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1.
Physiol Behav ; 194: 77-82, 2018 10 01.
Article in English | MEDLINE | ID: mdl-29746891

ABSTRACT

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.


Subject(s)
Exercise , Muscle, Skeletal/injuries , Myalgia/prevention & control , Plant Extracts/therapeutic use , Tea , Acetylcholinesterase/blood , Adult , Antioxidants/metabolism , Creatine Kinase/blood , Dietary Supplements , Double-Blind Method , Glutathione/blood , Humans , L-Lactate Dehydrogenase/blood , Male , Oxidative Stress/drug effects , Pain Measurement , Reactive Oxygen Species/blood , Serum/metabolism , Thiobarbituric Acid Reactive Substances/metabolism , Time Factors , Young Adult
2.
PLoS One ; 8(10): e78332, 2013.
Article in English | MEDLINE | ID: mdl-24205200

ABSTRACT

BACKGROUND AND AIMS: Glutaric aciduria type I (GA-I) is characterized by accumulation of glutaric acid (GA) and neurological symptoms, such as cognitive impairment. Although this disease is related to oxidative stress and inflammation, it is not known whether these processes facilitate the memory impairment. Our objective was to investigate the performance of rat pups chronically injected with GA and lipopolysaccharide (LPS) in spatial memory test, antioxidant defenses, cytokines levels, Na+, K+-ATPase activity, and hippocampal volume. We also evaluated the effect of N-acetylcysteine (NAC) on theses markers. METHODS: Rat pups were injected with GA (5 umol g of body weight-1, subcutaneously; twice per day; from 5th to 28th day of life), and were supplemented with NAC (150 mg/kg/day; intragastric gavage; for the same period). LPS (2 mg/kg; E.coli 055 B5) or vehicle (saline 0.9%) was injected intraperitoneally, once per day, from 25th to 28th day of life. Oxidative stress and inflammatory biomarkers as well as hippocampal volume were assessed. RESULTS: GA caused spatial learning deficit in the Barnes maze and LPS potentiated this effect. GA and LPS increased TNF-α and IL-1ß levels. The co-administration of these compounds potentiated the increase of IL-1ß levels but not TNF-α levels in the hippocampus. GA and LPS increased TBARS (thiobarbituric acid-reactive substance) content, reduced antioxidant defenses and inhibited Na+, K+-ATPase activity. GA and LPS co-administration did not have additive effect on oxidative stress markers and Na+, K+ pump. The hippocampal volume did not change after GA or LPS administration. NAC protected against impairment of spatial learning and increase of cytokines levels. NAC Also protected against inhibition of Na+,K+-ATPase activity and oxidative markers. CONCLUSIONS: These results suggest that inflammatory and oxidative markers may underlie at least in part of the neuropathology of GA-I in this model. Thus, NAC could represent a possible adjuvant therapy in treatment of children with GA-I.


Subject(s)
Acetylcysteine/pharmacology , Animals, Newborn/metabolism , Glutarates/adverse effects , Glutarates/metabolism , Lipopolysaccharides/adverse effects , Memory Disorders/drug therapy , Spatial Memory/drug effects , Animals , Antioxidants/metabolism , Hippocampus/drug effects , Hippocampus/metabolism , Interleukin-1beta/metabolism , Male , Memory Disorders/metabolism , Rats , Rats, Wistar , Sodium-Potassium-Exchanging ATPase/metabolism , Tumor Necrosis Factor-alpha/metabolism
3.
Article in English | MEDLINE | ID: mdl-24111085

ABSTRACT

The lack of perception in the hindfoot increases the plantar flexion, causing irregular posture due to the foot position, a disability known as equinus foot deformity. A portable device, named baropodometer, that measures the pressure at the forefoot and hindfoot regions was built to help this population in terms of balance and posture correction. Ten hemiparetic teenager volunteers with equinus foot participated in the experiments. The results demonstrated that the proposed device increased the weight-bearing in upright stance in the paretic side, decreasing the weight in the non-paretic side. After 10 experimental sessions, performed along 6 months, the distribution of the pressure in the lower limbs was very similar. The baropodometer facilitates the rehabilitation, by biofeedbacking the pressure of the calcaneus, using the volunteer's audiovisual system. The rehabilitation using the proposed device was able to recover the balance by posture correction, facilitating future gait training of these volunteers.


Subject(s)
Biofeedback, Psychology/instrumentation , Biofeedback, Psychology/methods , Equinus Deformity/rehabilitation , Adolescent , Child , Foot/physiopathology , Humans , Male , Posture , Pressure , Signal Processing, Computer-Assisted , Weight-Bearing
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