Integrative physiology studies have shown that immune system and central nervous system interplay very closely towards behavioural modulation. Since the 70-kDa heat shock proteins (HSP70s), whose heavy expression during exercise is well documented in the skeletal muscle and other tissues, is also extremely well conserved in nature during all evolutionary periods of species, it is conceivable that HSP70s might participate of physiologic responses such as fatigue induced by some types of physical exercise. In this way, increased circulating levels of extracellular HSP70 (eHSP70) could be envisaged as an immunomodulatory mechanism induced by exercise, besides other chemical messengers (e.g. cytokines) released during an exercise effort, that are able to binding a number of receptors in neural cells. Studies from this laboratory led us to believe that increased levels of eHSP70 in the plasma during exercise and the huge release of eHSP70 from lymphocytes during high-load exercise bouts may participate in the fatigue sensation, also acting as a danger signal from the immune system.

Exercise stimulates immune responses, but the appropriate "doses" for such achievements are unsettled. Conversely, in metabolic tissues, exercise improves the heat shock (HS) response, a universal cytoprotective response to proteostasis challenges that are centred on the expression of the 70-kDa family of intracellular heat shock proteins (iHSP70), which are anti-inflammatory. Concurrently, exercise triggers the export of HSP70 towards the extracellular milieu (eHSP70), where they work as pro-inflammatory cytokines. As the HS response is severely compromised in chronic degenerative diseases of inflammatory nature, we wondered whether acute exercise bouts of different intensities could alter the HS response of lymphocytes from secondary lymphoid organs and whether this would be related to immunoinflammatory responses. Adult male Wistar rats swam for 20 min at low, moderate, high or strenuous intensities as per an overload in tail base. Controls remained at rest under the same conditions. Afterwards, mesenteric lymph node lymphocytes were assessed for the potency of the HS response (42 °C for 2 h), NF-κB binding activity, mitogen-stimulated proliferation and cytokine production. Exercise stimulated cell proliferation in an "inverted-U" fashion peaking at moderate load, which was paralleled by suppression of NF-κB activation and nuclear location, and followed by enhanced HS response in relation to non-exercised animals. Comparative levels of eHSP70 to iHSP70 (H-index) matched IL-2/IL-10 ratios. We conclude that exercise, in a workload-dependent way, stimulates immunoinflammatory performance of lymphocytes of tissues far from the circulation and this is associated with H-index of stress response, which is useful to assess training status and immunosurveillance balance.

Moderate exercise positively impacts innate immune functions, bringing about a better resistance against infections and general immunosurveillance. Exercise of high workloads (i.e., high intensity and/or duration) such as elite marathon, on the other hand, may have detrimental effects over immune function, but neither how long nor how intense should be the exercise sessions to be deleterious is known, this being a matter of intense dispute. Exercise is, at the same time, one of the most powerful inducers of the 70 kDa family of heat shock proteins (HSPAs, formerly known as HSP70s), which are protein chaperones characterized by a marked anti-inflammatory potency, when located intracellularly (iHSPA), but may act as pro-inflammatory cytokines if in the extracellular space (eHSPA). The above observations led us to suppose that short-term exercise could impose long-lasting effects on macrophage function that should be related to the eHSPA-to-iHSPA ratio, viz. H-index. Sedentary adult male Wistar rats were then submitted to 20 min swimming sessions with an overload (as a percentage of body weight attached to the tail base) of either 2, 4, 6, or 8 %. Control animals were maintained at rest in shallow water. Monocyte/macrophage functions (phagocytic capacity, nitric oxide [NO], and hydrogen peroxide [H2O2]) were assessed just after and 12 h after exercise and compared with HSPA status and oxidative stress markers. The results showed that exercise increased phagocytosis and H2O2 immediately after the bouts in a workload-dependent way. This was accompanied by increased H-index but no alteration in the redox status. Enhanced phagocytic capacity persisted for up to 12 h, when a marked rise in NO production was also observed, but H-index resumes its control values, suggesting that immune alertness returned to basal levels. Of note was the detection of the cognate form of eHSPA (encoded by hspa8 gene and formerly known as HSP73) in the rat sera. In total, acute exercise may evoke 12 h long workload-dependent effects associated with HSPA status.

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Aim. The purpose of this study was to determine the response of circulating markers of lipid and protein oxidation following an incremental test to exhaustion before and after 4 weeks of high-intensity interval training performed in the heat. Methods. To address this question, 16 physically active men (age = 23 ± 2 years; body mass = 73 ± 12 kg; height = 173 ± 6 cm; % body fat = 12.5 ± 6 %; body mass index = 24 ± 4 kg/m2) were allocated into 2 groups: control group (n = 8) performing high-intensity interval training at 22°C, 55% relative humidity and heat group (n = 8) training under 35°C, 55% relative humidity. Both groups performed high-intensity interval training 3 times per week for 4 consecutive weeks, accumulating a total of 12 training sessions. Before and after the completion of 4 weeks of high-intensity interval training, participants performed an incremental cycling test until exhaustion under temperate environment (22°C, 55% relative humidity) where blood samples were collected after the test for determination of exercise-induced changes in oxidative damage biomarkers (thiobarbituric acid reactive species and protein carbonyls). Results. When high-intensity interval training was performed under control conditions, there was an increase in protein carbonyls (p < 0.05) following the incremental test to exhaustion with no changes in thiobarbituric acid reactive species. Conversely, high-intensity interval training performed in high environmental temperature enhanced the incremental exercise-induced increases in thiobarbituric acid reactive species (p < 0.05) with no changes in protein carbonyls. Conclusion. In conclusion, 4 weeks of high-intensity interval training performed in the heat enhances exercise-induced lipid peroxidation, but prevents protein oxidation following a maximal incremental exercise in healthy active men.