Publications by authors named "Alisson Luiz da Rocha"

The circadian-regulated transcriptional repressor REV-ERB-α is a key mediator of skeletal muscle oxidative capacity, enhancing exercise performance when activated. Conversely its global genetic ablation leads to impaired performance. Simultaneously the kynurenine (KYN) pathway, involved in tryptophan degradation, produces neurotoxic metabolites under stress and inflammation, contributing to CNS dysfunction and fatigue.

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Background: Aging increases the prevalence of prostate cancer. The circadian clock coordinates metabolism, cell cycle, and tumor suppressor p53. Although physical exercise has several effects on preventing prostate diseases, its effect on regulating genes and proteins of the circadian rhythm of the prostate needs to be better evaluated.

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High-fat diet consumption causes hypothalamic inflammation, dysregulating the leptin pathway, which, in turn, compromises the modulation of hypothalamic neuronal activities and predisposes obesity development. Intermittent fasting (IF) and exercise training (ET) have been demonstrated as efficient interventions to modulate hypothalamic inflammation and neuronal activity. However, no studies have evaluated whether combining these interventions could induce better results in reestablishing hypothalamic homeostasis disrupted by high-fat diet intake.

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The aim of this study is to verify the influence of the intensity on muscle and hepatic glycogen depletion and recovery kinetics of Wistar rats, submitted to three acute training sessions with equalized loads. 81 male Wistar rats performed an incremental test to determine maximal running speed (MRS) and divided into 4 groups: baseline group (Control; 9); low intensity training session (G; 24; 48 minutes at 50% of MRS); moderate intensity group (G; 24; 32 minutes at 75% of MRS) and high intensity group (G; 24; 5x5 minutes and 20 seconds at 90% of MRS). Immediately after the sessions and after 6, 12 and 24 hours, 6 animals from each subgroup were euthanized for glycogen quantification in soleus and EDL muscles and liver.

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Cardiovascular diseases are a leading cause of death for adults worldwide. Published articles have shown that toll-like receptor 4 (TLR4), a member of the toll-like receptor (TLR) family, is involved in several cardiovascular diseases and can be modulated by physical exercise. TLR4 is the most expressed TLR in cardiac tissue and is an essential mediator of the inflammatory and apoptosis processes in the heart, playing a pivotal role in the development of cardiovascular diseases.

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Excess of adipose tissue increases the concentration of proinflammatory cytokines, triggering a subclinical inflammatory condition. This inflammatory profile contributes to retina damage, which can lead to retinal dysfunction and reduced vision. Regularly practicing both aerobic and strength exercises is well known for promoting anti-inflammatory effects on different organs in the peripheral and central regions.

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Aims: The aim of this study was to evaluate the effects of aging on intracellular adiponectin signaling and the possible therapeutic effect of physical exercise.

Main Methods: Fischer 344 rats were distributed in the following groups: Young (3 months old); Sedentary Old (Old, 27 months old); and Old Exercised (Old-Exe, 27 months old), which were subjected to a short-term exercise training protocol.

Key Findings: The results showed that the old rats presented glucose intolerance without increased adiposity.

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Downhill running-based overtraining model increases the hypothalamic levels of IL-1β, TNF-α, SOCS3, and pSAPK-JNK. The aim of the present study was to verify the effects of 3 overtraining protocols on the levels of BiP, pIRE-1 (Ser724), pPERK (Thr981), pelF2α (Ser52), ATF-6, GRP-94, caspase 4, caspase 12, pAKT (Ser473), pmTOR (Ser2448), and pAMPK (Thr172) proteins in the mouse hypothalamus. The mice were randomized into the control, overtrained by downhill running (OTR/down), overtrained by uphill running (OTR/up), and overtrained by running without inclination (OTR) groups.

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