RESUMO
OBJECTIVE: Here we investigated the impact of chronic high-intensity interval training (HIIT) and caffeine consumption on the activities of Na+-K+-ATPase and enzymes of the antioxidant system, as well as anxiolytic-like behaviour in the rat brain. METHODS: Animals were divided into groups: control, caffeine (4â mg/kg), caffeine (8â mg/kg), HIIT, HIIT plus caffeine (4â mg/kg) and HIIT plus caffeine (8â mg/kg). Rats were trained three times per week for 6 weeks, and caffeine was administered 30 minutes before training. We assessed the anxiolytic-like behaviour, Na+-K+-ATPase, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, levels of reduced glutathione (GSH) and thiobarbituric acid reactive substances (TBARS) in the brain. RESULTS AND DISCUSSION: HIIT-induced anxiolytic-like behaviour increased Na+-K+-ATPase and GPx activities and TBARS levels, altered the activities of SOD and CAT in different brain regions, and decreased GSH levels. Caffeine, however, elicited anxiogenic-like behaviour and blocked HIIT effects. The combination of caffeine and HIIT prevented the increase in SOD activity in the cerebral cortex and GPx activity in three brain regions. Our results show that caffeine promoted anxiogenic behaviour and prevented HIIT-induced changes in the antioxidant system and Na+-K+-ATPase activities.
Assuntos
Ansiolíticos/uso terapêutico , Ansiedade/tratamento farmacológico , Ansiedade/metabolismo , Cafeína/uso terapêutico , ATPase Trocadora de Sódio-Potássio/metabolismo , Animais , Antioxidantes/metabolismo , Catalase/metabolismo , Glutationa/metabolismo , Glutationa Peroxidase/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismoRESUMO
The use of ergogenic substances such as caffeine has become a strategy to enhance sports performance. In the present study we evaluated the effects of high-intensity interval training (HIIT) associated with caffeine intake on acetylcholinesterase (AChE) and Ca2+ATPase activity and glycogen levels in the muscles of rats were evaluated. The animals were divided in groups: control, caffeine 4 or 8mg/kg, HIIT, HIIT plus caffeine 4 or caffeine 8mg/kg. Our results showed a decrease in glycogen levels in muscle in all trained groups after acute session exercise, while that an increase in glycogen levels was observed in all groups in relation to control in chronic exercise protocol. HIIT increases the thickness of the left ventricle and the Ca2+-ATPase activity and decrease the AChE activity in gastrocnemius muscle. Caffeine treatment prevents changes in enzymes activities as well as left ventricular hypertrophy adaptation induced by HIIT. Our findings suggest that caffeine modulates crucial pathways for muscle contraction in HIIT.
Assuntos
Cafeína/farmacologia , Treinamento Intervalado de Alta Intensidade , Músculo Esquelético/efeitos dos fármacos , Músculo Esquelético/fisiologia , Inibidores de Fosfodiesterase/farmacologia , Condicionamento Físico Animal/fisiologia , Acetilcolinesterase/metabolismo , Adaptação Fisiológica , Animais , ATPases Transportadoras de Cálcio/metabolismo , Glicogênio/metabolismo , Hipertrofia Ventricular Esquerda/prevenção & controle , Masculino , Músculo Esquelético/enzimologia , Ratos , Ratos Wistar , Natação/fisiologiaRESUMO
The aim of this study was to assess whether α-tocopherol administration prevented alterations in the ectonucleotidase activities and platelet aggregation induced by high-fat diet in rats. Thus, we examined four groups of male rats which received standard diet, high-fat diet (HFD), α-tocopherol (α-Toc), and high-fat diet plus α-tocopherol. HFD was administered ad libitum and α-Toc by gavage using a dose of 50 mg/kg. After 3 months of treatment, animals were submitted to euthanasia, and blood samples were collected for biochemical assays. Results demonstrate that NTPDase, ectonucleotide pyrophosphatase/phosphodiesterase, and 5'-nucleotidase activities were significantly decreased in platelets of HFD group, while that adenosine deaminase (ADA) activity was significantly increased in this group in comparison to the other groups (P < 0.05). When rats that received HFD were treated with α-Toc, the activities of these enzymes were similar to the control, but ADA activity was significantly increased in relation to the control and α-Toc group (P < 0.05). HFD group showed an increased in platelet aggregation in comparison to the other groups, and treatment with α-Toc significantly reduced platelet aggregation in this group. These findings demonstrated that HFD alters platelet aggregation and purinergic signaling in the platelets and that treatment with α-Toc was capable of modulating the adenine nucleotide hydrolysis in this experimental condition.
Assuntos
Dieta Hiperlipídica , Nucleotídeos/metabolismo , Agregação Plaquetária , alfa-Tocoferol/farmacologia , Animais , RatosRESUMO
We investigated the efficacy of rosmarinic acid (RA) in preventing lipid peroxidation and increased activity of acetylcholinesterase (AChE) in the brain of streptozotocin-induced diabetic rats. The animals were divided into six groups (n = 8): control, ethanol, RA 10 mg/kg, diabetic, diabetic/ethanol and diabetic/RA 10 mg/kg. After 21 days of treatment with RA, the cerebral structures (striatum, cortex and hippocampus) were removed for experimental assays. The results demonstrated that the treatment with RA (10 mg/kg) significantly reduced the level of lipid peroxidation in hippocampus (28%), cortex (38%) and striatum (47%) of diabetic rats when compared with the control. In addition, it was found that hyperglycaemia caused significant increased in the activity of AChE in hippocampus (58%), cortex (46%) and striatum (30%) in comparison with the control. On the other hand, the treatment with RA reversed this effect to the level of control after 3 weeks. In conclusion, the present findings showed that treatment with RA prevents the lipid peroxidation and consequently the increase in AChE activity in diabetic rats, demonstrating that this compound can modulate cholinergic neurotransmission and prevent damage oxidative in brain in the diabetic state. Thus, we can suggest that RA could be a promising compound in the complementary therapy in diabetes.
Assuntos
Acetilcolinesterase/metabolismo , Antioxidantes/farmacologia , Encéfalo/metabolismo , Cinamatos/farmacologia , Depsídeos/farmacologia , Diabetes Mellitus Experimental/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Animais , Diabetes Mellitus Experimental/induzido quimicamente , Masculino , Ratos , Ratos Wistar , Estreptozocina , Ácido RosmarínicoRESUMO
AIMS: We investigated whether the treatment with anthocyanins prevents the scopolamine-induced memory deficits and whether ectonucleotidase activities and purine levels are altered in the cerebral cortex (CC) and hippocampus (HC) in this model of mnemonic deficit in rats. MAIN METHODS: The animals were divided into 4 experimental groups: control (vehicle), anthocyanins (Antho), scopolamine (SCO), and scopolamine plus anthocyanins (SCO+Antho). After seven days of treatment, they were tested in the inhibitory avoidance task and open field test and submitted to euthanasia. The CC and the HC were collected for biochemical assays. The effect of treatment with Antho (200 mgkg(-1), i.p.) was investigated in rats trained to a stable level of performance and post-treated with SCO (1 mgkg(-1), i.p. 30 min after training). KEY FINDINGS: The treatment with SCO decreased the step-down latency in inhibitory avoidance task. Antho prevented the scopolamine-induced memory impairment and also the increase of NTPDase activity in the CC and HC. Furthermore, the treatment with anthocyanins prevents the decrease in 5'-nucleotidase activity and the increase in adenosine deaminase activity induced by SCO in HC. In addition, the treatment with Antho prevented the decrease in ATP levels induced by SCO in the CC and HC. SIGNIFICANCE: Our results show that scopolamine may affect purinergic enzymatic cascade or cause alterations in energy metabolism inducing loss of memory. In contrast Antho could reverse these changes, suggesting a neuroprotective effect of Antho on ectonucleotidase activities and neuronal energetic metabolism.