For example, an ample supply of vitamin A is essential for the innate immune system to operate at full capacity. However, in winter, nutrients like vitamin A found in red, orange and dark green fruits and vegetables tend to be in shorter supply in the diet because many people consume much smaller quantities of fruits and vegetables, preferring warm, stodgy and comforting foods instead.

The same is true of the acquired immune system, which needs an amply supply of a wide range of nutrients to operate at full potential. Any shortfall in just one single nutrient can adversely affect immunity.

This explains why your immunity can be used as an excellent barometer of your overall nutrition status. Key nutrients for immunity OK, given the above facts, what are the basic rules for bolstering immunity during the winter months? Make sure too that your alcohol intake is within recommended limits for health, as too much can result in significant immune depression.

The following nutrients and foods are especially important for maintaining maximum immunity: Vitamins Vitamin A — well supplied in liver, eggs, all orange and red fruits and vegetables such as carrots, sweet potatoes, apricots.

Vitamin C — found in citrus fruits such as oranges and grapefruits, kiwis, all the berries, also well supplied in tomatoes and peppers.

Vitamin D — good sources include eggs, milk, butter, cod liver oil see box on supplements and some other fish oils.

Essential fatty acids ie omega-3 and omega-6 oils — good sources include all the fatty fish trout, sardines, herrings, salmon, mackerel, pilchards, etc as well as unrefined whole grains and nuts and seeds, especially, hemp, flax, walnuts and pumpkin seeds.

Minerals Zinc — a vital immune nutrient; good sources are high quality, lean cuts of meat and fish and shellfish; also found in whole grains and some nuts and seeds, such as walnuts and pumpkin seeds.

Selenium — well supplied in unrefined whole grains eg wholemeal bread , all seafood and some nuts and seeds, especially Brazil nuts. Post-exercise nutritional strategy In recent years, a number of studies have shown that low carbohydrate consumption is associated with increased levels of stress hormones and lowered immunity.

The reason is that when carbohydrate stores are low, vigorous exercise promotes a process known as catabolism, where body tissue such as muscle is broken down in order to provide energy.

Catabolism is associated with higher levels of circulating stress hormones such as adrenaline and cortisol, which have a negative effect on immunity. This will help to reduce the extent of carbohydrate depletion during exercise.

Do supplements help boost immunity? However, some products have been scientifically investigated and are worth considering see below.

Bear in mind, however, that no amount of supplementation can make up for an inherently poor basic diet! Indeed, because we can synthesise and store vitamin D in the skin when exposed to spring and summer sunshine, some researchers now believe that this increased level of vitamin D is a major factor in our improved immunity during the summer months.

Vitamin C —The notion that vitamin C might be beneficial for combating URTIs is regarded as a universal truth by much of the general public, but unfortunately the evidence is somewhat mixed; some studies have shown that vitamin C supplementation reduces the incidence of URTIs, while other studies have reported no benefits.

On balance, though, the evidence suggests that some modest daily supplementation around mg is worthwhile. Garlic, chilli and ginger — these products have known antiviral and antibacterial effects — great news for curry lovers out there! They can also be used in a number of other dishes.

However, we really need more research in this area before we can confidently recommend routine daily use of these products specifically to boost immunity. Andrew Hamilton Andrew Hamilton BSc Hons, MRSC, ACSM, is the editor of Sports Performance Bulletin and a member of the American College of Sports Medicine.

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Great bang for your buck in terms of quality and content. There is robust evidence of causative links between exercise, improved immunity, and disease prevention. Indeed, an optimal functioning immune system plays a central role in health maintenance, promoting a well-balanced defense against microorganisms or aberrant cells.

In this light, exercise training is recommended as a multifaceted intervention for health 1 , 2. Nevertheless, intense and prolonged exercise bouts seem to produce a temporary immunodepression, associated with a decreased host protection and, in turn, an increased risk of diseases, particularly infections, as documented by studies on athletes 3 , 4.

The human immune system is intensely shaped by exercise and by a variety of stimuli, such as stress, lack of sleep, general health status, environmental extremes altitude , competition, and nutrients. Among others, vitamin D is a well-known regulator of the immune response, acting on several immune cell types, including macrophages, antigen-presenting cells APC , dendritic cells DCs , T cells, and B cells, which express vitamin D receptor VDR , either constitutively or upon activation 5.

Adequate levels of vitamin D are recommended to maintain immunity and prevent illness. Currently, overwhelming evidence suggests that D hypovitaminosis is similarly widespread in the general population and in athletes 6 — 9. A vitamin D-deficient athlete may be at an increased risk of potential problems like stress, fractures, respiratory infections, muscle injuries, and immune system depression.

Remarkably, vitamin D remodels and strengthens immunity, not only acting directly on immune cells but also modulating the so-called immune ability of nonproperly working immune tissues, such as the skeletal muscle 12 — Indeed, besides resident immune compartments, which exert inflammatory, protective, and reparative functions, the skeletal muscle can behave as a proper immune secretory organ, functioning as a checkpoint within a complex integrated network of immune-endocrine signals, malleable by exercise and vitamin D.

Thus, the interplay between exercise and vitamin D status seems to play a pivotal role in immune health homeostasis. This review aims to provide an overview of how vitamin D shapes human immunity, acting on both the immune system and skeletal muscle, and how it interplays with exercise to profile whole-body immune response, focusing on athletes.

In the first part of the paper, some aspects of exercise-related modifications in the immune system are summarized with pros and cons. A sedentary lifestyle is associated with an increased risk of comorbidities, including cardiovascular and metabolic diseases, cancer, neurodegeneration, and depression.

The expanded adipose tissue, along with infiltrated resident macrophages, is recognized to be the main source of prototypic inflammatory Th1 cytokines, such as tumor necrosis factor TNF -α Those positive effects are promoted by improvements in immune function and opposition to immune senescence, a biological age-related decline of immune surveillance, leading to higher susceptibility to infections, lower efficacy of vaccination, and higher risk of cancer 30 — In the elderly, physical activity is associated with better immune response and better protection of the influenza vaccine 33 , In addition to the benefits of some age-related alterations, excellently summarized in a recent review 35 , studies on young subjects document that exercise boosts the immune system by acting on circulating inflammatory cytokines and decreasing the secretion of several inflammatory cytokines, including TNF-α, interferon IFN -γ, interleukin IL -1β, IL-2, IL-6, and IL-8 36 , In early investigations, the anti-inflammatory effect was associated with an increased risk of infections due to exercise-induced immunodepression, as addressed hereafter.

The decrease of reactive oxygen and nitrogen species ROS and RNS, respectively and the simultaneous increase of antioxidant defense—by potentiating enzymatic activity of catalase, superoxide dismutase, glutathione peroxidase—are examples of the multiple mechanisms involved in exercise-induced support to the immune system 38 , Exercise significantly supports immune response by promoting immune cell recirculation from lymphoid tissues and their interchange with blood: intensity-dependent leukocytosis is followed by an increase in the number and redistribution of effector cells to peripheral tissues.

Leukocyte recirculation following exercise likely depends on cell mobilization and demargination of previously circulating cells, driven by surface modifications of adhesion molecules, rather than de novo bone marrow release It has been suggested that the modifications to natural killer NK and T-cell trafficking promoted by exercise might potentially have important implications for health, i.

Furthermore, during moderate exercise lasting less than 1 h , stress hormones do not reach the high concentration needed to act as a suppressor of immunocyte activity This transient effect results in immune surveillance boosting.

Stress hormone-induced modifications to cell number, surface molecule expression, and cell deformation, found in different cell subsets, are greater with prolonged intense exercise, as exhaustively reported elsewhere Exercise-induced positive regulation of the immune system involves several mechanisms, including the qualitative shift from a Th1 to a Th2 response, the enhancement of mitochondrial function in peripheral blood mononuclear cells, and the regulation of immunometabolism toward more oxidative phenotypes 48 — Thus far, albeit research in exercise immunology is still emergent and gaps in the knowledge exist, the summation of the effects induced by each bout of moderate exercise repeated over time significantly strengthens immune surveillance against pathogens, inflammatory disorders, and cancer cells by several mechanisms, collectively supporting the therapeutic potential of exercising 55 , 56 , as summarized in Table 1.

Nevertheless, it is undeniable that heavy exertion as practiced by athletes may be associated with increased inflammation, oxidative stress, and increased risk of illness. The attention on immune response in athletes is currently high since heavy training workloads might turn to an immune dysfunctional response and increased risk of illness.

This phenomenon gives rise to questions on a possible edge separating the immune-depressive from the immune-boosting effect of exercise, particularly in athletes 57 , The pioneering studies on changes in basic immune cell counts and function evidenced profound perturbations of leukocyte subsets linked to endeavor-related stress 57 , 59 — The relationship between the risk of URTI and exercise intensity in humans mostly emerged from self-reported sickness logs and was substantially confirmed in animals, albeit mechanistic experimental studies are often not immediately translated to humans, considering the difficult comparison across species due to the high variability of exercise protocols or adaptation 78 — To date, this hypothesis has been argued and it is still under debate In fact, exercise in a moderate regimen on a regular basis can decrease illness incidence by dampening inflammation and infections, as previously addressed 57 , This result persists after adjustment of confounders, such as age, gender, education level, marital status, and mental stress 56 , Athletes undergoing repeated heavy exertion cycles, i.

Albeit pure cause—effect relationships between heavy exertion and risk of diseases either infective or not have not yet been clarified, some chief organizations, such as the International Olympic Committee and the International Association of Athletic Federation, have introduced surveillance programs to prevent and manage this important problem 58 , 86 — Remarkably, exercise stress represents such a challenge for the immune system, requiring biosynthetic and oxygen bioavailability to promptly reprogram and support effector cell metabolism and production of specific mediators, like cytokines, involved in the inflammatory response.

Indeed, intensely trained athletes show important alterations in the bioactive lipidome and proteome, like metabolites from lipid super pathways oxylipins or immune-related proteins, largely involved in immune cell chemotaxis and migration, mediating organ cross-talk during inflammatory responses 90 — In this scenario, the multiomics approach highlights the importance of nutritional interaction on immune modifications in response to exercise.

Of several factors, vitamin D status is highly critical, considering that this molecule can control whole-body immunity, affecting the immune system and the immune activity of skeletal muscle. The diet of athletes should provide sufficient nutrients and micronutrients—proteins, carbohydrates, minerals, and vitamins—to meet their energy needs and maintain at best their immune health 4.

Furthermore, larger increases in circulating stress hormones and greater immune perturbation have been reported in athletes exercising in a carbohydrate-depleted state The explanation for this widespread D inadequacy is likely due to different factors. First, ultraviolet UV B sunrays insufficient exposure, which is the main source of vitamin D, in addition to the diet few foods naturally contain it or vitamin D-fortified foods, as previously reported Regardless of the cause, vitamin D hypovitaminosis is acknowledged in the global athletic population and attracts growing attention.

Instead, concerns should be addressed about general health rather than limited to performance, considering the tight control exerted by vitamin D on some important functions, broadly affecting health in all individuals, including athletes. Vitamin D, behaving as a typical steroid hormone or as a micronutrient with rapid mechanisms, exerts pleiotropic effects via interaction with vitamin D receptor VDR , virtually expressed by every human tissue , In addition to homeostasis regulation in bone, which is the classical tissue target of this molecule, it is well recognized that vitamin D significantly impacts the inflammatory status, which, in turn, is acknowledged as the common link in several noxious conditions, including infections, joint degenerative diseases, and disturbance of metabolism, to mention some — Unfortunately, the ability of vitamin D to modulate the immune response can be listed among the main mechanisms underlying its anti-inflammatory effects.

Vitamin D signaling, indeed, ensures the suppression of proinflammatory status, downregulating T cells and cytokines like IL-2, IL-6, IL-8, IL, tumor growth factor TGF -β, IFN-γ, IL, and IL, simultaneously enabling Treg subset expansion with increased production of protolerogenic mediators, such as IL-4, IL-5, IL, IL, and CCL2 — Interestingly, IL promotes long-lasting antigen-specific T-cell anergy and plays a driving role for type 1 T regulatory Tr1 cells, the cell subset known to be critical for maintaining tolerance to self and nonself antigens in humans and animals, in the presence of APC, as emerged from in vitro experiments — Of note, vitamin D induces macrophage and epithelial cells to produce cathelicidin, a protein with marked antimicrobial activity, able to improve macrophage bacterial capacity involved in host-first-line defense — Furthermore, vitamin D impairs macrophage inflammatory cascade by targeting cyclooxygenase 2 COX-2 and inducible nitric oxide synthase iNOS and, therefore, reducing nitric oxide NO and prostaglandin PG E2 Figure 1 summarizes the main effects induced by vitamin D in different types of immunocytes.

Figure 1 Vitamin D-induced immune regulation of the immune system and skeletal muscle. Vitamin D controls inflammation and promotes tolerogenic status, acting on several types of circulating immune cells, skeletal muscle cells, and intraorgan immune cells. Adequate vitamin D levels can downtone exercise-induced inflammatory-like response and converge to exercise-induced immunosurveillance boosting, with protective effects on whole-body health.

Overtraining athletes in hypovitaminosis D can be at higher risk of infectious and noninfectious diseases. The higher production of cathelicidin and defensin another host-defense peptide induced by vitamin D along with its anti-inflammatory action would promptly reduce the cytokine storm during infection by COVID Indeed, recent investigations in COVID patients document the usefulness of vitamin D administration due to the protective effects against mortality and intensive care unit admission , Adequate vitamin D status combined with the practice of exercise seems to promote positive outcomes in COVID, albeit the research on this specific topic is still in its infancy It has been reported that sex-dependent dimorphism in vitamin D metabolism likely explains the greater immune vulnerability to perinatal infections observed in male vs.

It would be interesting to extend this kind of investigation into adulthood to verify whether similar mechanism s may underlie some sex-dependent differences in response to infections including COVID , which are also seen in athletes and are frequently mistreated , In B cells, vitamin D inhibits proliferation and immunoglobulin production similarly to heavy exertion, whereas repeated bouts of moderate-intensity exercise enhance B-cell proliferation.

Exercise upregulates VDR expression in T cells regardless of exercise-induced T-cell mobilization , therefore enhancing the anti-inflammatory loop. Thus far, vitamin D can impact both innate and adaptive immunity with a decisive anti-inflammatory profile.

While this effect was initially simplistically considered immunosuppressive, the current concept focuses on the exquisite modulating role of vitamin D toward tolerogenic homeostasis Conversely, low vitamin D levels are associated with deficits in immune surveillance, including lower salivary IgA and increased risk of long-lasting respiratory infection, as observed in elite athletes Indeed, hypovitaminosis D-shaped modifications in the immune system often converge on and amplify heavy exertion-induced effects.

Furthermore, vitamin D deficiency is described in the pathophysiology of Th2-driven allergic diseases such as asthma, in which the lower hormone levels are associated with IL-4, IL-5, IL-9, and IL deregulation, increase in asthma markers IgE and eosinophil , and more severe clinical disease manifestation, as reported — To date, vitamin D deficit-dependent damage is not limited to the immune system but highly impacts the function of skeletal muscles; since this tissue exhibits important immunocompetent capacity, whole-body immune surveillance is further compromised.

Skeletal muscle is a nontraditional target tissue of vitamin D and is finely regulated by this molecule at several levels. According to experimental and human studies, insufficient vitamin D levels and VDR deletion cause critical muscular dysfunctions — Lower levels of vitamin D are associated with a significant reduction in muscle fiber size and atrophy mainly of type II fiber , and overall, determine muscular defects in energy handling as insulin resistance , plasticity, and contraction, in the general population and in athletes as well , Conversely, higher vitamin D levels are reported to be linked with lower injury rates and improved sports performance The beneficial effects of vitamin D on skeletal muscle function are related to the fine-tuned regulation exerted at the cell level through VDR interaction, albeit, in the past, the presence of this receptor in human muscle was questioned To date, VDR is mainly detected in fast-twitch muscle fibers committed to rapid actions and expressed at different levels in human isolated cells, depending on the cell fusion stage upregulation upon myotube formation , — Type II fiber atrophy significantly ameliorates with vitamin D, as documented in biopsies from vitamin D-deficient patients before and after the treatment with the hormone Vitamin D helps faster recovery from muscle injury and inflammation after high-intensity exercise , , whereas vitamin D-deficient athletes show a delayed recovery.

Generally, it can be stated that vitamin D affects almost all stages of the myogenic program toward regeneration, also acting on satellite cells.

Interestingly, regularly exercising maintains and enhances this functional feature Exercise is a well-known strategy against muscle wasting and atrophy, not only because it counteracts mass loss but because it exquisitely regulates the mitochondrial function and the internal immune component, both critical for muscle integrity maintenance during stress, as shown by multiomics analysis in astronauts during spaceflights Of note, exercise- and vitamin D-induced signals converge in the dynamic remodeling of mitochondria, promoting correct genomic reprogramming and skeletal muscle cell remodeling Beyond those beneficial effects, it is mandatory to highlight the function of vitamin D in maintaining the immune-secretory function of skeletal muscle, which is closely in line with the topic of this review.

Nowadays, the renewed and proven concept is that skeletal muscle is a proper secreting organ with immunoregulatory function. Currently, more than myokines are identified by the proteomic analysis of the muscular secretory profile, which is constantly updated Among this plethora of biomolecules, some myokines drew attention due to their ability to modulate the immune response, introducing a novel view of immunity-muscle crosstalk, which was previously considered to be a unidirectional route, with muscle being under immune system control and not vice versa.

Indeed, like other tissues, skeletal muscle has its resident immune cell population to warrant the regenerative potential and tissue homeostasis. Fiber damage due to different injuries, including contusions, strains, hyperextensions, avulsions, or ruptures, promptly activates neutrophils resident in skeletal muscle to release within the microenvironment high concentrations of inflammatory factors necessary for repair , Indeed, after neutrophils, macrophages represent the second subpopulation reaching the injured areas peak at 3 to 6 days and persisting 2 weeks after extensive damage , gradually shifting from a phagocytic to pro-myogenic phenotype, from M1 to M2 macrophages, respectively The shift in macrophage phenotype orchestrates the time of myogenic sequence, supporting first cell proliferation and migration, while delaying differentiation, and then facilitating alignment and fusion , During regenerative processes, soluble molecules as growth factors, cytokines, and prostaglandins regulate immune and muscle cell communications, but interestingly, close cell-to-cell contacts between myogenic cells and macrophages occur via adhesion molecules, macrophage pseudopodial extensions, and myogenic cell cytoplasmic protrusions , , T cells show a delayed response, roughly 4 days after the initial damage , Interleukin-6 is the prototypic myokine, the first one and most extensively studied.

Exercise-related pulsatile release of IL-6 promotes the anti-inflammatory macrophage subset M2-like , involving suppressor of cytokine signaling 3 SOCS3 ablation, and IL-1 receptor antagonist IL-1ra and IL, resulting in overall downregulation of inflammatory responses 52 , Interleukin-6 likely plays a central role in exercise-induced leukocytosis and late lymphopenia mediated by cortisol, as shown by IL-6 infusion in athletes In humans, IL-6 is known to counteract TNFα production and signaling from monocytes , Thus far, the myokine IL-6 likely characterizes exercise adaptation, as it is involved in long-term beneficial effects, related to an exercise-training reduction in abdominal fat and anti-inflammatory actions Vitamin D can enhance the biological effects of IL-6, as shown by the improved metabolic function observed in vitamin D-deficient trained men after a single intramuscular injection of vitamin D, which was associated with a significant rise of IL-6 1 h after resistance exercise The lack of modification in inflammatory parameters is likely due to the short duration of the treatment and the use of a single dose.

Interleukin-6 output from human skeletal muscle cells maintained in nutrient restriction, to mimic energy-demanding conditions such as postexercise, was significantly increased after the treatment with a VDR agonist Conversely, the addition of a VDR agonist to human muscle cells challenged by a strong proinflammatory environment significantly counteracted inflammation-induced intracellular cascade underlying Th1-type chemokine release Thus far, vitamin D modulation seems to be beneficial with prometabolic or anti-inflammatory effects, depending on the microenvironmental needs of skeletal myocytes.

Muscle-derived IL regulates macrophage differentiation, B-cell proliferation, neutrophil migration, and naïve T-cell survival This myokine tightly cooperates with vitamin D, promoting the conversion into the active hormone, the upregulation of VDR, and the induction of cathelicidin , IL-7 also plays a pivotal role in first-line immune defense; the age-dependent decline of this myokine can be counteracted by exercise and by vitamin D, which can help to restore aberrant ILdependent signal, i.

The main immune regulatory effects of vitamin D on intraorgan immunocytes and myocytes are depicted in Figure 1.

Athletes are thought to be in good health almost by definition, considering that many human diseases are tightly related to sedentary behavior and inflammation; importantly, the latter is a well-recognized bridge linking different and clustering illnesses. Nevertheless, the condition of overexercising, too often experienced in several sports disciplines, exposes athletes to a higher risk of inflammation and, consequently, a higher risk of diseases.

In this scenario, vitamin D status plays a critical role in immune health, as possible exercise-induced detrimental effects might merge with the poor immune health status determined by hypovitaminosis D.

Conversely, vitamin D adequacy counteracts inflammation, enhancing the immune defense and shaping the immune response of skeletal muscle, which is recognized to be a proper secreting organ with immune-like features.

Thus far, screening for vitamin D status would be mandatory in the athletic population as well. The lack of discussion on these aspects is among the limits of this review, which does not include sex-dependent differences in immune response or in vitamin D levels, or cardiovascular features.

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The effects of endurance running on the immune system have been well researched. In one study, a group of runners had blood drawn at regular intervals while running for three hours. Afterward, researchers looked at their white blood cells and hormone levels.

They observed an initial increase in most types of white blood cells and both cortisol and adrenaline levels. Following the endurance exercise, there was a subsequent reduction in some types of white blood cells. The immune system returned to normal within 24 hours of recovery.

Researchers have found a relationship between the intensity and duration of runs and immune function. Moderately intense workouts tend to strengthen the immune system.

For most people, this means an hour run at a steady pace. Running 10 miles or more or running to exhaustion, however, may temporarily weaken the immune system.

This impairment of immune function generally lasts only for a few hours, although for some people, it may take several days to recover, especially for those with an already weakened immune system.

Marathon runners have been observed to be up to six times more likely to get the common cold after a race. The answer is not to avoid long or hard runs, but rather to run smarter. Prevention is key.

Simple steps can be taken to reduce your risk of illness:. The data is currently mixed as to whether antioxidant supplements are of benefit to runners trying to prevent infection. Supplementation of vitamins is only helpful if someone is deficient in a vitamin more is not better.