Exercise and oxidative stress in hypoxia

Abstract

There is considerable indirect proof that a hypobaric-hypoxic environment increases oxidative stress, which is usually reflected by an increase in hepatic TBARS levels and a decrease in Mn-SOD levels. In a hypobaric chamber experiment designed to simulate the summit of Mt. Fuji, we detected an increase in hydroperoxide, an oxidative stress marker, although the percentage increase was lower than that observed at Mt. Fuji. This highlights the compounding effects of environmental factors (ultraviolet rays, temperature differences, etc.) and indicates the importance of conducting measurements in the field. Although the production of oxygen radicals increases with accelerated aerobic metabolism, it has been reported that oxidative stress increases even in hypoxic environments. Activation of xanthine oxidase (XO), that accompanies ischemia-reperfusion (I/R) or an increase in white blood cells, etc. are considered as potential mechanisms by which oxidative stress increases in hypoxic environments. However, these mechanisms have not been fully clarified.

Effect of Normobaric Hypoxia on Alterations in Redox Homeostasis, Nitrosative Stress, Inflammation, and Lysosomal Function following Acute Physical Exercise

“…During tissue hypoxia (as during tissue ischemia), xanthine dehydrogenase is converted to XO, donating an electron to molecular oxygen. The reaction catalyzed by XO produces superoxide anions and hydrogen peroxide [2,30,31,70], explaining the increase in SOD and CAT activity under hypoxic exercise. However, overactivation of nitric oxide synthases (NOS), especially inducible NOS (iNOS), also occurs in these conditions [71,72].…”

“…Therefore, improvements in aerobic and anaerobic capacity may occur. However, hypoxia and subsequent reoxygenation are also responsible for ROS/RNS overproduction, during prolonged exposure to altitude, as well as during intermittent hypoxic training [29][30][31]. This is caused by disruption of the mitochondrial respiratory chain, disturbances in arachidonic acid metabolism, or migration/activation of immune cells during regular physical activity [24,25,30,31].…”

“…However, hypoxia and subsequent reoxygenation are also responsible for ROS/RNS overproduction, during prolonged exposure to altitude, as well as during intermittent hypoxic training [29][30][31]. This is caused by disruption of the mitochondrial respiratory chain, disturbances in arachidonic acid metabolism, or migration/activation of immune cells during regular physical activity [24,25,30,31]. Nevertheless, there is a lack of studies evaluating the relationship between antioxidant systems, oxidative and nitrosative cell damage, inflammation, and lysosomal function under normoxic and hypoxic conditions.…”

“…As interest in high-altitude sports grows, it is essential to understand the differences in redox homeostasis between various protocols of acute physical intervention. Previous studies have examined only a few aspects of redox homeostasis [30,32,33] and ultimately have not systematically studied the effects of normoxia and hypoxia during acute exercise. Therefore, the present study is aimed at evaluating the relationship between (1) enzymatic and nonenzymatic antioxidant barrier, (2) total antioxidant/ oxidant status, (3) oxidative and (4) nitrosative cell damage, (5) biomarkers of inflammation, and (6) lysosomal function in different protocols (different intensity and duration) performed under normoxic and hypoxic conditions.…”