Hydrogen Gas Protects Brain from Exercise-Related Inflammation in Rats
- Authors
- Jonatas E. Nogueira, Junia L. de Deus, Mateus R. Amorim, Marcelo E. Batalhão, Ricardo M. Leão, Evelin C. Carnio, Luiz G.S. Branco
- Journal
- Neuroscience Letters
- Year
- 2020
- DOI
- 10.1016/j.neulet.2019.134577
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Brazil
- Health Condition
- Exercise-Induced Inflammation
- Body System
- Nervous System
TL;DR
Inhaling molecular hydrogen (H2) gas can reduce inflammation in the brain caused by intense exercise without affecting oxidative stress.
Key Finding
Inhaled hydrogen gas reduced exercise-induced inflammation in the rat brain by decreasing pro-inflammatory molecules and increasing anti-inflammatory molecules immediately after intense exercise.
Summary
Researchers gave sedentary rats either hydrogen gas or regular air while they ran intensely on a treadmill, then measured inflammation markers in the hippocampus (a brain region involved in memory). Rats breathing hydrogen gas showed reduced levels of inflammatory molecules that promote inflammation (TNF-α and IL-6) and increased levels of anti-inflammatory molecules (IL-10) compared to control rats, suggesting hydrogen gas may help protect the brain from harmful inflammation caused by sudden intense exercise.
Practical Takeaway
This is an early-stage animal study suggesting hydrogen gas may help reduce brain inflammation from intense exercise in untrained individuals, but results are limited to rats and a single exercise session. Human studies would be needed to determine if these findings apply to people, and whether the effect persists with regular training or different exercise intensities.
Abstract
Physical exercise-induced inflammation may be beneficial when exercise is regular but it may be harmful when exercise is intense and performed by unaccustomed individuals/rats. Molecular hydrogen (H2) has recently emerged as a powerful anti-inflammatory, antioxidant and anti-apoptotic molecule in a number of pathological conditions, but little is known about its putative role under physiological conditions such as physical exercise. Therefore, we tested the hypothesis that H2 decreases intense acute exercise-induced inflammation in the hippocampus, since it is a brain region particularly susceptible to inflammation. Moreover, we also assessed hippocampus oxidative status. Rats ran on a sealed treadmill inhaling either the H2 (2% H2, 21% O2, balanced with N2) or the control gas (0% H2, 21% O2, balanced with N2) and hippocampal samples were collected immediately or 3 h after exercise. We measured hippocampal levels of cytokines [tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 and IL-10] and oxidative markers [superoxide dismutase (SOD), thiobarbituric acid reactive species (TBARS) and nitrite/nitrate (NOx)]. Exercise increased TNF-α, IL-6 and IL-10 immediately after the session, whereas no change in IL-1β levels was observed. Conversely, exercise did not cause any change in SOD activity, TBARS and NOx levels. H2 inhibited the exercise-induced surges in TNF-α and IL-6, and potentiated the IL-10 surge, immediately after the exercise. Moreover, no change in IL1-β levels of rats inhaling H2 was observed. Regarding the oxidative stress markers, H2 failed to cause any change in SOD activity, TBARS and NOx levels. No significant change was observed in any of the assessed parameters 3 h after the exercise bout. These data are consistent with the notion that H2 acts as a powerful anti-inflammatory agent not only down-modulating pro-inflammatory cytokines (TNF-α and IL-6) but also upregulating an anti-inflammatory cytokine (IL-10) production without affecting the local oxidative stress status. These data indicate that H2 effectively decreases exercise-induced inflammation in the hippocampus, despite the fact that this region is particularly prone to inflammatory insults.