Bloomer, R.J., A.H. Goldfarb, L. Wideman, M.J. McKenzie, and L.A. Consitt. Effects of acute aerobic and anaerobic exercise on blood markers of oxidative stress. J. Strength Cond. Res. 19(2):276-285. 2005.-The purpose of this study was to compare oxidative modification of blood proteins, lipids, DNA, and glutathione in the 24 hours following aerobic and anaerobic exercise using similar muscle groups. Ten cross-trained men (24.3 Ϯ 3.8 years, [mean Ϯ SEM]) performed in random order 30 minutes of continuous cycling at 70% of V O 2 max and intermittent dumbbell squatting at 70% of 1 repetition maximum (1RM), separated by 1-2 weeks, in a crossover design. Blood samples taken before, and immediately, 1, 6, and 24 hours postexercise were analyzed for plasma protein carbonyls (PC), plasma malondialdehyde (MDA), and whole-blood total (TGSH), oxidized (GSSG), and reduced (GSH) glutathione. Blood samples taken before and 24 hours postexercise were analyzed for serum 8-hydroxy-2Ј-deoxyguanosine (8-OHdG). PC values were greater at 6 and 24 hours postexercise compared with pre-exercise for squatting, with greater PC values at 24 hours postexercise for squatting compared with cycling (0.634 Ϯ 0.053 vs. 0.359 Ϯ 0.018 nM·mg protein Ϫ1 ). There was no significant interaction or main effects for MDA or 8-OHdG. GSSG experienced a shortlived increase and GSH a transient decrease immediately following both exercise modes. These data suggest that 30 minutes of aerobic and anaerobic exercise performed by young, crosstrained men (a) can increase certain biomarkers of oxidative stress in blood, (b) differentially affect oxidative stress biomarkers, and (c) result in a different magnitude of oxidation based on the macromolecule studied. Practical applications: While protein and glutathione oxidation was increased following acute exercise as performed in this study, future research may investigate methods of reducing macromolecule oxidation, possibly through the use of antioxidant therapy.

Purpose. The current study sought to expand implications of physiological weathering through the application of latent profile analysis to stress biomarkers to address limitations of traditional allostatic load calculations.Methods. Latent profile analysis was applied biomarkers used in traditional allostatic load metrics to identify physiological risk profiles in the 2007-20010 National Health and Nutritional and Examination Survey. Multinomial logistic regression was used to determine the probability of risk profiles by race/ethnicity, age, gender, and poverty income ratio (PIR). Mean allostatic load score was assessed across each risk profile.Results. Latent profile analysis identified four distinct profiles labeled low risk, inflammatory risk, cardiovascular risk, and hypertension risk. Race, age, and gender significantly increased odds of exhibiting a risk profile. Compared to Whites, Hispanics had significant higher odds of inflammatory (OR=1.43, 95% CI [1.06-1.92]) and cardiovascular risk profiles (OR=1.63, 95% CI [1.09-2.43]) while Blacks had higher odds of inflammatory (OR=1.76 95% CI [1.25-2.47]), cardiovascular (OR=2.12, 95% CI, [1.39-3.27]) and hypertension risk profiles (OR= 1.78, 95% CI [1.21-2.59]). Females held significant greater odds of all risk categories except hypertension in which they held the lowest odds (OR= .19, 95% CI [.14-.25]). Mean allostatic load scores were highest in the inflammatory (M=3.99, SD=1.66) and cardiovascular risk profiles (M=4.4, SD=1.84). Conclusions.Employing latent profile analysis may expand traditional allostatic load methodology by identifying physiological risk patterns among those who experience allostatic load early in life. This may be useful for examining how cultural specific interventions may reduce cardiovascular risk among those exhibiting physiological risk profiles.

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Obesity has been linked with elevation of the inflammatory protein, C‐reactive protein (CRP), which increases risk of developing chronic disease. Weight loss, specifically loss of abdominal fat, may decrease CRP. The Healthy Eating Index (HEI), which measures overall diet quality, may also be associated with CRP levels. These scores are based on the intake of 12 different food components with a maximum score of 100. The objective of this study was to determine the effect of weight loss and dietary quality on CRP in 36 overweight, postpartum (PP) women from two randomized, controlled weight loss trials. Weight, height, and body composition (determined by DXA) were measured at baseline (4‐14 weeks PP) and endpoint (18‐26 weeks PP). Concentrations of CRP were measured by ELISA. HEI scores were calculated from two 24‐hour recalls obtained using the Nutrition Data System for Research. The intervention group lost significantly more weight than the control group (‐6.86 ± 1.04 kg, ‐3.65 ± 1.14 kg, p=0.02). There were no significant differences between groups for CRP or HEI scores. When analyzing data from all participants, there was a significant positive association between change in CRP (‐0.13 ± 0.49 mg/L) and change in weight (R2=0.12) and trunk fat (R2=0.15). Also, while change in HEI scores was not significantly associated with change in CRP, HEI score at baseline (59.9 ± 2.6) tended to be negatively associated with change in CRP (R2=0.09, p=0.09). The relationship between change in trunk fat and change in CRP was strengthened when HEI scores at baseline were added to the model (R2=0.19). These results suggest that loss of total weight and abdominal fat is associated with a reduction of CRP. Diet quality may mediate the relationship seen between body composition and CRP.