Hydrogen Gas Protects Muscles from Exercise Damage in Sedentary Rats
- Authors
- Jonatas E. Nogueira, Mateus R. Amorim, Ana P. Pinto, Alisson L. da Rocha, Adelino S.R. da Silva, Luiz G.S. Branco
- Journal
- Canadian Journal of Physiology and Pharmacology
- Year
- 2020
- DOI
- 10.1139/cjpp-2020-0297
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Brazil
- Health Condition
- Exercise-Induced Muscle Damage
- Body System
- Musculoskeletal
TL;DR
Breathing in hydrogen gas while exercising intensely can reduce muscle damage, inflammation, and cell death in rats that aren't used to physical activity.
Key Finding
Molecular hydrogen inhalation reduced exercise-induced muscle damage in sedentary rats by decreasing oxidative stress, inflammatory markers, and cell death pathways.
Summary
Researchers tested whether molecular hydrogen (H2) could protect muscles from damage caused by exhausting exercise in sedentary rats. When rats breathed a mixture containing hydrogen gas while running to exhaustion, those receiving hydrogen showed less muscle damage compared to controls. The hydrogen reduced three harmful processes: oxidative stress (cellular damage from unstable molecules), inflammation (swelling and immune response), and apoptosis (programmed cell death).
Practical Takeaway
This rat study suggests hydrogen gas may help protect muscles from damage during intense exercise, but these are early findings in animals only. Whether this would apply to humans, what dose would be needed, or how it compares to other protective strategies remains unknown. Anyone considering hydrogen therapy should consult a healthcare provider, as human research is still very limited.
Abstract
Physical exercise-induced skeletal muscle damage may be characterized by increased oxidative stress, inflammation, and apoptosis which may be beneficial when exercise is regular, but it is rather harmful when exercise is exhaustive and performed acutely by unaccustomed individuals. Molecular hydrogen (H2) has emerged as a potent antioxidant, anti-inflammatory, and anti-apoptotic agent, but its action on the deleterious effects of acute exhaustive exercise in muscle damage remain unknown. Therefore, we tested the hypothesis that H2 decreases acute exhaustive exercise-induced skeletal muscle damage of sedentary rats. Rats ran to exhaustion on a sealed treadmill inhaling an H2-containing mixture or the control gas. We measured oxidative stress (SOD, GSH, and TBARS), inflammatory (TNF-α, IL-1β, IL-6, IL-10, and NF-κB phosphorylation), and apoptotic (expression of caspase-3, Bcl-2, and HSP70) markers. Exercise caused no changes in SOD activity but increased TBARS levels. H2 caused increases in exercise-induced SOD activity and blunted exercise-induced increased TBARS levels. We observed exercise-induced TNF-α and IL-6 surges as well as NF-κB phosphorylation, which were blunted by H2. Exercise increased cleaved caspase-3 expression, and H2 reduced this response. In conclusion, H2 effectively downregulates muscle damage, reducing oxidative stress, inflammation, and apoptosis after acute exhaustive exercise performed by an unaccustomed organism.