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 1β (IL-1β), 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-1β 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.

Ultramarathon Evaluation above 180 km in relation to Peak Age and Performance

“…On the other hand, interestingly, competitions over 360 km began to become common in 2017, a fact that should be further explored. In part, it can be explained by the increase in psychological resilience [9]. 4.2.…”

“…However, currently, the participation in challenges over 180 km is advancing. These competitions are considered extreme events exceeding 1000 km, making them a superior challenge, which presents the athletes with a series of adversities (i.e., extreme weather conditions and nutritional care) [ 9 ]. Thus, an understanding of the profile of athletes is important to guide their training and preparation for long-term performance.…”

Effects of Ibuprofen Use on Lymphocyte Count and Oxidative Stress in Elite Paralympic Powerlifting

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Neuroprotective Effects of Physical Activity via the Adaptation of Astrocytes

“…In contrast, long-term treadmill exercise reduced the number of hippocampal GFAP+ astrocytes in APP/PS1 mice model of AD, and voluntary running decreased the intensity and size of activated astrocytes in the cortex and hippocampus in the double transgenic APPswe/PS1ΔE9 mouse model of AD [ 89 , 90 ]. Moreover, ultra-endurance race simulation after high-volume training in rodents altered the GFAP isoform profile, suggesting impaired astrocyte reactivity in the cerebellum [ 91 ], where, in normal conditions, astrocytes regulate the homeostasis of this region, locomotor performance, and represent an antioxidant resource [ 92 ]. A combination of treadmill and running wheel for 4 weeks significantly increased the extent of astrocyte processes in adult mice.…”