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Objective: Determine whether sleeping and resting energy expenditure and sleeping, resting, and 24‐hour fuel use distinguish obesity‐prone from obesity‐resistant women and whether these metabolic factors explain long‐term weight gain. Research Methods and Procedures: Forty‐nine previously overweight but currently normal‐weight women were compared with 49 never‐overweight controls. To date, 87% of the 98 women have been re‐evaluated after 1 year of follow‐up, without intervention, and 38% after 2 years. Subjects were studied at a General Clinical Research Center after 4 weeks of tightly controlled conditions of energy balance and macronutrient intake. Forty‐nine obesity‐prone weight‐reduced women were group‐matched with 49 never‐overweight obesity‐resistant controls. All were premenopausal, sedentary, and normoglycemic. Energy expenditure and fuel use were assessed using chamber calorimetry. Body composition was assessed using DXA. Results: At baseline, percent body fat was not different between the obesity‐prone and control women (33 ± 4% vs. 32 ± 5%, respectively; p= 0.22). Analysis of covariance results show that after adjusting for lean and fat mass, sleeping and resting energy expenditure of obesity‐prone women was within 2% of controls. Neither sleeping nor resting energy expenditure nor sleeping, resting, or 24‐hour fuel use was significantly different between the groups (p> 0.25). None of the metabolic variables contributed significantly to patterns of weight gain at 1 or 2 years of follow‐up. Discussion: The results suggest that when resting and sleeping energy expenditure and fuel use are assessed under tightly controlled conditions, these metabolic factors do not distinguish obesity‐prone from obesity‐resistant women or explain long‐term weight changes.

Objective: To investigate the role of genetic admixture in explaining phenotypic variation in obesity‐related traits in a sample of African‐American women (n= 145) and to determine significant associations between obesity traits and admixture genetic markers. Research Methods and Procedures: Associations between genetic admixture and BMI, resting metabolic rate, fat mass, fat‐free mass, and bone mineral density were tested using linear regression considering the estimation of admixture by 1) a maximum‐likelihood approach (MLA) and 2) a Bayesian analysis. Results: Both the conservative MLA and the Bayesian approach support an association between African genetic admixture and BMI. Evidence for the associations of African genetic admixture with fat mass and fat‐free mass was supported by the Bayesian analysis; the MLA supported an association with bone mineral density. When the individual ancestry informative markers that were used to estimate admixture were tested for associations with BMI, significant associations were identified in chromosomes 1, 11, and 12. Discussion: These results provide evidence supporting the application of admixture mapping methods to the identification of genes that result in higher levels of obesity among African‐American women. Further research is needed to replicate and further explore these findings.

LAREW, K., G. R. HUNTER, D. E. LARSON-MEYER, B. R. NEWCOMER, J. P. MCCARTHY, and R. L. WEINSIER. Muscle Metabolic Function, Exercise Performance, and Weight Gain. Med. Sci. Sports Exerc., Vol. 35, No. 2, pp. 230–236, 2003.

Oxidant formation in the vasculature contributes to vascular disease and dysfunction associated with obesity. In contrast, exercise‐dependent production of oxidants may stimulate adaptive responses that protect against the development of such diseases. In this review, we discuss current concepts in the biology of reactive oxygen and nitrogen species and how their function is modulated in the context of vascular disease, obesity, and aerobic exercise.

Objective:To determine the effects of fat gain, time, and race on the accumulation of visceral adipose tissue (VAT) in a group of normal‐weight premenopausal women. Research Methods and Procedures:Sixty‐five women participated in the study (32 African American and 33 white). The mean age of subjects was 34 ± 6 years (range, 22 to 47 years). Eligible subjects were women who had body mass indices <25 kg/m2at baseline and who had completed evaluations at baseline and at follow‐up year 1, without intervention. A subset of subjects was reevaluated annually for up to 4 years. Body composition was assessed by DXA, and VAT was determined from a single computed tomography scan. A linear mixed model was used to examine changes in VAT over time, with total body fat as a covariate Results:Total fat mass was not significantly different between races at baseline and increased significantly in both groups over time (p< 0.001). Time‐related increases in total body fat were greater in African‐American women (p< 0.01). VAT was significantly higher in white women at baseline (p< 0.01) and increased significantly over time in both races (p< 0.01), but remained higher in white women (p< 0.001). Increases in VAT, relative to total body fat, were greater than the increases in total body fat over time, independent of age and race (p< 0.001). Discussion:Gaining total body‐fat mass results in a higher increase in VAT, relative to total body fat, regardless of race and age, although African‐American women maintain a lower VAT levels across time.

The purpose of this study was to determine whether muscle metabolic capacity was inversely related to age after adjusting for physical activity in sedentary premenopausal women. Eighty-three women (ages 23–47 yr) had their free-living, activity-related energy expenditure evaluated with doubly labeled water procedures, and room calorimeter determined sleeping energy expenditure. Maximum O2uptake and strength were evaluated in all subjects, whereas 31P-magnetic resonance spectroscopy determined metabolic economy during maximal exercise, and muscle biopsy maximal enzyme activity was evaluated in subsets of the sample (48 and 18 subjects, respectively). Age was significantly related to whole body treadmill endurance time (r= −0.32), plantar flexion strength (r= −0.29), maximum O2uptake (r= −0.27),31P-magnetic resonance spectroscopy ADP recovery rate (r= −0.44), and anaerobic glycolytic capacity (r= −0.37), and muscle biopsy citrate synthase activity (r= −0.48), glyceraldehyde-3-phosphate dehydrogenase (r= −0.54), phosphofructokinase (r= −0.62), and phosphorylase (r= −0.58) activity even after adjusting for activity-related energy expenditure. These data suggest that, in sedentary premenopausal women, both oxidative and glycolytic muscle capacity decrease with age even when physical activity is taken into account.

The relationships between in vivo ³¹P magnetic resonance spectroscopy (MRS) and in vitro markers of oxidative capacity (mitochondrial function) were determined in 27 women with varying levels of physical fitness. Following 90-s isometric plantar flexion exercises, calf muscle mitochondrial function was determined from the phosphocreatine (PCr) recovery time constant, the adenosine diphosphate (ADP) recovery time constant, the rate of change of PCr during the initial 14 s of recovery, and the apparent maximum rate of oxidative adenosine triphosphate (ATP) synthesis (Qmax). Muscle fiber type distribution (I, IIa, IIx), citrate synthase (CS) activity, and cytochrome c oxidase (COX) activity were determined from a biopsy sample of lateral gastrocnemius. MRS markers of mitochondrial function correlated moderately (P &lt; 0.05) with the percentage of type IIa oxidative fibers (r = 0.41 to 0.66) and CS activity (r = 0.48 to 0.64), but only weakly with COX activity (r = 0.03 to 0.26, P > 0.05). These results support the use of MRS to determine mitochondrial function in vivo. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 1665–1676, 2001

The relationships between in vivo 31P magnetic resonance spectroscopy (MRS) and in vitro markers of oxidative capacity (mitochondrial function) were determined in 27 women with varying levels of physical fitness. Following 90‐s isometric plantar flexion exercises, calf muscle mitochondrial function was determined from the phosphocreatine (PCr) recovery time constant, the adenosine diphosphate (ADP) recovery time constant, the rate of change of PCr during the initial 14 s of recovery, and the apparent maximum rate of oxidative adenosine triphosphate (ATP) synthesis (Qmax). Muscle fiber type distribution (I, IIa, IIx), citrate synthase (CS) activity, and cytochrome c oxidase (COX) activity were determined from a biopsy sample of lateral gastrocnemius. MRS markers of mitochondrial function correlated moderately (P< 0.05) with the percentage of type IIa oxidative fibers (r= 0.41 to 0.66) and CS activity (r= 0.48 to 0.64), but only weakly with COX activity (r= 0.03 to 0.26, P> 0.05). These results support the use of MRS to determine mitochondrial function in vivo. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 1665–1676, 2001

HUNTER, G. R., R. L. WEINSIER, J. P. MCCARTHY, D. E. LARSON-MEYER, and B. R. NEWCOMER. Hemoglobin, muscle oxidative capacity, and 2maxin African-American and Caucasian women. Med. Sci. Sports Exerc., Vol. 33, No. 10, 2001, pp. 1739–1743. PurposeThe purpose of this paper was to determine whether differences in hemoglobin (Hb) and muscle aerobic capacity exist between African-American (AA) and Caucasian (CA) premenopausal women and to determine whether Hb and aerobic capacity of the muscle are associated with the racial differences in maximum oxygen uptake (2max). Methods43 AA and 46 CA sedentary premenopausal women were subjects. Percent body fat was determined by four-compartment model, leg lean tissue by dual energy x-ray absorptiometry, 2maxduring a graded exercise test, aerobic capacity of the calf muscle by 31P magnetic resonance spectroscopy, and serum Hb by the cyanide method. ResultsAA women had reduced 2max(AA 29.3 ± 3.0 vs CA 33.6 ± 5.6 mL·kg−1bdw−1·min, P< 0.01), reduced muscle aerobic capacity (AA 24.3 ± 5.8 vs CA 21.3 ± 4.8 s, P0.01, where lower values indicate higher aerobic capacity), and reduced Hb (AA 11.8 ± 1.3 vs CA 12.9 ± 0.8 g·dL−1, P< 0.01). The racial difference in 2maxpersisted whether the values were unadjusted or adjusted for fat-free mass or leg lean tissue. Multiple regression analysis revealed that both Hb and muscle aerobic capacity were related to 2maxafter adjusting for each other, race, and either fat-free mass or leg lean tissue. Being AA was associated with reduced 2maxin mL O2·kg leg lean tissue−1.min−1(zero-order simple Pearson-product correlation −0.60, P< 0.01). When multiple regression was used, the correlation between race and 2maxdecreased but persisted (−0.40, <0.01) after adjusting for Hb and muscle aerobic capacity. ConclusionsThese data suggest that differences in Hb and aerobic capacity of muscle are related to reduced 2maxin AA women. However, Hb and aerobic capacity of the muscle can only partially explain the racial differences in 2max.

The number of physical activity measures and indexes used in the human literature is large and may result in some difficulty for the average investigator to choose the most appropriate measure. Accordingly, this review is intended to provide information on the utility and limitations of the various measures. Its primary focus is the objective assessment of free‐living physical activity in humans based on physiological and biomechanical methods. The physical activity measures have been classified into three categories: 1. Measures based on energy expenditure or oxygen uptake, such as activity energy expenditure, activity‐related time equivalent, physical activity level, physical activity ratio, metabolic equivalent, and a new index of potential interest, daytime physical activity level.2. Measures based on heart rate monitoring, such as net heart rate, physical activity ratio heart rate, physical activity level heart rate, activity‐related time equivalent, and daytime physical activity level heart rate.3. Measures based on whole‐body accelerometry (counts/U time). . Measures based on energy expenditure or oxygen uptake, such as activity energy expenditure, activity‐related time equivalent, physical activity level, physical activity ratio, metabolic equivalent, and a new index of potential interest, daytime physical activity level. . Measures based on heart rate monitoring, such as net heart rate, physical activity ratio heart rate, physical activity level heart rate, activity‐related time equivalent, and daytime physical activity level heart rate. . Measures based on whole‐body accelerometry (counts/U time). Quantification of the velocity and duration of displacement in outdoor conditions by satellites using the Differential Global Positioning System may constitute a surrogate for physical activity, because walking is the primary activity of man in free‐living conditions. A general outline of the measures and indexes described above is presented in tabular form, along with their respective definition, usual applications, advantages, and shortcomings. A practical example is given with typical values in obese and non‐obese subjects. The various factors to be considered in the selection of physical activity methods include experimental goals, sample size, budget, cultural and social/environmental factors, physical burden for the subject, and statistical factors, such as accuracy and precision. It is concluded that no single current technique is able to quantify all aspects of physical activity under free‐living conditions, requiring the use of complementary methods. In the future, physical activity sensors, which are of low‐cost, small‐sized, and convenient for subjects, investigators, and clinicians, are needed to reliably monitor, during extended periods in free‐living situations, small changes in movements and grade as well as duration and intensity of typical physical activities.

It is not known what causes the well‐established inverse relationship between whole‐body exercise economy and exercise intensity. The purpose of this study was to: (1) evaluate muscle exercise economy at 45%, 70%, and maximum isometric strength using 31P magnetic resonance spectroscopy (31P‐MRS); and (2) determine the relationship between percent type II muscle fiber cross‐section, whole‐body exercise economy, and muscle exercise economy. Subjects included 32 premenopausal women. Muscle exercise economy was significantly different across the three exercise intensities (28.1 ± 10.4, 24.8 ± 8.2, and 20.2 ± 7.5 N/cm2· mmol/L adenosine triphosphate [ATP] for the 45%, 70%, and maximum intensities, respectively). Percent type II muscle area was significantly related to whole‐body metabolic economy during activities of daily living (r= −0.68) and 31P‐MRS muscle metabolic economy during isometric plantar flexion (r= −0.53). These data suggest that skeletal muscle becomes less economical as force production increases, and that these decreases in metabolic economy may be related to increased dependence on inefficient type II muscle. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 654–661, 2001

BAMMAN, M. M., B. R. NEWCOMER, D. E. LARSON-MEYER, R. L. WEINSIER, and G. R. HUNTER. Evaluation of the strength-size relationship in vivousing various muscle size indices. Med. Sci. Sports Exerc.,Vol. 32, No. 7, pp. 1307–1313, 2000.

REINALDO FIGUEROA-COLON, GARY R. HUNTER, MATTHEW S. MAYO, RUBY A. ALDRIDGE, MICHAEL I. GORAN, and ROLAND L. WEINSIER. Reliability of treadmill measures and criteria to determine O2maxin prepubertal girls. Med. Sci. Sports Exerc.,Vol. 32, No. 4, pp. 865–869, 2000.

The reliability, relation to whole‐body maximal oxygen uptake (VO2max), and force‐level sensitivity of 31P MRS markers of mitochondrial function were studied in 39 normal‐weight women. Following 90 s isometric plantar‐flexion exercises at 45, 70 and 100% of maximum voluntary contraction, skeletal muscle mitochondrial function was determined from the phosphocreatine recovery time constant (TCPCr), the ADP recovery time constant (TCADP), and the rate of change in PCr during the first 14 s of recovery (OxPhos). VO2maxwas measured on a treadmill. Test–retest measurements were obtained in a subset of seven women. Overall, TCPCr, TCADPand OxPhos were reproducible for all exercises (coefficients of variation = 2.3–19.3%). With increasing force‐level, TCPCrwas prolonged (29.0 ± 8.2, 31.9 ± 9.0 and 35.4 ± 9.5 s), OxPhos was increased (0.159 ± 0.081, 0.247 ± 0.090 and 0.310 ± 0.114), and TCADPwas shortened (22.4 ± 7.9, 21.3 ± 6.2, and 19.5 ± 6.7; p< 0.01). All MRS markers of mitochondrial function were correlated with VO2max(r= 0.41–0.72; p< 0.05). These results suggest that measurements of TCPCr, TCADPand OxPhos yield reproducible results that correlate with whole‐body VO2maxand that vary in force‐level sensitivity. Copyright © 2000 John Wiley & Sons, Ltd.

The reliability, relation to whole-body maximal oxygen uptake (VO2max), and force-level sensitivity of ³¹P MRS markers of mitochondrial function were studied in 39 normal-weight women. Following 90 s isometric plantar-flexion exercises at 45, 70 and 100% of maximum voluntary contraction, skeletal muscle mitochondrial function was determined from the phosphocreatine recovery time constant (TCPCr), the ADP recovery time constant (TCADP), and the rate of change in PCr during the first 14 s of recovery (OxPhos). VO2max was measured on a treadmill. Test–retest measurements were obtained in a subset of seven women. Overall, TCPCr, TCADP and OxPhos were reproducible for all exercises (coefficients of variation = 2.3–19.3%). With increasing force-level, TCPCr was prolonged (29.0 ± 8.2, 31.9 ± 9.0 and 35.4 ± 9.5 s), OxPhos was increased (0.159 ± 0.081, 0.247 ± 0.090 and 0.310 ± 0.114), and TCADP was shortened (22.4 ± 7.9, 21.3 ± 6.2, and 19.5 ± 6.7; p &lt; 0.01). All MRS markers of mitochondrial function were correlated with VO2max (r = 0.41–0.72; p &lt; 0.05). These results suggest that measurements of TCPCr, TCADP and OxPhos yield reproducible results that correlate with whole-body VO2max and that vary in force-level sensitivity. Copyright © 2000 John Wiley & Sons, Ltd.

Obesity is associated with increased bile stasis and cholesterol saturation, and an increased risk of gallstone development. Conversely, bile composition is normalized following reduction in body weight. It would appear advantageous to promote weight loss in obesity, which would reduce the predisposition to gallstone formation. Despite the potential health benefits of weight reduction, very‐low‐calorie diets appear to increase the risk for cholesterol crystal and gallstone formation. The incidence of gallstone formation seems to be dependent on the degree of caloric restriction, the rate of weight loss, and the duration of the dietary intervention. Thus, faster rates of weight loss for longer periods of time are associated with increased risk. Available data obtained from prospective studies of subjects during active weight loss suggest that newly formed gallstones occur within 4 weeks and with incidence rates 15 to 25‐fold higher than in the general obese population. The stones produce symptoms in approximately one‐third of the subjects, of whom approximately one‐half will undergo surgery. Proposed mechanisms underlying gallstone formation during weight reduction include bile stasis due to reduced caloric intake, increased biliary cholesterol saturation secondary to increased cholesterol mobilization, and increased nucleation due to changes in bile arachidonate and givcoprotein concentrations. Data are lacking on the effects of gradual rates of weight loss and risk of gallstone formation.

This study examined the effect of weight loss (separate from energy restriction) and weight maintenance/rebound over time on blood pressure, serum lipids, and body composition in 24 obese (mean 137% ideal body weight (IEW)) females with mild to moderate hypertension. Weight loss was induced under tightly controlled General Clinical Research Center conditions until each subject had lost at least 10 kg (mean 13 kg) and attained normal body weight (<120% IBW). After 4 years subjects returned for repeat evaluation. Weight changes were compared with 24 pair‐matched normal weight controls who were also followed for 4 years. With weight loss, significant improvements were seen in standing mean arterial pressure (MAP), serum total cholesterol, low‐density lipoprotein cholesterol, and triglycerides. Subjects regained 11 kg (87% of the weight lost) over the 4 year follow‐up period while control subjects gained only 2 kg. Subjects who chose self‐selected exercise gained less weight than nonexercisers (6 kg vs. 13 kg, P<0.05). With weight regain there were significant increases in standing and supine MAP, total cholesterol, and high‐density lipoprotein (HDL) cholesterol. The amount of weight regained was significantly correlated with standing MAP (r=0.73), triglycerides (r=0.43), and HDL cholesterol (r=‐0.47). The percentage fat of the weight regained was no greater than that of the weight previously lost. Weight loss, distinct from energy restriction, was associated with improvements in blood pressure and serum lipid levels. The ability to sustain these improvements in the co‐morbidities of obesity was directly related to the persistence and magnitude of weight loss maintenance.

Objective: Satiety plays an important role in weight control. The meaning of fasting hormone levels and satiety feelings, and how post‐absorptive changes after meals high in carbohydrate regulate appetite remains to be demonstrated. Research Methods and Procedures: Prospective metabolic study with 25 non‐diabetic obese women at the Energy Metabolism Research Unit of the Department of Nutrition Sciences, University of Alabama at Birmingham. We analyzed fasting and postprandial ratings of hunger‐satiety and values of various metabolic parameters (serum glucose and insulin, plasma cholecystokinin, respiratory quotient) during controlled weight loss. The postprandial measures were assessed following a test meal providing 320 kcal and yielding a food quotient of 0.89. Results: In the fasting state, there was no correlation between hunger‐satiety ratings and any of the measured metabolic parameters. Under postprandial conditions, satiety was positively related to glucose (p = 0.002) and insulin (p = 0.002) responses to the test meal. In multivariate analysis including glucose, insulin, cholecystokinin, hunger‐satiety ratings and respiratory quotient, insulin was the only independent predictor of satiety in the postprandial state. Discussion: These data suggest an association between the endogenous insulin response and feelings of postprandial satiety. Insulin's satiation properties, which could well be mediated by other hormones, may represent a primary factor of food intake regulation after meals relatively high in carbohydrate.

Objective: Regulation of growth and development, clinical assessment, and obesity are among the areas of nutritionrelated research, wherein accurate assessment of body composition is important. We want to test the hypothesis that dual‐energy X‐ray absorptiometry (DXA) measurements are reproducible in healthy girls. Research Methods and Procedures: We determined total body composition measurements in healthy prepubertal girls using DXA twice, 6 weeks apart. Results: We studied 61 healthy, normal‐weight, prepubertal girls, aged 4.8 years to 10.3 years. The girls' DXA‐derived mean weight between visits 1 and 2 significantly increased (27.14 kg vs. 27.80 kg, P<0.0001). The increased weight was due to significant increases in total body fat‐free mass (FFM) (19.53 kg vs. 19.89 kg,P

Objective: This study was designed to determine if serum leptin concentrations (adjusted for fat mass) after weight loss on a low‐calorie diet predict subsequent weight gain. Research Methods and Procedures: Body composition and serum leptin concentrations were determined on 14 moderately obese, postmenopausal, nondiabetic women with a familial predisposition to obesity. Assessments were obtained under tightly controlled metabolic ward conditions of macronutrient intake and weight maintenance both before (obese state) and after a mean weight loss of 12.0 kg to normal body weight (postobese state). Four years later, without intervention, body weight and body composition were reassessed. Results: Weight loss resulted in significant decreases in fat mass (29.7 ± 5.4 vs. 20.3 ± 4.7; kg), body mass index (27.7 ± 1.6 vs. 23.0 ± 1.5; kg/m2), percent body fat (40.7 ± 4.3 vs. 33.1 ± 5.0), and serum leptin concentrations (31.8 ± 16.0 vs. 11.5 ± 5.4; ng/mL). Serum leptin concentrations were positively correlated (p<<0.05) with fat mass in both the obese and postobese states (r= 0.67 and r= 0.56, respectively). However, residual serum leptin concentrations (adjusted for fat mass) in the obese and postobese states were not related to changes in body weight (p<= 0.61 and 0.52), fat mass (p= 0.72 and 0.42), body mass index (p= 0.59 and 0.33), or percent body fat (p= 0.84 and 0.46) over the follow‐up period. Discussion: These finding do not support the hypothesis that relatively low concentrations of leptin predict weight regain after weight loss. However, because the number of subjects in this study was limited, further studies are warranted.

The literature regarding the association of personality with obesity has been generally confusing and contradictory with very different pictures of the obese person emerging. An alternative to identifying either personality types or personality traits associated with the condition is to construct a typology of obese individuals. Rather than seeking the “obesity personality”, the method utilized in the current research sought to differentiate the obese population of an outpatient weight-control clinic into distinct subgroups. For purposes of this study, the Eating Disorder Inventory (EDI) was employed as the measure of personality. The typing procedure using the eight EDI factor scores yielded four distinct subgroups: normal obese, normal/drive-for-thinness group, normal/perfectionist group, and distressed/bulimic group. Issues regarding treatment format, treatment needs, and treatment outcome are discussed.