Sedentary aging increases resting and exercise-induced intramuscular free radical formation
Abstract
Mitochondrial free radical formation has been implicated as a potential mechanism underlying degenerative senescence, although human data are lacking. Therefore, the present study was designed to examine if resting and exercise induced intramuscular free radical-mediated lipid per oxidation is indeed increased across the spectrum of sedentary aging. Biopsies were obtained from the vastus lateralis in six young (26 +/- 6 yr) and six aged (71 +/- 6 yr) sedentary males at rest and after maximal knee extensor exercise. Aged tissue exhibited greater (P < 0.05 vs. the young group) electron paramagnetic resonance signal intensity of the mitochondrial ubisemiquinone radical both at rest (138 +/- 62%) and during exercise (143 +/- 40%), and this was further complemented by a greater increase in alpha-phenyl-N-tert-butylnitrone adducts identified as a combination of lipid-derived alkoxyl-alkyl radicals (295 +/- 96% and 298 +/- 120%). Lipid hydroperoxides were also elevated at rest (0.190 +/- 0.169 vs. 0.148 +/- 0.071 nmol/mg total protein) and during exercise (0.567 +/- 0.259 vs. 0.320 +/- 0.263 nmol/mg total protein) despite a more marked depletion of ascorbate and uptake of alpha,beta-carotene, retinol, and lycopene (P < 0.05 vs. the young group). The impact of senescence was especially apparent when oxidative stress biomarkers were expressed relative to the age-related decline in mitochondrial volume density and absolute power output at maximal exercise. In conclusion, these findings confirm that intramuscular free radical-mediated lipid peroxidation is elevated at rest and during acute exercise in aged humans.