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Regular exercise can decrease the deleterious effects of aging and limit the development and progression of chronic disease in elderly people, depending on the type, intensity, frequency, and duration of exercise. This study aimed to investigate the potential protective effects of different physical training programs on oxidative stress parameters and inflammatory and neurotrophic mediators in the serum of elderly men. Healthy male volunteers [60 to 80 years; n=55] were divided into four groups: control [Ctr, n=14], aerobic training on dry land [ATdl, n=12]; and combined training on dry land [CTdl, n=12] or in water [CTw, n=17]. The training protocols were performed over 8 weeks, three times per week. Each 1 h session included 5 min warming-up exercise, 50 min specific training [aerobic, strength, or combined], and 5 min stretching. Blood samples were drawn 72 h before [baseline] the beginning of the 8 weeks' protocol and 48 h after the last training session, processed, and the serum was aliquoted and stored at -70 °C until biochemical assessment of oxidative damage, antioxidant system and neurotrophic, growth and inflammatory factors. Elevated BDNF or IGF-1 levels were observed in the ATdl or CTdl groups, respectively. Overall oxidative stress parameters were improved including reduced lipid oxidative damage and increased thioredoxin reductase and glutathione peroxidase activities and total glutathione. Significant decreases in the inflammatory mediators IL-6 and IL-8 were observed; IL-6 was more susceptible to the effects of type of physical training. Thus, the effects of training in elderly men vary in an exercise type-dependent manner.

The tissue response to acute myocardial infarction (AMI) is key to avoiding heart complications due to inflammation, mitochondrial dysfunction, and oxidative stress. Antioxidant and anti-inflammatory agents can minimize the effects of AMI. This study investigated the role of 2-methoxy-isobutyl-isonitrile (MIBI)-associated gold nanoparticles (AuNP) on reperfusion injury after ischemia and its effect on cardiac remodeling in an experimental AMI model. Three-month-old Wistar rats were subjected to a temporary blockade of the anterior descending artery for 30 min followed by reperfusion after 24 h and 7 days by intraventricularly administering 0.4, 1.3, and 3 mg/kg AuNP-MIBI. The cardiac toxicity and renal and hepatic function levels were determined, and the infarct and peri-infarct regions were surgically removed for histopathology, analysis of inflammation from oxidative stress, and echocardiography. MIBI-conjugated AuNP promoted changes in oxidative stress and inflammation depending on the concentrations used, suggesting promising applicability for therapeutic purposes.

OBJECTIVES: Progressive decline of physiological processes with aging is normal. Aging is also associated with decreased functional capacity and onset of many diseases. This study evaluated the changes in physical fitness (PF), body composition (BC), and lipid profile (LP) in elderly men completing different training protocols. METHODS: Fifty-five men (age 60-80 years) were randomized into the following groups: without training, aerobic training on dry land, combined training on dry land, and combined training in water. Training was conducted for 8 weeks, and PF, LP, and BC were assessed at the beginning and end of the intervention. RESULTS: Significant improvements were observed in all parameters; however, combined programs on land or in water were more effective at improving strength and aerobic fitness. Combined exercise produced greater effects on BC and LP and some muscle fitness parameters; however, improvements in muscular and aerobic capacities occurred independently of exercise type or model. CONCLUSION: These results indicate that the effects of training occur regardless of training type or model, and are directly associated with training periodization, adherence, and regularity.

Age-associated decline in skeletal muscle mass and strength is associated with oxidative stress and Ca(2+) homeostasis disturbance. Exercise should be considered a viable modality to combat aging of skeletal muscle. This study aimed to investigate whether continuous and fractionated training could be useful tools to attenuate oxidative damage and retain calcium-handling proteins. We conducted the study using 24-month-old male Wistar rats, divided into control, continuous, and fractionated groups. Animals ran at 13 m min(-1) for five consecutive days (except weekends) for 6 weeks, for a total period of 42 days. Each session comprised 45 min of exercise, either continuous or divided into three daily sessions of 15 min each. Metabolic and oxidative stress markers, protein levels of mitochondrial transcription factors, and calcium-handling proteins were analyzed. Continuous exercise resulted in reduced ROS production as well as showed a decrease in TBARS levels and carbonyl content. On the other hand, fractionated training increased the antioxidant enzyme activities. The ryanodine receptor and phospholamban protein were regulated by continuous training while sodium calcium exchange protein was increased by the fractionated training. These data suggest that intracellular Ca(2+) can be modulated by various training stimuli. In addition, the modulation of oxidative stress by continuous and fractionated training may play an important regulatory role in the muscular contraction mechanism of aged rats, due to changes in calcium metabolism.

Skeletal muscle aging is associated with loss of mass, function, and strength-a condition known as sarcopenia. It has been reported that sarcopenia can be attenuated by physical exercise. Therefore, we investigated whether 2 different physical exercise protocols could modulate and induce changes in oxidative and inflammatory parameters, as well as in BDNF and DNA repair enzyme levels in skeletal muscle tissue of aged rats. Aging Wistar rats performed treadmill or strength training for 50 min 3 to 4 times a week for 8 weeks. Strength training decreased 2′,7′-dichlorofluorescein (DCFH) oxidation (P = 0.0062); however, nitric oxide, protein deglycase DJ-1, and tumor necrosis factor alpha (TNF-α) levels increased after aerobic training (P = 0.04, P = 0.027 and P = 0.009, respectively). Both exercise protocols increased superoxide dismutase (SOD) and catalase (CAT) activity (P = 0.0017 and P = 0.0326) whereas the activity of glutathione (GSH) (P = 0.0001) was decreased. Brain-derived neurotropic factor (BDNF) levels were not affected by exercise, but 8-oxoguanine glycosylase (OGG1) decreased after strength training (P = 0.0007). In conclusion, oxidative parameters showed that skeletal muscle adapt to increased ROS levels, reducing the risk of free radical damage to the tissue after both exercise protocols. These results show that the effects of physical exercise on skeletal muscle are mediated in an exercise type-dependent manner.

The aim of this study was to investigate the regulatory effects of taurine on the biochemical parameters of muscle injury by overuse.Male Swiss mice were divided into four groups: control (Ctrl), overuse (Ov), taurine (Tau), and overuse plus taurine (OvTau). High-intensity exercise sessions were administered for 21 d with concomitant subcutaneous injections of taurine (150 mg/kg). The mice were then sacrificed. The quadriceps muscles were surgically removed for subsequent histologic analysis and evaluation of mitochondrial function, oxidative stress parameters, tissue repair, and DNA damage markers.The Ov group showed significant differences compared with the Ctrl group (all P 0.05). The fiber area decreased by 49.34%, whereas the centralized nuclei contents (Ctrl = 1.33%; Ov = 28.67%), membrane potential (CtrlTaken together, these data suggest that taurine supplementation modulates various cellular remodeling parameters after overuse-induced muscle damage, and that these positive effects may be related to its antioxidant capacity.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) caused by demyelination, immune cell infiltration, and axonal damage. Herein, we sought to investigate the influence of physical exercise on mice experimental autoimmune encephalomyelitis (EAE), a reported MS model. Data show that both strength and endurance training protocols consistently prevented clinical signs of EAE and decreased oxidative stress, an effect which was likely due to improving genomic antioxidant defense-nuclear factor erythroid 2-related factor (Nrf2)/antioxidant response elements (ARE) pathway-in the CNS. In addition, physical exercise inhibited the production of pro-inflammatory cytokines interferon (IFN)-γ, interleukin (IL)-17, and IL-1β in the spinal cord of mice with EAE. Of note, spleen cells obtained from strength training group incubated with MOG35-55 showed a significant upregulation of CD25 and IL-10 levels, with a decrease of IL-6, MCP-1, and tumor necrosis factor (TNF)-α production, mainly, during acute and chronic phase of EAE. Moreover, these immunomodulatory effects of exercise were associated with reduced expression of adhesion molecules, especially of platelet and endothelial cell adhesion molecule 1 (PECAM-1). Finally, physical exercise also restored the expression of tight junctions in spinal cord. Together, these results demonstrate that mild/moderate physical exercise, when performed regularly in mice, consistently attenuates the progression and pathological hallmarks of EAE, thereby representing an important non-pharmacological intervention for the improvement of immune-mediated diseases such as MS. Graphical Abstract Schematic diagram illustrating the beneficial effects of physical exercise during experimental model of MS. Physical exercise, especially strength (ST) and endurance (ET) training protocols, inhibits the development and progression of disease, measured by the mean maximal clinical score (1.5 and 1.0, respectively), with inhibition of 30 % and 50 %, respectively, based on the AUC, compared with EAEuntreated group. In addition, ST and ET decreased oxidative stress, possibly, through genomic antioxidant defense, Nrf2-Keap1 signaling pathway, in the CNS. Physical exercise inhibited the production of inflammatory cytokines, such as IFN-γ, IL-17 and IL-1β in the spinal cord after EAE induction, as well as spleen cells obtained from ST group showed a significant upregulation of regulatory T cell markers, such as CD25 and IL-10 levels, and blocked IL-6, MCP-1 and TNF-α production, mainly, during acute and chronic phase of EAE. Finally, these immunomodulatory effects of exercise were associated with inhibition of adhesion molecules and reestablishment of tight junctions expression in spinal cord tissue, thereby limiting BBB permeability and transmigration of autoreactive T cells to the CNS. NO, nitric oxide; GPx, glutathione peroxidase, GSH, glutathione; Nrf2, nuclear factor (erythroid-derived 2)-like 2; CNS, central nervous system; BBB, blood-brain barrier; IFN-g, interferon-gamma; IL-17, interleukin 17; IL-1b, interleukin-1beta.

This study aimed to evaluate the effects of two different protocols for physical exercise (strength and aerobic training) on mitochondrial and inflammatory parameters in the 6-OHDA experimental model of Parkinson’s disease. Six experimental groups were used (n=12per group): untrained + vehicle (Sham), strength training + vehicle (STR), treadmill training + vehicle (TTR), untrained + 6-OHDA (U + 6-OHDA), strength training + 6-OHDA (STR + 6-OHDA), and treadmill training + 6-OHDA (TTR + 6-OHDA). The mice were subjected to strength or treadmill training for 8 weeks. PD was inducedviastriatal injection of 6-OHDA 24 h after the last exercise session. Mice were euthanized by cervical dislocation and the striatum and hippocampus were homogenized to determine levels of tyrosine hydroxylase (TH), nuclear factor kappa B (NF-κB) p65, and sirtuin 1 (Sirt1) by western blot; tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), IL-17, interferon-γ(IFN-γ), and transforming growth factorβ1 (TGF-β1) levels by ELISA; NO content; and complex I (CI) activity. STR + 6-OHDA mice had higher TH levels and CI activity and lower NF-κB p65 and IFN-γlevels in the striatum compared to U + 6-OHDA mice, while TTR + 6-OHDA mice had higher Sirt1 levels and CI activity in both the striatum and the hippocampus, compared to U + 6-OHDA mice. Strength training increased CI activity and TH and Sirt1 levels and reduced NO, NF-κB p65, TNF-α, IFN-γ, IL-1β, and TGF-β1 levels in 6-OHDA mice, while treadmill exercise increased CI activity and NO, TH, and Sirt1 levels and reduced NF-κB p65, TNF-α, IFN-γ, and IL-1βlevels. Our results demonstrated that both treadmill training and strength training promote neuroprotection, possibly by stimulating Sirt1 activity, which may in turn regulate both mitochondrial function and neuroinflammationviadeacetylation of NF-κB p65. Changes in nitric oxide levels may also be a mechanism by which 6-OHDA-induced inflammation is controlled.