Acute immune response in respect to exercise-induced oxidative stress
Introduction
One of the most actual problems of sports medicine is to prevent athletes from disease and infections during intensive training and competition periods. The risk of infection near the decisive competition is significantly elevated, especially when, during training camps, the athletes live together and infection can be spread and ruin the work of several years. Although, moderate training enhances many aspects of immune function, exhaustive exercise may impair immune responses increasing athlete's susceptibility to infection [1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12] and, possibly, to autoimmune diseases and cancer [13], [14]. Epidemiological data suggest that endurance athletes are at increased risk for upper respiratory tract infection (URTI) during periods of heavy training and up to 2-weeks period following competition [15]. Exercise-related immunological changes include signs of inflammation, such as release of cytokines, activation of immunocompetent cell lines, complement, and the induction of acute phase proteins [7], [8], [16], [17], [18], [19]. However, the signs of immunosuppression, such as decreased T and B cell function and impaired cytotoxic or phagocytic activity, can also be observed [20], [21], [22]. The immunological response to exercise comprises numerous alterations within the immune system; but how these processes are regulated is still largely unknown. There has been substantial evidence for link between the neurohormonal and the immune system [23], [24], [25]. It is thought that stress hormones like adrenaline and cortisol cause the mobilization of granulocytes from extracirculatory pool [26]. Plasma concentrations of adrenaline and noradrenaline increase almost linearly with the duration of exercise and exponentially with its intensity when expressed relative to individual maximal oxygen uptake [27], [28]. The expression of β-adrenoreceptors on T, B and NK cells, macrophages and neutrophiles provides the molecular basis for these cells to be targets for catecholamine signaling [29], [30]. On the other hand, it has been reported that catecholamines can autooxidize and lead to free radical production [31], [32] or undergo metal ion-catalyzed oxidation to free radical products [33]. Hence, they provide a potential source of free radical production during exercise.
Heavy exercise is associated with substantial increases in oxygen consumption and production of reactive oxygen species (ROS) [34], [35], [36], [37]. Strenuous exercise is known to induce oxidative stress [35], [37], [38], [39], [40], a state where pro-oxidants overwhelm the antioxidant defense capacity [41], [42], [43]. Previously, it has been shown that physical exercise may cause depletion and oxidation of GSH, a crucial factor in the maintenance of tissue-antioxidant defenses and in the regulation of redox sensitive-signal transduction [44], [45], [46], [47], [48]. Likewise, reactive oxygen species promote complement activation [49], as well as facilitate vascular translocation of leukocytes by inducing expression of adhesion molecules [50]. Despite the substantial evidence indicating that strenuous exercise induces oxidative stress and acute immune response, information concerning interactions between antioxidant defense and immune system within exercise is scanty. This study was, therefore, primarily focussed on monitoring of oxidative stress markers and cellular immune response within exercise until volitional exhaustion.
Increased knowledge about the cross talk between exercise-induced oxidative stress and acute immune response is important for developing means for maximizing the health benefits of exercise and improving sports performance.
Section snippets
Material and methods
Nineteen male endurance-trained athletes (age 22.21±5.58 years, VO2max 69.79±8.22 ml/kg/min) were recruited into the study after obtaining an informed consent. The experimental procedures and protocol conformed to the principles of the Declaration of Helsinki and were approved by the Human Ethics Committee of the University of Tartu. Reasons for exclusion included any deviation from the criteria of good health, smoking, chronic medication or vitamin supplementation.
Maximal oxygen consumption
The mean VO2max (69.72±8.73 ml/kg/min) indicated that the men were highly fit.
Hemoglobin and hematocrit
Both Hb concentration and Hct rose markedly with exercise (P=0.0004–0.0014), but returned to pre-exercise level in 30-min recovery period (Table 1).
Cellular immune response
Exercise until volitional exhaustion induced leukocytosis (P<0.00001) in the peripheral blood, which returned to pre-exercise level during 30-min recovery (Table 2). Neutrophilia was prominent (P<0.00001) immediately after exercise, but returned to pre-exercise level in
Discussion
Exercise until volitional exhaustion caused oxidative stress as evident from the lipid peroxidation data. Our finding of elevated serum TBARS and DC in post-exercise samples is consistent with previous reports [58], [59].
We found that serum total antioxidant status (ability to scavenge free radicals) increased significantly in 30-min recovery, which may indicate compensation in response to exhaustive exercise. Previously, it has been shown that half-marathon in 17 trained male runners induced
Acknowledgements
This work was supported by Estonian Science Foundation and Finnish Center for International Mobility.
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