While more likely to be obese than white women, black women have greater muscle mass than whites. In addition, black women have more resistance to insulin-mediated glucose utilization in muscle. Whether the combination of both high lean mass (LM), insulin resistance and chronic hyperinsulinemia leads to a race difference in exercise performance is unknown. One hundred forty non-diabetic sedentary overweight women 64% black;age 4511 years (meanSD), body mass index (BMI) range 25.3 to 57.7 kg/m2 underwent body composition measurements by dual-energy X-ray absorptiometry. Insulin sensitivity index (SI) was calculated from the minimal model, and chronic insulin exposure by fasting insulin level. Exercise performance was measured by peak oxygen consumption (VO2 peak) during graded treadmill exercise.Both total body LM (49.76.6 vs 44.86.2 kg, P<0.001) and lower extremity LM (18.32.9 vs 15.92.5 kg, P<0.001) were greater in blacks than whites, even after adjustment for BMI or total fat mass. SI was lower in blacks than whites (3.11.8 vs 4.72.7 L.U-1min-1, P<0.001): Lower SI was negatively (r= -0.505, r= -0.342) and higher fasting insulin was positively (r= 0.428, r= 0.428) associated with increased total body and lower extremity LM in blacks (all P<0.01), but did not achieve statistical significance in whites. Blacks had reduced VO2 peak (21.34.6 vs 26.34.8 ml/kg/min, P<0.001) than whites: both total body (beta= -0.15, P=0.004) and lower extremity LM (beta= -0.47, P=0.002) were independently predictive of reduced VO2 peak in black women, even when age, relative fat mass load and SI were entered into the multiple regression model. By contrast, neither LM was independently predictive of VO2 peak in white women. Thus, overweight black women had more LM, associated with greater chronic insulin exposure, but lower exercise performance than white women. The contributions of hyperinsulinemia to LM and poor exercise tolerance in black women need to be explored. Diet-induced weight loss in overweight women may be associated with decreases not only in total cholesterol and low-density lipoprotein cholesterol (LDL-C), but also in high-density lipoprotein cholesterol (HDL-C) levels. Whether a decrease in HDL-C level is associated with altered HDL function is unknown.One hundred overweight women (60 black, 35 white, 3 Asian, 2 Hispanic;12 diabetic;age 46 11 years;BMI 33.5 6.1 kg/m2) were enrolled in a six month worksite wellness program, which included a reduced fat and total energy diet and low-intensity exercise to achieve weight loss. Serum cholesterol efflux capacity was measured by incubating 1% apolipoprotein B-depleted serum with 3H-cholesterol-labeled BHK cells expressing ABCA1, ABCG1 or SR-B1 transporters. Antioxidant properties of HDL were estimated by paraoxonase-1 (PON1) activity and the oxygen radical absorbance capacity (ORAC). Endothelial nitric oxide synthase (eNOS) activation was measured by incubating HDL from 49 subjects with cultured endothelial cells and by measuring conversion of L-arginine to L-citrulline. All baseline and six month samples were assayed in pairs. Data are reported as mean value SD. Participants achieved an average weight loss of 2.2 3.9 kg (P<0.001), associated with reductions in all plasma cholesterol values: total cholesterol: -11 24 mg/dL, P<0.001;LDL-C: -6 21 mg/dL, P=0.004;HDL-C: -3 9 mg/dL, P=0.016. Cholesterol efflux capacity by the ABCA1 transporter decreased by 10% (P=0.006);efflux capacities by the ABCG1 and SR-B1 transporters were not significantly altered (both <2%, P>0.736). ORAC decreased by 15% (P=0.018);neither PON1 activity (+1%, P=0.314) nor eNOS activation (-5%, p=0.174) was significantly altered by reduction in HDL-C.Weight loss in overweight women is associated with significant decrease in cholesterol levels, including HDL-C, but small changes in HDL-mediated cholesterol efflux capacity, oxidative protection and eNOS activation.

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