Obesity exacerbates oxidative stress levels after acute exercise.

INTRODUCTION/
PURPOSE: This study compared oxidative stress levels and antioxidant capacity in nonobese and obese participants after acute resistance (RX) and aerobic exercise (AX).
METHODS: Blood samples were collected from 28 nonobese (mean = 20.8% body fat) and obese (mean = 35.0% body fat) participants pre- and immediately post-RX and AX. Lipid hydroperoxides (PEROX), malondialdehyde (TBARS) and total antioxidant status (TAS) were measured. Oxygen consumption (VO2) and minute ventilation (VE) values were determined during each exercise session.
RESULTS: In both groups, PEROX and TBARS were elevated post-RX and AX, with the greater elevations occurring in the obese group in each case (P < 0.05). In the obese, TBARS increased by 42% and 41% post-RX and AX, respectively, compared with 7.1% and 26.9% in the nonobese group. PEROX increased by 100% and 70% post-RX and AX, respectively, in the obese, and by 85% and 62% in the nonobese. TAS was 17% higher (P < 0.05) post-RX in the nonobese compared with the obese, whereas TAS values were not different post-AX. Peak and average VE, and relative VO2). rates were higher in the obese post-AX compared with the nonobese (P < 0.05) Correlations existed between the exercise-induced change in PEROX and body fat, vitamin C and A intake, peak oxygen consumption, and exercise ventilation rates in the obese group (r = 0.784-0.776, P < 0.05). In both groups, the exercise-induced changes in PEROX were associated with vitamin C intake, exercise ventilation rates, VO2peak, and plasma triglycerides (r = 0.669-0.558, P < 0.05).
CONCLUSION: Lipid peroxidation is elevated in both RX and AX, and it is exacerbated in the obese. The mechanisms underlying this response in each exercise may be different but could involve plasma triglycerides, oxygen consumption, and antioxidant intake.