Exercise-induced Immune Changes Research Articles

Aerobic physical training does not condition against strenuous exercise-induced changes in immune function but modulates T cell proliferative responses.

Exercise-induced stress induces considerable changes in the immune system. To better understand the mechanisms related to these immune changes during acute and chronic physical stress, we studied the effects of aerobic physical training (APT) on several parameters of the immune system. Previously untrained males (18-25 years of age) were divided into a group that was subjected to 6 months of APT (N.=10) and a sedentary control group (N.=7). The subjects performed a cardiopulmonary exercise test (CET) at 0, 3, and 6 months of the APT program. B cell (CD19+), T cell (CD4+ and CD8+), and natural killer cell (CD56+) levels, and mitogen-induced T cell proliferation and cytokine production (interleukin-1, interleukin-4, interleukin-12, and interferon-γ) were evaluated before and at 30 seconds and 24 hours after the CET. There was a significant increase in CD4+ T cells and natural killer cells and a significant reduction in T cell proliferation in both groups 30 seconds after the CET at 0, 3 and 6 months of the APT program. Of note, the trained group showed significantly lower resting T cell proliferation (before and 24 hour after the CET) than the sedentary control groups at 0, 3 and 6 months of the APT program. There were no significant differences in cytokine production after the CET between both groups at any time point of the APT program. These data show that APT does not condition against strenuous exercise-induced immune changes but significantly modulates T cell proliferative responses.

Anti-inflammatory Dietary Interventions and Supplements to Improve Performance during Athletic Training

Despite the numerous positive effects of physical exercise, some negative physiological changes occur in long-lasting heavy training with transient dysfunction of the immune system, increased inflammation, and oxidative stress. This is the case of elite athletes, who train intensively to compete at the highest levels. However, these athletes can counteract the negative effects of heavy training, reducing acute and chronic inflammations and supporting the immune system, with nutritional and supplementation countermeasures. For this purpose, macronutrient manipulation with an appropriate use of certain supplements can be considered as an intervention to reduce exercise-induced immune changes and inflammatory risk. For example, branched-chain amino acid (BCAA) supplementation may promote such immune responses in skeletal muscle. Furthermore, micronutrients play an important role in immune function; in particular, the antioxidant capacity of several dietary micronutrients (e.g., tocopherols, docosahexaenoate, and flavonoids) is very interesting to support the endogenous antioxidant defense systems of the athletes, counterbalancing the negative effects of oxidative damage due to free radicals. Some of these nutrients have potential anti-inflammatory properties as assessed by the attenuated levels of interleukin-6 (IL-6) and C-reactive protein (CRP).Key Teaching Points• Long-lasting heavy training plan and competition can lead to chronic immune suppression in athletes, increasing infection risk.• Chronic exercise increases mobilization of neutrophils, decreases mobilization of lymphocytes, and decreases the absolute and relative numbers of neutrophils at rest.• Nutritional deficiencies alter the immuno-system and increase infection risk.• Nutrition can influence exercise-induced immune suppression.• Elite athletes competing at the highest levels can benefit from nutritional and supplementation support to improve immunity and reduce acute and chronic inflammations.

76. The influence of running volume on CD4+ T cell subpopulations and the role of stress

The purpose of this study was to determine the influence of stress on exercise-induced immune changes. Twenty-nine recreational runners were recruited for this study. Each recorded the number of miles that they ran in the week leading up to the study visit, completed the State Trait Anxiety Inventory (STAI) and the Penn State Worry Questionnaire (PSWQ), and donated blood for assessment of CD4+ T cell subpopulations and cytokine production. Participants ran an average of 30 (13.4) miles per week and had average STAI and PSWQ scores of 32.6 (12.6) and 40 (16.6), respectively. Average values (SD) for immune biomarkers were as follows: Treg, 3.2% (1.2); Tr1, 27.1% (8.3); Th3, 7.4 (6.1); IFNγ, 32,027 pg/ml (26,404); IL4, 8.1 pg/ml (13.7); IFNγ/IL4, 10,610 (12,485); IL10, 512 pg/ml (288). Overall, there were significant correlations between Treg and running volume (beta = 0.051%, p = 0.002) and IL10 production and running volume (beta = −10.57 pg/ml, p = 0.007), and a borderline significant correlation between Tr1 and running volume (beta = −0.198%, p = 0.093). High levels of anxiety and worry were associated with a significant negative correlation between Tr1 and running volume and a significant positive correlation between IFNγ and running volume while low levels of anxiety and worry were not. These data indicate that high levels psychological stress can potentiate immunological changes resulting from endurance-based exercise.

Physiological and leukocyte subset responses to exercise and cold exposure in cold-acclimatized skaters.

We investigated physiological responses and changes in circulating immune cells following exercise in cold and thermoneutral conditions. Participants were short track skaters (n=9) who were acclimatized to cold conditions, and inline skaters (n=10) who were not acclimatized. All skaters were young, and skating at a recreational level three days per week for at least one year. Using a cross-over design, study variables were measured during 60 min of submaximal cycling (65% O2max) in cold (ambient temperature: 5±1°C, relative humidity: 41±9%) and thermoneutral conditions (ambient temperature: 21±1°C, relative humidity: 35±5%). Heart rate, blood lactate and tympanic temperature were measured at rest, during exercise and recovery. Plasma cortisol, calprotectin and circulating blood cell numbers were measured before and after 60 min of cold or thermoneutral conditions, and during recovery from exercise. Heart rate was lower in both groups during exercise in cold versus thermoneutral conditions (P<0.05). The increase in total leukocytes during recovery was primarily due to an increase in neutrophils in both groups. The cold-acclimatized group activated neutrophils after exercise in cold exposure, whereas the non-acclimatized group activated lymphocyte and cortisol after exercise in cold exposure. Lymphocyte subsets significantly changed in both groups over time during recovery as compared to rest. Immediately after exercise in both groups, CD16+ and CD69+ cells were elevated compared to rest or before exercise in both conditions. Acclimatization to exercise in the cold does not appear to influence exercise-induced immune changes in cold conditions, with the possible exception of neutrophils, lymphocytes and cortisol concentration.

Immunonutrition support for athletes

Multiple components of the immune systems in athletes exhibit transient dysfunction after prolonged, heavy exertion. During this "open window" of impaired immunity, pathogens may gain a foothold, increasing infection risk. Nutritional supplements have been studied as countermeasures to exercise-induced immune changes and infection risk. This review focuses on findings from recent exercise-based studies with macro- and micronutrient supplements, and "advanced" immunonutrition supplements including beta-glucan, curcumin, and quercetin. Results from these studies indicate that immunonutrition supplements have the potential to lessen the magnitude of exercise-induced perturbations in immune function and to reduce the risk of upper respiratory tract infections.

Effect of Whey Protein Isolate on Oxidative Stress, Exercise Performance, and Immunity

1183 PURPOSE: The purpose of this study was to evaluate the effect of a whey protein isolate (WPI), a reported glutathione (GSH) booster, on exercise performance, immune function, and antioxidant status during weight maintenance and energy restriction in athletes. METHODS: Twenty, college-age, male cyclists performed a submaximal cycling exercise test for 45 min immediately followed by a performance test set at 90% VO2peak until exhaustion. Blood samples were collected prior to, after 45 min, at exhaustion and 1 h after exercise and analyzed for tGSH, GSH/GSSG ratio, white blood cell (WBC) GSH, glutathione peroxidase (GPx), lipid hydroperoxides (LPO), and several immunity measures. Subjects consumed 40 g/day of WPI or casein placebo (P) along with their normal diet for 2 wk, repeated the exercise test, and then began a low energy diet (20 kcal/kg/d), continuing the same supplementation, for 4 d before the final exercise test. RESULTS: WPI was not associated with superior exercise performance, antioxidant status, or immune function following exercise or weight loss. There was a nonsignificant increase following 2 wk supplementation in tGSH for WPI (trial 1 = 1288 ± 39, trial 2 = 1416 ± 54μmol/mg protein) compared to P (trial 1 = 1359 ± 35, trial 2 = 1399 ± 54μmol/mg protein). Following exhaustive exercise for all trials, tGSH and GPx increased 7% and 11%, respectively, while WBCGSH decreased 13%. Exhaustive exercise caused a 28% increase in CD8+ T-cells and decreased CD4+ (34%), CD3+ (15%), the CD4+/8+ ratio (45%), and phagocytosis (8%) (p<0.05), with all values returning to baseline after 1 h recovery. Weight loss was not different between groups with WPI losing 2.4 ± 0.4 kg and P losing 2.9 ± 0.3 kg. Energy restriction resulted in increases in phagocytosis (65%), WBCGSH (40%), and GPx (35%) while decreasing the GSH/GSSG ratio (55%) and LPO (16%) (p<0.05). CONCLUSIONS: Supplementation with WPI did not enhance GSH status, exercise performance, or exercise-induced immune changes, in trained cyclists, during weight maintenance or energy restriction. Energy restriction reduced indicators of oxidative stress.

Exercise and hypoxia: effects on leukocytes and interleukin-6-shared mechanisms?

Stress-induced immunological reactions to exercise have stimulated much research into stress immunology and neuroimmunology. It has been suggested that exercise can be employed as a model of temporary immunosuppression, which occurs during physical stress, such as hypoxia. Acute exercise and acute hypoxia mediate in principle identical effects on circulating lymphocyte and neutrophil numbers. Thus, during exercise and hypoxia, lymphocytes are recruited to the blood. After the stress, the number of lymphocytes declines after the stress, whereas the neutrophil number continues to increase. When exercise is performed during hypoxia, the exercise-induced immune changes are pronounced. There is some evidence that the exercise- and hypoxia-induced changes in leukocyte subpopulations are mediated by neuroendocrinological factors such as catecholamines, growth hormone, and cortisol. In contrast, although exercise, as well as hypoxia, is associated with increased plasma levels of IL-6, the mechanisms are not likely to be the same. Thus, during exercise, contracting skeletal muscles are the main source of IL-6 production, whereas the source of IL-6 during hypoxia has not been demonstrated. The increased level of adrenaline contributes to the enormous increase in plasma IL-6 only to a minor degree during strenuous exercise. However, the only modest increase in IL-6 during hypoxia may be linked to hormonal changes, whereas the prolonged increase in IL-6 during chronic hypoxia is likely to be multifactorial.

Nutrition and sport

Nutrition and sport

Exercise and the immune system: regulation, integration, and adaptation.

Stress-induced immunological reactions to exercise have stimulated much research into stress immunology and neuroimmunology. It is suggested that exercise can be employed as a model of temporary immunosuppression that occurs after severe physical stress. The exercise-stress model can be easily manipulated experimentally and allows for the study of interactions between the nervous, the endocrine, and the immune systems. This review focuses on mechanisms underlying exercise-induced immune changes such as neuroendocrinological factors including catecholamines, growth hormone, cortisol, beta-endorphin, and sex steroids. The contribution of a metabolic link between skeletal muscles and the lymphoid system is also reviewed. The mechanisms of exercise-associated muscle damage and the initiation of the inflammatory cytokine cascade are discussed. Given that exercise modulates the immune system in healthy individuals, considerations of the clinical ramifications of exercise in the prevention of diseases for which the immune system has a role is of importance. Accordingly, drawing on the experimental, clinical, and epidemiological literature, we address the interactions between exercise and infectious diseases as well as exercise and neoplasia within the context of both aging and nutrition.

Exercise and immune function: effect of ageing and nutrition.

Strenuous exercise is followed by lymphopenia, neutrophilia, impaired natural immunity, decreased lymphocyte proliferative responses to mitogens, a low level of secretory immunoglobulin A in saliva, but high circulating levels of pro- and anti-inflammatory cytokines. These exercise-induced immune changes may provide the physiological basis of altered resistance to infections. The mechanisms underlying exercise-induced immune changes are multifactorial and include neuroendocrinological and metabolic mechanisms. Nutritional supplementation with glutamine abolishes the exercise-induced decline in plasma glutamine, but does not influence post-exercise immune impairment. However, carbohydrate loading diminishes most exercise effects of cytokines, lymphocyte and neutrophils. The diminished neutrophilia and elastase (EC 3.4.21.37) responses to eccentric exercise in elderly subjects were enhanced to levels comparable with those of young subjects by fish oil or vitamin E supplements. However, although vitamin C supplementation may diminish the risk of contracting an infection after strenuous exercise, it is not obvious that this effect is linked to an effect of vitamin C on exercise-induced immune changes. In conclusion, it is premature to make recommendations regarding nutritional supplementation to avoid post-exercise impairment of the immune system.