Hydrogen Gas Reduces Exercise-Induced Inflammation and Oxidative Stress
- Authors
- Jonatas E. Nogueira, Patricia Passaglia, Clarissa M.D. Mota, Bruna M. Santos, Marcelo E. Batalhão, Evelin C. Carnio, Luiz G.S. Branco
- Journal
- Free Radical Biology and Medicine
- Year
- 2018
- DOI
- 10.1016/j.freeradbiomed.2018.09.028
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Brazil
- Health Condition
- Exercise-Induced Inflammation
- Body System
- Muscular
TL;DR
Inhaling hydrogen gas can reduce inflammation and oxidative stress caused by intense exercise in sedentary rats.
Key Finding
Molecular hydrogen gas inhalation reduced exercise-induced inflammatory markers (TNF-α and IL-6) and decreased oxidative stress indicators in sedentary rats.
Summary
Researchers had sedentary rats run on a treadmill while breathing either hydrogen gas or regular air, then measured inflammatory and stress markers in their blood. They found that rats breathing hydrogen gas had lower levels of inflammatory chemicals (TNF-α and IL-6) after exercise and showed better antioxidant responses (higher SOD activity and lower TBARS, which indicates less cellular damage) compared to rats breathing regular air.
Practical Takeaway
This is an early-stage animal study suggesting hydrogen gas may help reduce inflammation and oxidative stress from acute exercise. However, these results are from rats only, and it's unclear whether similar effects would occur in humans or with other hydrogen delivery methods (like hydrogen water). More research in humans would be needed before drawing conclusions about practical benefits.
Abstract
Physical exercise induces inflammatory and oxidative markers production in the skeletal muscle and this process is under the control of both endogenous and exogenous modulators. Recently, molecular hydrogen (H2) has been described as a therapeutic gas able to reduced oxidative stress in a number of conditions. However, nothing is known about its putative role in the inflammatory and oxidative status during a session of acute physical exercise in sedentary rats. Therefore, we tested the hypothesis that H2 attenuates both inflammation and oxidative stress induced by acute physical exercise. Rats ran at 80% of their maximum running velocity on a closed treadmill inhaling either the H2 gas (2% H2, 21% O2, balanced with N2) or the control gas (0% H2, 21% O2, balanced with N2) and were euthanized immediately or 3 h after exercise. We assessed plasma levels of inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6] and oxidative markers [superoxide dismutase (SOD), thiobarbituric acid reactive species (TBARS) and nitrite/nitrate (NOx)]. In addition, we evaluated the phosphorylation status of intracellular signaling proteins [glycogen synthase kinase type 3 (GSK3α/β) and the cAMP responsive element binding protein (CREB)] that modulate several processes in the skeletal muscle during exercise, including changes in exercise-induced reactive oxygen species (ROS) production. As expected, physical exercise increased virtually all the analyzed parameters. In the running rats, H2 blunted exercise-induced plasma inflammatory cytokines (TNF-α and IL-6) surges. Regarding the oxidative stress markers, H2 caused further increases in exercise-induced SOD activity and attenuated the exercise-induced increases in TBARS 3 h after exercise. Moreover, GSK3α/β phosphorylation was not affected by exercise or H2 inhalation. Otherwise, exercise caused an increased CREB phosphorylation which was attenuated by H2. These data are consistent with the notion that H2 plays a key role in decreasing exercise-induced inflammation, oxidative stress, and cellular stress.