The aim of this study was to compare the effect of low-load resistance exercise (LLRE) with continuous and intermittent blood flow restriction (BFR) on the creatine kinase (CK), lactate dehydrogenase (LDH), protein carbonyl (PC), thiobarbituric acid-reactive substance (TBARS) and uric acid (UA) levels in military men. The study included 10 recreationally trained men aged 19 ± 0.82 years who underwent the following experimental protocols in random order on separate days (72-96 h): 4 LLRE sessions at a 20% 1RM (one-repetition maximum [1RM]) with continuous BFR (LLRE + CBFR); 4 LLRE sessions at 20% 1RM with intermittent BFR (LLRE + IBFR) and 4 high-intensity resistance exercise (HIRE) sessions at 80% 1RM. The CK and LDH (markers of muscle damage) levels were measured before exercise (BE), 24 h post-exercise and 48 h post-exercise, and the PC, TBARS and UA (markers of oxidative stress) levels were measured BE and immediately after each exercise session. There was a significant increase in CK in the HIRE 24 post-exercise samples compared with the LLRE + CBFR and LLRE + IBFR (P = 0.035, P = 0.036, respectively), as well as between HIRE 48 post-exercise and LLRE + CBFR (P = 0.049). Additionally, there was a significant increase in CK in the LLRE + CBFR samples BE and immediately after each exercise (Δ = 21.9%) and in the HIRE samples BE and immediately after each exercise, BE and 24 post-exercise, and BE and 48 post-exercise (Δ values of 35%, 177.6%, and 177.6%, respectively). However, there were no significant changes in LDH, PC, TBARS, and UA between the protocols (P > 0.05). Therefore, a physical exercise session with continuous or intermittent BFR did not promote muscle damage; moreover, neither protocol seemed to affect the oxidative stress markers.

This study compared the acute effects of low-intensity resistance exercise (RE) sessions for the upper limb with continuous and intermittent blood flow restriction (BFR) and high-intensity RE with no BFR on lactate, heart rate, double product (DP; heart rate times systolic blood pressure), and perceived exertion (RPE). Ten recreationally trained men (1-5 years strength training; age mean = 19 ± 0.82 years) performed three experimental protocols in random order: (a) low-intensity RE at 20% one-repetition maximum (1RM) with intermittent BFR (LI + IBFR), (b) low-intensity RE at 20% 1RM with continuous BFR (LI + CBFR), and (c) high-intensity RE at 80% 1RM. The three RE protocols increased lactate and DP at the end of the session ( p < .05) and increased heart rate at the end of each exercise ( p < .05). However, greater local and general RPE was observed in the high-intensity protocol compared with LI + IBFR and LI + CBFR in the lat pull-down, triceps curl, and biceps curl exercises ( p < .05). A greater percentage change in DP and lactate was observed for continuous BFR compared with intermittent BFR; however, RPE was lower for intermittent BFR. In conclusion, intermittent BFR appears to be an excellent option for physical training because it did not differ significantly from continuous BFR in any variable and promoted a lower percentage change in DP and RPE.

Introduction: Over the last century, people have become less active, adopting more sedentary habits. This scenario has increased the incidence of chronic diseases such as cardiovascular diseases, type 2 diabetes and metabolic syndrome. The practice of physical activities can influence healthiness by altering the metabolic state and also the immune system. Objective: To review the literature for studies that address the effects promoted by physical exercise on the development of immune responses and the possible signal transduction pathways. Methods: The SciELO and PubMed data bases were consulted. Results: The available literature shows that during the practice of exercise, various subpopulations of leukocytes are altered in accordance with the intensity and duration of the activity performed. Exercise of moderate intensity stimulates a pro-inflammatory response, while those of high intensity tend to promote antiinflammatory responses that could decrease damage to skeletal muscle. Such alterations are observed in cells that present antigens (such as macrophages and dendritic cells), neutrophils, natural killer cells (NK) and in surface molecules like Toll-like receptors (TLR) and major histocompatibility complex class II, as well as the entire repertoire of cytokines. Conclusion: The current state of knowledge suggests that the alterations in the immune system are dependent on parameters inherent to exercise and that in order to have all these alterations occurring, some cell signaling cascades are activated, giving rise to a complex process of phosphorylation/dephosphorylation that culminates in the activation of transcription factors, translation of mRNA's, protein synthesis and cell proliferation.

Physical exercise can improve health and may lead to changes in the functionality of the immune system. Moderate intensity exercise can reduce the risk of infection by shifting the overall immune response towards a T helper type 1 pattern. This study investigates the effect of 12 weeks of swimming on the cytokine profile of lymph node cells and macrophages and of the nitric oxide production by these cells. BALB/c mice were divided into 2 groups. The exercise group was subjected to swimming exercise. Lymph node cells culture showed that concentrations of interferon-γ and tumour necrosis factor-α were higher in the exercised group, while levels of interleukine-4 and interleukine-10 were significantly decreased in this group. The interleukine-10/interferon-γ ratio tended towards a T helper type 1 profile. Moreover, macrophages isolated from exercised mice produced more interleukine-12 and tumour necrosis factor-α following lipopolysaccharide stimulus. Challenging these macrophages with Leishmania major resulted in higher interleukine-12 production than was observed with macrophages from the control group. Nitric oxide production was increased in macrophages isolated from exercised group following lipopolysaccharide stimulus but not following infection with Leishmania major. These data suggest that exercise biases the immune system towards a T helper type 1 response profile.

Both acute exercise and excessive training can cause oxidative stress. The resulting increase in free radicals and the inadequate response from antioxidant systems can lead to a framework of cellular damage. An association between affected tissue and the biomarkers of oxidative stress that appear in plasma has not been clearly established. The aim of this study was to evaluate the source of oxidative stress biomarkers found in the plasma of untrained rats after a single bout of swimming exercise at 2 different intensities: low intensity (SBLIE) or high intensity (SBHIE). Immediately after the exercise, aspartate transaminase (AST), alanine transaminase (ALT), γ-glutamyltransferase (GGT), and lactate dehydrogenase (LDH) were measured in plasma to characterize cell damage. Oxidative stress was assessed using protein carbonylation (PC), total antioxidant capacity (TAC), and thiobarbituric acid reactive substances (TBARS) quantified by malondialdehyde concentration. SBHIE raised levels of plasma AST (93%) and ALT (17%), and both exercise regimens produced an increase in GGT (7%) and LDH (∼55%). Plasma levels of PC and TBARS were greater in the SBHIE group; there were no changes in TAC. SBLIE caused only a modest increase in TBARS. In muscle, there were no changes in TAC, PC, or TBARS, regardless of exercise intensity, In the liver, TAC and TBARS increased significantly in both the SBLIE and SBHIE groups. This indicates that the oxidative stress biomarkers measured in the plasma immediately after a single bout of swimming exercise were generated primarily in the liver, not in muscle.

Purpose. Investigate free radical production and antioxidant buffering in military pentathletes' saliva after their performance of a standardized, running-based anaerobic sprint test (RAST). Methods. Seven members of the Brazilian Navy pentathlon team were recruited to perform a running-based anaerobic test (~90 sec). The participants provided samples of saliva before and after the test that were analyzed for biomarkers of oxidative stress such as lipid peroxidation, total antioxidant capacity and the quantity of two specific antioxidants, glutathione and uric acid. Results. The lipid peroxidation increased ~2 fold after RAST, despite an increase in total antioxidant capacity (46%). The concentration of reduced glutathione did not change, while the uric acid concentration increased by 65%. Conclusions. The evaluation in saliva following a sprint test that lasted no more than 90 sec was sensitive enough to reveal changes in redox state.

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Thyroid dysfunction can compromise physical capacity. Here, we analyze the effects of hyperthyroidism and hypothyroidism on maximum swim time in rats subjected to acute forced swimming, as an indicator of anaerobic capacity. Animals were forced to swim against a load (5% of body weight) attached to the tail and were killed 48 hours after the last test. Hyperthyroid rats were treated with thyroxine (50 mug/100 g body weight, i. p. for 7 days). The hypothyroid group received 0.03% methimazole in the drinking water for 4 weeks. Thyroid state was confirmed by alterations in serum thyroid-stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), and liver mitochondrial glycerol phosphate dehydrogenase (mGPD) activity. Hyperthyroid rats presented significantly lower visceral fat mass (VFM) and higher food intake (p<0.05) with unchanged body weight. Maximum swim time (MST), glycogen content (skeletal muscle and liver), and leptin levels were lower while corticosterone was higher (p<0.05). In hypothyroid rats body weight was lower (p<0.05), without changes in VFM. Tested at 7-day intervals, MST was lower for tests 2, 3, and 4 (p<0.05). Muscle glycogen was higher in extensor digitorum longus (EDL) and soleus (p<0.05), without changes in liver. Serum corticosterone was lower, while leptin was higher (p<0.05). These results suggest that in hyperthyroid and hypothyroid rats, thyroid hormones together with corticosterone and/or leptin may impair exercise capacity differently through its known effects on glycogen metabolism.