Operation Everest III (Comex'97): the effect of simulated severe hypobaric hypoxia on lipid peroxidation and antioxidant defence systems in human blood at rest and after maximal exercise

Eight subjects were placed in a decompression chamber for 31 days at pressures from sea level (SL) to 8848 in altitude equivalent. Whole blood lipid peroxidation (LP) was increased at 6000 in by a mean of 23% (P < 0.05), at 8000 m by 79% (P < 0.01) and at 8848 rn by 94% (P < 0.01). (All figures are means.) Two days after return to sea level (RSL), it remained high, by 81% (P < 0.01), while corresponding erythrocyte GSH/GSSG ratios decreased by 31, 46, 49, 48%, respectively (each P < 0.01). Erythrocyte SOD and plasma ascorbate did not change significantly. At sea level, maximal exercise induced a 49% increase in LP (P < 0.01), and a 27% decrease in erythrocyte GSH/GSSG ratio relative to resting values (P < 0.05). At 6000 m, the LP was enhanced further from 23 (P < 0.05) to 66% (P < 0.01), and after RSL from 81 (P < 0.01) to 232% (P < 0.01), while pre-exercise GSH/GSSG ratios did not change significantly. Exercise did not change plasma ascorbate relative to sea level or to 6000 in, but decreased after RSL by 32% (P < 0.01). These findings suggest that oxidative stress is induced by prolonged hypobaric hypoxia, and is maintained by rapid return to sea level, similar to the post-hypoxic re-oxygenation process. It is increased by physical exercise. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.