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Ultra-Endurance Associated With Moderate Exercise in Rats Induces Cerebellar Oxidative Stress and Impairs Reactive GFAP Isoform Profile.

ABSTRACT: Ultra-endurance (UE) race has been associated with brain metabolic changes, but it is still unknown which regions are vulnerable. This study investigated whether high-volume training in rodents, even under moderate intensity, can induce cerebellar oxidative and inflammatory status. Forty-five adult rats were divided into six groups according to a training period, followed or not by an exhaustion test (ET) that simulated UE: control (C), control + ET (C-ET), moderate-volume (MV) training and MV-ET, high-volume training (HV) and HV-ET. The training period was 30 (MV) and 90 (HV) min/day, 5 times/week for 3 months as a continuous running on a treadmill at a maximum velocity of 12 m/min. After 24 h, the ET was performed at 50% maximum velocities up to the animals refused to run, and then serum lactate levels were evaluated. Serum and cerebellar homogenates were obtained 24 h after ET. Serum creatine kinase (CK), lactate dehydrogenase (LDH), and corticosterone levels were assessed. Lipid peroxidation (LP), nitric oxide (NO), Interleukin 1? (IL-1?), and GFAP proteins, reduced and oxidized glutathione (GSH and GSSG) levels, superoxide dismutase (SOD) and catalase (CAT) activities were quantified in the cerebellum. Serum lactate concentrations were lower in MV-ET (?20%) and HV-ET (?40%) compared to the C-ET group. CK and corticosterone levels were increased more than ? twofold by HV training compared to control. ET increased CK levels in MV-ET vs. MV group (P = 0.026). HV induced higher LP levels (?40%), but an additive effect of ET was only seen in the MV-ET group (P = 0.02). SOD activity was higher in all trained groups vs. C and C-ET (P < 0.05). CAT activity, however, was intensified only in the MV group (P < 0.02). The 50 kDa GFAP levels were enhanced in C-ET and MV-ET vs. respective controls, while 42 kDa (?40%) and 39 kDa (?26%) isoform levels were reduced. In the HV-ET group, the 50 KDa isoform amount was reduced ?40-60% compared to the other groups and the 39 KDa isoform, increased sevenfold. LDH levels, GSH/GSSG ratio, and NO production were not modified. ET elevated IL-1? levels in the CT and MV groups. Data shows that cerebellar resilience to oxidative damage may be maintained under moderate-volume training, but it is reduced by UE running. High-volume training per se provoked systemic metabolic changes, cerebellar lipid peroxidation, and unbalanced enzymatic antioxidant resource. UE after high-volume training modified the GFAP isoform profile suggesting impaired astrocyte reactivity in the cerebellum.

SUBMITTER: de Souza RF

PROVIDER: S-EPMC7492828 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Ultra-Endurance Associated With Moderate Exercise in Rats Induces Cerebellar Oxidative Stress and Impairs Reactive GFAP Isoform Profile.

de Souza Raphael Fabricio RF Augusto Ricielle Lopes RL de Moraes Silvia Regina Arruda SRA de Souza Fabio Borges FB Gonçalves Lílian Vanessa da Penha LVDP Pereira Danielle Dutra DD Moreno Gisele Machado Magalhães GMM de Souza Fernanda Maria Araujo FMA Andrade-da-Costa Belmira Lara da Silveira BLDS

Frontiers in molecular neuroscience 20200902

Ultra-endurance (UE) race has been associated with brain metabolic changes, but it is still unknown which regions are vulnerable. This study investigated whether high-volume training in rodents, even under moderate intensity, can induce cerebellar oxidative and inflammatory status. Forty-five adult rats were divided into six groups according to a training period, followed or not by an exhaustion test (ET) that simulated UE: control (C), control + ET (C-ET), moderate-volume (MV) training and MV-E ...[more]

PMID: 32982688

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Project description:(1) Background: Participation in ultra-endurance sports, particularly ultra-running, has increased over the previous three decades. These are accompanied by high energetic demands, which may be further exacerbated by extreme environmental conditions. Preparation is long-term, comprising of sufficient exercise management, supportive dietary habits, and nutritional intakes for optimal adaptations. Gastrointestinal symptoms are often cited as causing underperformance and incompletion of events. Though the majority do not pose serious long-term health risks, they may still arise. It has been suggested that the nutritional interventions employed by such athletes prior to, during, and after exercise have the potential to alter symptom incidence, severity, and duration. A summary of such interventions does not yet exist, making it difficult for relevant personnel to develop recommendations that simultaneously improve athletic performance by attenuating gastrointestinal symptoms. The aim of this research is to systematically review the literature investigating the effects of a nutrition intervention on ultra-endurance athletes exercise-induced gastrointestinal symptom incidence, severity, or duration. (2) Methods: A systematic review of the literature was conducted (PubMed, CINAHL, Web of Science, and Sports Discus) in January 2023 to investigate the effects of various nutrition interventions on ultra-endurance athletes' (regardless of irritable bowel syndrome diagnosis) exercise-induced gastrointestinal symptoms. Variations of key words such as "ultra-endurance", "gastrointestinal", and "nutrition" were searched. The risk of bias in each paper was assessed using the ADA quality criteria checklist. (3) Results: Of the seven eligible studies, one was a single field-based case study, while the majority employed a crossover intervention design. A total of n = 105 participants (n = 50 male; n = 55 female) were included in this review. Practicing a diet low in short-chain, poorly absorbed carbohydrates, known as fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs), as well as employing repetitive gut challenges of carbohydrates, remain the most promising of strategies for exercise-induced gastrointestinal symptom management. (4) Conclusion: Avoiding high-FODMAP foods and practicing repetitive gut challenges are promising methods to manage gastrointestinal symptoms. However, sample sizes are often small and lack supportive power calculations.

Project description:Glial fibrillary acidic protein (GFAP) is an intermediate filament (IF) protein specific to central nervous system (CNS) astrocytes. It has been the subject of intense interest due to its association with neurodegenerative diseases, and because of growing evidence that IF proteins not only modulate cellular structure, but also cellular function. Moreover, GFAP has a family of splicing isoforms apparently more complex than that of other CNS IF proteins, consistent with it possessing a range of functional and structural roles. The gene consists of 9 exons, and to date all isoforms associated with 3' end splicing have been identified from modifications within intron 7, resulting in the generation of exon 7a (GFAPδ/ε) and 7b (GFAPκ). To better understand the nature and functional significance of variation in this region, we used a Bayesian multiple change-point approach to identify conserved regions. This is the first successful application of this method to a single gene--it has previously only been used in whole-genome analyses. We identified several highly or moderately conserved regions throughout the intron 7/7a/7b regions, including untranslated regions and regulatory features, consistent with the biology of GFAP. Several putative unconfirmed features were also identified, including a possible new isoform. We then integrated multiple computational analyses on both the DNA and protein sequences from the mouse, rat and human, showing that the major isoform, GFAPα, has highly conserved structure and features across the three species, whereas the minor isoforms GFAPδ/ε and GFAPκ have low conservation of structure and features at the distal 3' end, both relative to each other and relative to GFAPα. The overall picture suggests distinct and tightly regulated functions for the 3' end isoforms, consistent with complex astrocyte biology. The results illustrate a computational approach for characterising splicing isoform families, using both DNA and protein sequences.

Dataset Information

Ultra-Endurance Associated With Moderate Exercise in Rats Induces Cerebellar Oxidative Stress and Impairs Reactive GFAP Isoform Profile.

Publications

Ultra-Endurance Associated With Moderate Exercise in Rats Induces Cerebellar Oxidative Stress and Impairs Reactive GFAP Isoform Profile.

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