OXIDATIVE STRESS AFTER HUMAN EXERCISE - EFFECT OF N-ACETYLCYSTEINE SUPPLEMENTATION

Citation
Ck. Sen et al., OXIDATIVE STRESS AFTER HUMAN EXERCISE - EFFECT OF N-ACETYLCYSTEINE SUPPLEMENTATION, Journal of applied physiology, 76(6), 1994, pp. 2570-2577
Citations number
37
Categorie Soggetti
Physiology
ISSN journal
87507587
Volume
76
Issue
6
Year of publication
1994
Pages
2570 - 2577
Database
ISI
SICI code
8750-7587(1994)76:6<2570:OSAHE->2.0.ZU;2-1
Abstract
The association between exercise intensity and related oxidative stres s was investigated in nine men who exercised for 30 min at their aerob ic (AeT) and anaerobic (AnaeT) thresholds. We also tested the effect o f oral N-acetylcysteine (NAC) on exercise-associated rapid blood gluta thione (GSH) oxidation in subjects performing two identical maximal bi cycle ergometer exercise (Max) tests. Before the second test {Max with NAC supplementation [Max(NAC)]}, the men took 200 X 4 mg/day of NAC t ablets for 2 days and an additional 800 mg on the test morning. Blood samples were drawn before, immediately after, and 24 h after the tests . Total and oxidized GSH levels in blood were determined. Plasma thiob arbituric acid-reactive substances and net peroxyl radical scavenging capacity (PSC) were assayed. Exercise-associated damage in leukocyte D NA was estimated by fluorometric analysis of DNA unwinding. A single b out of exercise at Max, AeT, and AnaeT resulted in a significant incre ase in blood GSH oxidation but did not influence net PSC of plasma. Al though an association between a single bout of exercise and leukocyte DNA damage was apparent, this study suggests that the parameter may no t serve as a sensitive index to assess the role of exercise intensity in the extent of exercise-associated oxidative stress. Plasma thiobarb ituric acid-reactive substances did not change after either Max or Max (NAC) tests. NAC supplementation resulted in an increase in preexercis e PSC, indicating a higher net antioxidant capacity of the plasma, but did not affect blood GSH. Max-associated rapid decline in blood thiol redox status was markedly attenuated by NAC supplementation, indicati ng that the supplementation may have spared exercise-associated blood GSH oxidation and the thiol redox status perturbation.