Compared to soy, whey protein is higher in leucine, absorbed quicker and results in a more pronounced increase in muscle protein synthesis. Objective: To determine whether supplementation with whey promotes greater increases in muscle mass compared to soy or carbohydrate, we randomized non-resistance-trained men and women into groups who consumed daily isocaloric supplements containing carbohydrate (carb; n = 22), whey protein (whey; n = 19), or soy protein (soy; n = 22). Methods: All subjects completed a supervised, whole-body periodized resistance training program consisting of 96 workouts (∼9 months). Body composition was determined at baseline and after 3, 6, and 9 months. Plasma amino acid responses to resistance exercise followed by supplement ingestion were determined at baseline and 9 months. Results: Daily protein intake (including the supplement) for carb, whey, and soy was 1.1, 1.4, and 1.4 g·kg body mass⁻¹, respectively. Lean body mass gains were significantly (p < 0.05) greater in whey (3.3 ± 1.5 kg) than carb (2.3 ± 1.7 kg) and soy (1.8 ± 1.6 kg). Fat mass decreased slightly but there were no differences between groups. Fasting concentrations of leucine were significantly elevated (20%) and postexercise plasma leucine increased more than 2-fold in whey. Fasting leucine concentrations were positively correlated with lean body mass responses. Conclusions: Despite consuming similar calories and protein during resistance training, daily supplementation with whey was more effective than soy protein or isocaloric carbohydrate control treatment conditions in promoting gains in lean body mass. These results highlight the importance of protein quality as an important determinant of lean body mass responses to resistance training.

Dyslipidemia and oxidative stress contribute to atherogenesis. Astaxanthin (ASTX) is a red-colored carotenoid well known for its high antioxidant cap

The incidence of nonalcoholic fatty liver disease (NAFLD) has risen along with the ongoing obesity epidemic. Green tea extract (GTE) inhibits intestinal lipid absorption and may regulate hepatic lipid accumulation. The objective of this study was to determine whether GTE protects against hepatic lipid accumulation during the development of NAFLD in an obese mouse model. Five-wk-old ob/ob (obese) mice and their lean littermates (8 mice·genotype⁻¹·dietary treatment⁻¹) were fed GTE at 0, 1, or 2% (wt:wt) for 6 wk. The body weights of obese mice and lean littermates fed diets containing GTE were 23–25% and 11–20% lower (P < 0.05) than their respective controls fed no GTE. Histologic evaluation showed a significant reduction in hepatic steatosis in GTE-fed obese mice only and histologic scores were correlated with hepatic lipid concentration (r = 0.84; P < 0.05), which was reduced dose dependently by GTE. GTE protected against hepatic injury as suggested by 30–41% and 22–33% lower serum alanine aminotransferase and aspartate aminotransferase activities, respectively. Hepatic α-tocopherol was 36% higher in obese mice than lean mice. GTE tended (P = 0.06) to lower hepatic α-tocopherol, which was not fully explained by the GTE-mediated reduction in hepatic lipid. Hepatic ascorbic acid was lower in obese mice than in lean mice (P < 0.05) and was unaltered by GTE. Obese mice had lower serum adiponectin than lean mice and this was not affected by GTE. The results suggest that GTE protects against NAFLD by limiting hepatic lipid accumulation and injury without affecting hepatic antioxidant status and adiponectin-mediated lipid metabolism. Further study is underway to define the events by which GTE protects against obesity-triggered NAFLD.