasma glutamine concentrations could be transiently increased in sedentary horses by feeding common dietary ingredients or by glutamine supplementation (either as glutamine or glutamyl-peptide). This finding is important, because glutamine is also the preferred fuel for intestinal enterocytes; thus, the ability to raise plasma glutamine levels in response to feeding or supplementation indicates at least some of the dietary supply will become available to immune cells outside the gut. However, it remains to be determined whether glutamine supplementation following exercise has any impact on exercise-associated declines in immune function in horses.
Carbohydrate Supplementation
Many aspects of depressed immune function brought on by strenuous exercise seem to be caused by elevated levels of stress hormones (Pedersen and Hoffman-Goetz, 2000). Therefore, nutritional strategies that reduce the stress hormone response to exercise would be expected to limit the degree of exercise-induced immune dysfunction. It is well established that a reduction in blood glucose triggers an increased release of cortisol and growth hormone, with variable effects on adrenalin. Given that prolonged exercise typically results in a decline in blood glucose, it has been suggested that consumption of carbohydrate during exercise could attenuate the rise in stress hormones, thereby countering negative immune changes. Carbohydrate supplementation may also alter immunity following exercise by increasing the availability of energy substrate to immune cells. Glucose is the major energy substrate for immune cells.

Several studies with runners and cyclists have shown that ingestion of beverages with carbohydrates can attenuate changes in immunity when the athlete experiences physiological stress and depletion of carbohydrate stores in the body during prolonged exercise (see Nieman and Pedersen, 1999). Carbohydrate ingestion (about 1 liter/hour of a typical sports drink) compared to a placebo has been shown to significantly lower blood cortisol and adrenaline, reduce changes in blood immune cell counts, and lower pro- and anti-inflammatory cytokines.

While carbohydrate feeding during exercise appears to be effective in minimizing some of the immune perturbations associated with prolonged continuous exercise, it seems less effective for less-demanding exercise of an intermittent nature or when prolonged exercise is performed to the point of fatigue (see Gleeson, 2006). Furthermore, it is not clear if the magnitude of effects observed with carbohydrate feeding during prolonged exercise is sufficient to reduce the risk of infection.

In the horse, there has been a considerable amount of study investigating carbohydrate supplementation with respect to reducing glycogen depletion during exercise and promoting glycogen repletion after exercise; however, the impact these practices have on immune function has not been addressed. In humans, the size of the glycogen stores in muscle and liver at the onset of exercise has also been shown to influence the hormonal and immune response to exercise. For example, Mitchell et al. (1998) observed that exercising for one hour in a glycogen-depleted state resulted in greater decreases in lymphocyte numbers following exercise in humans. Based on the promising findings in humans, the immunomodulating effects of carbohydrate supplementation, as well as the impact of reduced glycogen stores, deserves study in horses participating in endurance-type activities. 
Antioxidant Supplementation
Immune cells are very active, resulting in the production of reactive oxygen species as a part of normal cellular metabolism. In addition, oxidative burst, a mechanism by which neutrophils and macrophages (the “Kamikazes”) use to destroy ingested pathogens also produces superoxide and hydrogen peroxide. Increased formation of reactive oxygen species also accompanies the dramatic rise in oxidative metabolism during exercise. Reactive oxygen species are capable of damaging cell membranes, proteins and DNA, if not kept in check by antioxidants.

In theory, antioxidant supplementation may neutralize the reactive oxygen species generated during exercise, thereby mitigating exercise-induced immunosuppression. In practice, however, supplementation of athletes with various antioxidants have produced variable results. The most positive responses have been noted with vitamin C. For example, daily supplementation with vitamin C for 3 weeks prior to a 90-km ultra-marathon reduced the self-reported symptoms of upper respiratory infections in the 2 week period following the competition (Peters et al., 1993). Vitamin C was also shown to attenuate the increases in serum cortisol and pro-inflammatory cytokines in ultra-marathon runners when ingested at 1000–1500 mg/day, but not at 500 mg/day (Peters et al., 2001). A combination of fat- and water-soluble antioxidant vitamins does not appear to be more successful in attenuating the post-exercise infection risk that vitamin C alone. For example, ultra-marathon runners supplied daily with vitamin C + E or vitamin C + E + beta-carotene for 3 weeks prior to competition had fewer symptoms of upper respiratory infections compared to runners given a placebo, but they were not enhanced over runners receiving vitamin C only (Peters et al., 1996).

Supplementation of equine athletes with vitamin E and/or vitamin C has been investigated for potential mitigation of exercise-induced oxidative stress. However, the potential role of these and other antioxidants in attenuating perturbations in immunity following strenuous exercise have not been researched in horses.
Polyunsaturated Fatty Acid Supplementation
Two groups of polyunsaturated fatty acids (PUFA) are essential to the body: omega-6 (n-6) fatty acids, derived from linoleic acid; and omega-3 (n-3) fatty acids, derived from -linolenic acid. These fatty acids cannot be synthesized by the body and therefore must be supplied in the diet.

The biological activity of PUFA can, in part, be attributed to their conversion to eicosanoids, which include prostaglandins. Metabolism of arachidonic acid (an n-6 fatty acid) yields the 2-series prostaglandins (eg, PGE2). Although PGE2 exhibits pro-inflammatory effects, including inducing fever, increasing vascular permeability and vasodilation, and enhancing pain and edema, PGE2 has long been regarded as one of the most powerful immuno-suppressants (Smith, 2003). In this respect, PGE2 suppresses the proliferation of T- and B-cells and inhibits production of pro-inflammatory cytokines (TNFα, IL-1, IL-6) from macrophages (Calder et al., 2002). Pedersen et al. (1990) reported that PGE2 production by monocytes increased 270% following an acute bout of exercise. The PGE2 released from macrophages and neutrophils in response to exercise was shown to suppress Natural killer cell activity for up to 7 days (Gannon et al., 1995).

The n-3 fatty acid, eicosapentaenoic acid (EPA), is a substrate for the synthesis of an alternate family of eicosanoids, including the 3-series prostaglandins. In general, the EPA-derived eicosanoids are weaker inflammatory agents than those synthesized from arachidonic acid. In addition, EPA suppresses the production of eicosanoids from arachidonic acid by competing for placement in cell membranes and for the enzymes responsible for oxidizing EPA and arachidonic acid to their respective eicosanoids. Consequently, dietary supplementation with n-3 fatty acids has been shown to modify immune and inflammatory responses in healthy, sedentary individuals and chronic disease states (Calder et al., 2002; Sijben & Calder 2007).

Surprisingly little is known about the potential contribution of dietary fatty acids to the regulation of exercise-induced alterations in immunity. In fact, only one study appears to have addressed immunomodulation of fatty acids in relation to exercise. Fish oil (a rich source of EPA) supplementation for 6 weeks prior to a marathon had no impact on plasma cytokine levels and neutrophil, B-cell, and T-cell blood counts in male runners (Toft et al. 2000).

Similar to the observations in other species, n-3 fatty acids in the form of flaxseed (rich in α-linolenic acid) or fish oil (rich in EPA) have been shown to modify biomarkers of inflammation and some aspects of immune function in sedentary horses (Warren, 2006). Research has also included the provision of n-3 fatty acids to exercising horses. However, the use of dietary fatty acids to minimize the depression in immune function following strenuous exercise has not yet been addressed in the horse.
Conclusions
The application of immunonutrition to the horse is a relatively new area of study. Yet interest in this area is gaining momentum as horse owners seek complementary and holistic methods to maintain the health of their horses. Further, many horses compete or participate in a variety of athletic events, which can challenge the immune system and increase risk of infection. Therefore, nutrition and feeding strategies that help alleviate perturbations in immune function resulting from strenuous exercise and training are needed. In humans, carbohydrate supplementation during and after prolonged continuous exercise has shown to mitigate many aspects of exercise-induced immunosuppression. Similarly, supplementation with antioxidants, particularly vitamin C alone or in combination with vitamin E, appears to bolster immune function and reduce symptoms of disease in athletes competing in strenuous events. Other immunomodulating nutrients (e.g., omega-3 fatty acids) have shown potential in sedentary subjects, but require greater evaluation in the exercising subject.

Ultimately, multiple endocrine and metabolic factors are involved in exercise-induced immune modulation. Therefore, it is unlikely that one single nutrient supplement will completely eliminate exercise-related immune dysfunction and risk of infection in performance horses. Synergistic effects between various immunomodulatory nutrients deserves further investigation in the athlete. Additionally, it is important to remember that mega-doses of nutrients can potentially impair immune function and have other toxic effects. Therefore, strategic provision of immunomodulatory nutrients should be undertaken with caution until research has confirmed safe and effective application in the horse. For the time being, it is recommended to provide performance horses with a balanced diet, minimize stress, and keep current with vaccinations.
References:
Calder, PC et al. (2002) Nutrition and Immune Function. CABI Publishing, New York, New York.
Castell, LM (2003) Glutamine supplementation in vitro and in vivo, in exercise and immunodepression. Sports Med. 33:323-345.
Gannon, GA et al. (1995) Natural killer cells: modulation by intensity and duration of exercise. Exerc. Immunol. Rev. 1:26-48.
Gleeson, M (2006) Can nutrition limit exercise-induced immunodepression? Nutr. Rev. 64:119-131.
Gleeson, M (2007) Immune function in sport and exercise. J. Appl. Physiol. 103:693-699.
Harris, RC et al. (2006) Plasma glutamine concentrations in the horse following feeding and oral glutamine supplementation. Equine Vet. J. 30 (Suppl.):612-616.
Kryzwkowski, K et al. (2001a) Effect of glutamine supplementation on exercise-induced changes in lymphocyte function. Amer. J. Cell Physiol. 281:C1259-C1265.
Kryzwkowski, K et al. (2001b). Effect of glutamine and protein supplementation on exercise-induced decrease in saliva secretory IgA in athletes. J. Appl. Physiol. 91:832-838.
Mitchell, JB et al. (1998) Influence of carbohydrate status on immune responses before and after endurance exercise. J Appl. Physiol. 84:1917-1925.
Nieman, DC and Pedersen, BK (1999) Exercise and immune function. Sports Med. 27:73-80.
Pedersen, BK et al. (1990) Indomethacin in vitro and in vivo abolishes postexercise suppression of natural killer cell activity in peripheral blood. Int. J. Sports Med. 11:127-131.
Pedersen, BK et al. (2000) Exercise and the immune system: regulation, integration, and adaptation. Physiol. Rev. 80, 1055-1081.
Peters, EM et al. (1993) Vitamin C supplementation reduces the incidence of post-race symptoms of upper respiratory tract infection in ultramarathon runners. Am. J. Clin. Nutr. 75: 170-174.
Peters, EM et al. (1996) Vitamin C as effective as combinations of antioxidant nutrients in reducing symptoms of upper respiratory tract infections in ultramarathon runners. South African J. Sports Med. 11:23-27.
Peters, EM et al. (2001) Vitamin C supplementation attenuates the increases in circulating cortisol, adrenaline and anti-inflammatory polypeptides following ultramarathon running. Int. J. Sports Med. 22:537-543.
Raidal, SL et al. (2000) Effect of single bouts of moderate and high intensity exercise and training on equine peripheral blood neutrophil function. Res. Vet. Sci. 68:141-146.
Rohde, T et al. (1998) Competitive sustained exercise in humans, lymphokine activated killer cell activity, and glutamine – an intervention study. Eur. J. Appl. Physiol. 78:448-453.
Routledge, NBH et al. (1999) Plasma glutamine status in the equine at rest, during exercise and following viral challenge. Equine Vet. J. 30 (Suppl.):612-616.
Sijben, JWC and Calder, PC (2007) Differential immunomodulation with long-chain n-3 PUFA in health and chronic disease. Proc. Nutr. Soc. 66:237-259.
Smith, LL (2003) Overtraining, excessive exercise, and altered immunity. Sports Med. 33:347-364.
Toft, AD et al. (2000) N-3 polyunsaturated fatty acids do not affect cytokine response to strenuous exercise. J. Appl. Physiol. 89:2401-2406.
Warren, LK (2006) Feeding omega-3 fatty acids. Proceedings of the Alberta Horse Owners and Breeders Conference. Pp 69-76.



 

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