Exercise-induced oxidative stress in older adults as measured by antipyrine oxidation

Abstract

Aging is associated with increased susceptibility to free radical-mediated tissue damage. Measuring exercise-induced oxidative stress, however, is a major problem in free radical research. We used an exogenous marker (antipyrine) to measure oxidative stress in older adults during submaximal exercise. Antipyrine pharmacokinetics is independent of blood flow to the liver. Furthermore, antipyrine reacts quickly with hydroxyl radicals (1010-1011 L [middot] mol[minus ]1 [middot] s[minus ]1) to form para- and ortho-hydroxyantipyrine (o-APOH). o-APOH is not formed in man through the mono-oxygenase pathway of cytochrome P450. Thirty-four subjects (62 [plusmn] 1 years) orally ingested 10 mg antipyrine/kg body mass. One hour after ingestion subjects cycled 45 minutes at 50% maximal power output. Exercise significantly increased the ratio of para-hydroxyantipyrine (p-APOH) to native antipyrine in plasma (.0014 [plusmn] .0001 v .0021 [plusmn] .0002; P [lt ] .0001). Also, the ratio of o-APOH was significantly increased after exercise (.0014 [plusmn] .0001 v .0019 [plusmn] .0002; P [lt ] .0001). Exercise significantly increased plasma levels of plasma malondialdehyde MDA) (.55 [plusmn] .07 v .92 [plusmn] .21 [mu ]mol/L; P [lt ] .01). In conclusion, in older adults, oxidative stress occurs during cycling at submaximal intensity as measured with free radical reaction products of antipyrine.