Moderate altitude but not additional endurance training increases markers of oxidative stress in exhaled breath condensate

Abstract

Oxidative stress occurs at altitude, and physical exertion might enhance this stress. In the present study, we investigated the combined effects of exercise and moderate altitude on redox balance in ten endurance exercising biathletes, and five sedentary volunteers during a 6 week stay at 2800 m. As a marker for oxidative stress, hydrogen peroxide (H 2 O 2 ) was analyzed by the biosensor measuring system Ecocheck TM , and 8-iso prostaglandin F2α (8-iso PGF2α) was determined by enzyme immunoassay in exhaled breath condensate (EBC). To determine the whole blood antioxidative capacity, we measured reduced glutathione (GSH) enzymatically using Ellman's reagent. Exercising athletes and sedentary volunteers showed increased levels of oxidative markers at moderate altitude, contrary to our expectations, there was no difference between both groups. Therefore, all subjects' data were pooled to examine the oxidative stress response exclusively due to altitude exposure. H 2 O 2 levels increased at altitude and remained elevated for 3 days after returning to sea level (p ≤ 0.05). On the other hand, 8-iso PGF2α levels showed a tendency to increase at altitude, but declined immediately after returning to sea level (p ≤ 0.001).Hypoxic exposure during the first day at altitude resulted in elevated GSH levels (p ≤ 0.05), that decreased during prolonged sojourn at altitude (p ≤ 0.001). In conclusion, a stay at moderate altitude for up to 6 weeks increases markers of oxidative stress in EBC independent of additional endurance training. Notably, this oxidative stress is still detectable 3 days upon return to sea level.

Exercise modulation of total antioxidant capacity (TAC): towards a molecular signature of healthy aging

“…Training at higher altitudes also decreased TAC of elite swimmers (Subudhi et al 2004), confirming previous research which demonstrated increased oxidative stress at higher altitudes after nutritional supplementation with antioxidants (Heinicke et al 2009;Castell et al 2010). However, in high-fitness trained military marine men, the total antioxidant capacity remained Child et al (1999) 2.730 ± 0.07 Urine (at rest) Child et al (1999) 3.130 ± 0.11 * protein precipitation by perchloric acid.…”

“…Regular practice of physical activity and exercise can improve TAC by modulating the synthesis of both enzymatic (SOD, CAT, GPX) and non-enzymatic (uric acid, albumin, ceruloplasmin, metallothioneins) cell antioxidants in skeletal muscles, liver, heart, brain and other organs, and can reduce lipid peroxidation, postprandial oxidative and nitrosative stresses and LDL cholesterol oxidation (Heitkamp et al 2008;Neubauer et al 2008;Bloomer et al 2009;Heinicke et al 2009;Ji et al 2009;Castell et al 2010). DNA damage can be reduced with regular physical exercise by enhancing expression of genome repairing enzymes on striatal skeletal muscles (Radák et al 2003;Kim et al 2010).…”

Oxygen-induced regulation of the intracellular glutathione levels in erythrocytes

“…We are replying to Dr. Böning's comments to our recently published paper on oxidative stress parameters at moderate altitude (Heinicke et al 2009). Half cell redox potential for the couple reduced (GSH)-oxidized (GSSG) glutathione is widely accepted as a reliable measure of the intracellular redox state (Schafer and Buettner 2001).…”

“…Thus, glutathione reductase activity should be signiWcantly up-regulated to aVord it. Mild hypoxia triggered an increase in GSH of 12-20% in humans exposed to moderate altitude (Heinicke et al 2009). However, further deoxygenation may cause further up-regulation of the intracellular GSH content which is much more pronounced (to about 50%), (Bogdanova et al 2003.…”

Oxidative damage is present in plasma and circulating neutrophils 4 weeks after a high mountain expedition

“…Exposure to high altitudes aVects antioxidant enzymes, resulting in impaired free-radical scavenging (Heinicke et al 2009;Dosek et al 2007;Joanny et al 2001). Radak et al (1994) described for the Wrst time that intermittent exposure to 4,000 m for 6 months resulted in a decrease in the activity of mitochondrial Mn-superoxide dismutase (Mn-SOD) in rat skeletal muscle as a consequence of altered gene transcription due to hypoxia.…”