Molecular hydrogen reduces acute exercise-induced inflammatory and oxidative stress status

Author(s)

Nogueira, Jonatas E. ^{[1, 2]} ; Passaglia, Patricia ^[3] ; Mota, Clarissa M. D. ^[3] ; Santos, Bruna M. ^[3] ; Batalhao, Marcelo E. ^[4] ; Carnio, Evelin C. ^{[3, 4]} ; Branco, Luiz G. S. ^{[5, 3, 2]}

Affiliation

^[1] Univ Sao Paulo, Sch Phys Educ & Sports Ribeirao Preto, Ribeirao Preto, SP - Brazil

^[2] Univ Sao Paulo, Postgrad Program Rehabil & Funct Performance, Ribeirao Preto, SP - Brazil

^[3] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Physiol, Ribeirao Preto, SP - Brazil

^[4] Univ Sao Paulo, Sch Nursing Ribeirao Preto, Dept Gen & Specialized Nursing, Ribeirao Preto, SP - Brazil

^[5] Univ Sao Paulo, Dent Sch Ribeirao Preto, Dept Morphol Physiol & Basic Pathol, BR-14040904 Ribeirao Preto, SP - Brazil

• Document type: Journal article
• Source: Free Radical Biology and Medicine; v. 129, p. 186-193, DEC 2018.
• Web of Science Citations: 6

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 (H-2) 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 H-2 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 H-2 gas (2% H-2, 21% O-2, balanced with N-2) or the control gas (0% H-2, 21% O-2, balanced with N-2) and were euthanized immediately or 3 h after exercise. We assessed plasma levels of inflammatory cytokines {[}tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta 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 (GSK3 alpha/beta) 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, H-2 blunted exercise-induced plasma inflammatory cytokines (TNF-alpha and IL-6) surges. Regarding the oxidative stress markers, H-2 caused further increases in exercise-induced SOD activity and attenuated the exercise-induced increases in TBARS 3 h after exercise. Moreover, GSK3 alpha/beta phosphorylation was not affected by exercise or H-2 inhalation. Otherwise, exercise caused an increased CREB phosphorylation which was attenuated by H-2. These data are consistent with the notion that H-2 plays a key role in decreasing exercise-induced inflammation, oxidative stress, and cellular stress. (AU)

• FAPESP's process: 16/17681-9 - Pathophysiological changes during systemic inflammation
• Grantee: Luiz Guilherme de Siqueira Branco
• Support Opportunities: Research Projects - Thematic Grants