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Previous studies addressed the antioxidant and anti-inflammatory role of compounds from green tea in different human tissues. Positive antioxidant and anti-inflammatory effects were described for brain tissues. Whether similar effects are observed in the skeletal muscle, green tea supplementation could be a strategy to reduce delayed onset muscle soreness resultant of exercise. Here we determine the effect of green tea extract supplementation on exercise-induced muscle soreness, muscle damage and oxidative stress. We performed a randomized triple blind placebo control study. Twenty non-trained men performed sessions of exercise to induce delayed onset muscle soreness in the triceps sural muscle group before and after 15 days of supplementation (500 mg/day) with green tea extract (n = 10) or a placebo (n = 10). Muscle soreness was evaluated using a visual scale. Blood samples were taken at different moments to determine serum blood markers of muscle damage, oxidative stress and antioxidant status. We found that exercise induced delayed onset muscle soreness. Supplementation reduced muscle damage but muscle soreness did not change. Plasma oxidative damage marker and antioxidant status did not show an effect of supplementation. As a conclusion, green tea extract supplementation did not reduce the sensation of delayed onset muscle soreness but reduces the marker of muscle damage after exercise. It suggests the green tea extract supplementation has positive effects on muscle recovery after strenuous exercise.

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Ischemic stroke is a major cause of morbidity and mortality all over the world. Among impairments observed in survivors there is a significant cognitive learning and memory deficit. Neuroprotective strategies are being investigated to minimize such deficits after an ischemia event. Here we investigated the neuroprotective potential of physical exercise and green tea in an animal model of ischemia-reperfusion. Eighty male rats were divided in 8 groups and submitted to either transient brain ischemia-reperfusion or a sham surgery after 8 weeks of physical exercise and/or green tea supplementation. Ischemia-reperfusion was performed by bilateral occlusion of the common carotid arteries during 30 min. Later, their memory was evaluated in an aversive and in a non-aversive task, and hippocampus and prefrontal cortex were removed for biochemical analyses of possible oxidative stress effects. Ischemia-reperfusion impaired learning and memory. Reactive oxygen species were increased in the hippocampus and prefrontal cortex. Eight weeks of physical exercise and/or green tea supplementation before the ischemia-reperfusion event showed a neuroprotective effect; both treatments in separate or together reduced the cognitive deficits and were able to maintain the functional levels of antioxidant enzymes and glutathione.

Recently, nongenetic animal models to study the onset and development of Alzheimer's disease (AD) have appeared, such as the intrahippocampal infusion of peptides present in Alzheimer amyloid plaques [i.e., amyloid-β (Aβ)]. Nonpharmacological approaches to AD treatment also have been advanced recently, which involve combinations of behavioral interventions whose specific effects are often difficult to determine. Here we isolate the neuroprotective effects of three of these interventions-environmental enrichment (EE), anaerobic physical exercise (AnPE), and social enrichment (SE)-on Aβ-induced oxidative stress and on impairments in learning and memory induced by Aβ. Wistar rats were submitted to 8 wk of EE, AnPE, or SE, followed by Aβ infusion in the dorsal hippocampus. Short-term memory (STM) and long-term memory (LTM) of object recognition (OR) and social recognition (SR) were evaluated. Biochemical assays determined hippocampal oxidative status: reactive oxygen species, lipid peroxidation by thiobarbituric acid reactive substance (TBARS) test, and total antioxidant capacity by ferric reducing/antioxidant power (FRAP), as well as acetylcholinesterase activity. Aβ infusion resulted in memory deficits and hippocampal oxidative damage. EE and AnPE prevented all memory deficits (STM and LTM of OR and SR) and lipid peroxidation (i.e., TBARS). SE prevented only the SR memory deficits and the decrease of total antioxidant capacity decrease (i.e., FRAP). Traditionally, findings obtained with EE protocols do not allow discrimination of the roles of the three individual factors involved. Here we demonstrate that EE and physical exercise have better neuroprotective effects than SE in memory deficits related to Aβ neurotoxicity in the AD model tested.

Purpose. Many falls in older people occur after tripping or slipping, mainly due to unsuccessful vertical clearances or horizontal distances. A first fall may be explained by several factors related to aging and can be a trigger to subsequent falls. It is unclear if a history of fall changes the kinematics of obstacle crossing, increasing the risk of trips. Here, we determined whether older women reporting a fall history showed different spatial-temporal kinematic parameters during obstacle crossing than non-fallers. In addition, we investigated the presence of asymmetries between the preferred and non-preferred lower limb during obstacle crossing in fallers and non-fallers. Methods. This cross-sectional study recruited older women with a history of fall (n = 10) and without falls (n = 10). They had their kinematic parameters evaluated when walking at self-selected speed along an 8-m walkway, crossing an obstacle positioned in the middle of the walkway, with both preferred and non-preferred limb as the lead limb. The groups were compared, and effects of lower limb preference were also determined in both groups. Results. No main effects of group were observed regarding the kinematic variables. An effect of leg preference was found for post-obstacle horizontal distance, which was greater for the preferred limb in both groups. Conclusions. In conclusion, the kinematics of gait with obstacle crossing does not differentiate between older women with or without a history of recent fall.

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