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Strength Exercise Improves Muscle Mass and Hepatic Insulin Sensitivity in Obese Youth


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Medicine & Science in Sports & Exercise: November 2010 - Volume 42 - Issue 11 - p 1973-1980
doi: 10.1249/MSS.0b013e3181df16d9
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Physical activity is a primary intervention in the combat against obesity and obesity-related disorders in children and adolescents. According to the American Academy of Pediatrics, both aerobic (running, biking, and swimming) and resistance exercise (strength training) should be part of a multifaceted approach to stimulate exercise and improve fitness in children and adolescents (23).

We and others have demonstrated positive effects of aerobic exercise programs on abdominal fat distribution, hepatic fat content, and peripheral as well as hepatic insulin sensitivity in children and adolescents (12,13,27,41,42). In contrast, there are only limited data on the effect of programs containing resistance training alone or in combination with a diet intervention on body composition and insulin sensitivity in children and adolescents (4,8,24,32,39). Increased strength and lean body mass (LBM; muscle mass) were observed in three of these studies (24,32,39), while one (32) reported improved insulin sensitivity. Studies in adults have demonstrated increased strength (6,15,16), muscle mass (6,15), and insulin sensitivity (6,15,16) in response to resistance exercise programs.

There is no published information on the effect of a resistance exercise program on hepatic and intramyocellular fat contents or on glucose and lipid metabolism in adolescents. Neither has peripheral and hepatic insulin sensitivity (representing different mechanisms to maintain glucose homeostasis) been determined separately in response to resistance training.

Resistance exercise might be an attractive alternative to aerobic training for obese individuals because of its lower aerobic intensity and the positive feedback from the visible strength gain. Studies investigating the effects of resistance exercise programs on metabolic and body composition parameters are crucial in designing strategies that provide various intervention options to prevent obesity-related disease.

The aim of the present study was to determine the effect of a controlled resistance exercise program alone, without additional dietary intervention or weight loss, on body composition; abdominal, hepatic, and intramyocellular fat contents; peripheral and hepatic insulin sensitivity; and glucose and lipid metabolism in obese adolescents. We focused on sedentary obese Hispanics because of their high risk of obesity-related illnesses (25,29,31).

We hypothesized that, in these adolescents, a 12-wk resistance exercise program would increase LBM; reduce visceral, hepatic, and intramyocellular fat accumulation (IMCL); and improve peripheral and hepatic insulin sensitivity.



After approval of the protocol by the Baylor College of Medicine Institutional Review Board for Human Subject Research and the General Clinical Research Center Advisory Board, obese adolescents were recruited by local advertisement. Adolescents were screened and enrolled in the study after written assent from the adolescents and consent from the legal guardian were obtained.

Twelve postpubertal (Tanner IV = 2 and Tanner V = 10) obese Hispanic adolescents (six males and six females, age = 15.5 ± 0.5 yr) were studied (Table 1). All participants had BMI >95th percentile for age (20). Participants had been obese for ≥5 yr and reported stable body weight for at least 6 months. Only sedentary adolescents were included, i.e., they did not participate in any school or after-school organized athletic activities and performed <45 min of light to moderate physical activity per week (by self-report).

Body composition and fat distribution at baseline and postexercise (mean ± SE).

All participants were Hispanic (parents and grandparents of Hispanic descent by self-report). They were in good health as determined by a medical history, a physical examination, and a standard blood chemistry analysis including blood lipids, liver and kidney function tests, hemoglobin, hematocrit, hemoglobin A1c, and fasting and 2-h postprandial glucose response. Participants were taking no medications including birth control pills and had no first-degree relatives with diabetes. Adolescents with morbid obesity (% body fat > 50%, sleep apnea, pickwickian syndrome, or cor pulmonale) were excluded.

Study design.

Each participant was studied on two occasions: 1) the weekend before start of the exercise program (baseline) and 2) 3 d after the final exercise session of the 12-wk program (postexercise). All procedures were identical on both study occasions.

To exclude effects of dietary intake on measurements obtained at baseline versus postexercise, before both studies, each participant received an identical 7-d low-CHO/high-fat diet at home (30% CHO, 55% fat, and 15% protein; 20% of the total CHO content as fructose) (33,34,40-42). Total energy intake was calculated to correspond to each individual's requirement according to the Institute of Medicine Dietary Reference Intakes (30). We have previously shown that estimating energy requirements on the basis of these criteria results in accurate energy balance (33,34,40). A pack-out strategy with return and examination of nonconsumed food was used (33,34,40). To determine the effect of exercise alone, participants were told not to make lifestyle changes and keep to their habitual diet except adhere to the controlled diet provided the week before both study occasions.

On both occasions, the participants were admitted to the General Clinical Research Center at Texas Children's Hospital (Houston, TX) in the evening before the metabolic study. After dinner and a snack, participants were fasted overnight (except for water), i.e., from 2000 h until completion of the isotope infusion study at 1300 h the next day. Subsequently, the participants were transferred to the radiology department at Texas Children's Hospital for magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) of abdominal, hepatic, and intramyocellular fat contents.

Resistance exercise program.

For the duration of 12 wk, participants came to the Physiotherapy Unit at Texas Children's Hospital twice a week for a 1-h resistance exercise session. The program was based on the guidelines of the American College of Sport Medicine (1). Briefly, during weeks 1 and 2, the program starts with resistance (weights) corresponding to ∼50% of three repetitions max (3R max) with two to three sets of 8-12 repetitions. The weights and repetitions are then increased gradually according to each individual's ability reaching ∼80%-85% of 3R max with three sets of 15-20 repetitions during weeks 9-12.

The 1-h session included 10 min of warm-up, 40 min of resistance training, and 10 min of cool down. There was at least 1 d of rest between sessions. All major muscle groups were trained during each exercise session using one of the alternative exercises for each muscle group outlined in Table 2. During the exercise program, first the number of repetitions and, subsequently, resistance (weight) was increased.

Resistance exercises.

We present the result of the program as the dynamic strength gain by comparing sets × repetitions and (strength) weights for corresponding exercises at the start and completion of the program. Specifically, we evaluated strength improvements in chest, triceps, biceps, quadriceps, and hamstring muscles (Table 3). Quadriceps strength gain was evaluated using a Biodex isokinetic dynamometer (Shirley, NY) at a velocity of 180°·s−1 as described by Wiggin et al. (44). All exercise sessions were supervised by trained exercise physiologists. Participants performed no exercise outside the program. Their weight was assessed twice a week in conjunction with the exercise sessions to ensure that no weight loss occurred. The purpose of the study was to determine the acute effects of the exercise program and not the acute effect of an exercise session. Therefore, the last exercise session took place 3 d before the metabolic and MRI/MRS measurements.

Strength improvements in response to the exercise program (mean ± SE).


Deuterium oxide (99% 2H), [2H5]glycerol (99% [2H], 95% [2H5]), [1-13C]glucose (99% [13C]), and [6,6-2H2]glucose (99% [2H], 98% [2H2]) were purchased from Cambridge Isotope Laboratories (Andover, MA). The isotopes were tested for sterility and pyrogenicity by the investigation pharmacy at Texas Children's Hospital. The infusates were filtered through a Millex GP syringe filter (0.22 μm; Millipore Corporation, Bedford, MA) and were stored at 4°C for no more than 24-48 h before administration.

Administration of tracers.

On each study occasion, the participants received the following stable isotopically labeled tracers as previously described (33-35).

  1. During the overnight fast at 2100, 2300, 0100, and 0300 h, deuterium oxide (a total of 3 g·kg LBM−1) was administered orally to measure total gluconeogenesis (7).
  2. Between 0600 and 1300 h, a simultaneous, primed (60× the minute infusion rate), constant rate intravenous infusion of [1-13C]glucose (0.33 ± 0 μmol·kg LBM−1·min−1) and [2H5]glycerol (0.14 ± 0 μmol·kg LBM−1·min−1) was administered to measure glucose production and the plasma turnover of glycerol, an indicator of lipolysis (33-35).
  3. The stable-label intravenous glucose tolerance test (SLIVGTT) was started at 0900 h after the 0-min blood sample (see below). A bolus injection of glucose, 0.35 ± 0 g·kg LBM−1 containing 10% [6,6-2H2]glucose, was administered for 90-120 s to measure insulin sensitivity (33-35).

Blood sampling.

Blood samples were obtained just before start of the primed constant rate infusion of the [1-13C]glucose and [2H5]glycerol (designated as t = −180; 13 mL) and, subsequently, at t = −30, −20, −10, and 0 min (8 mL per sample). The injection of the SLIVGTT bolus (after the 0-min sample) was followed by blood sampling (3.6 mL per sample) at +2, 3, 4, 5, 8, 10, 18, 20, 23, 28, 32, 40, 60, 120, 180, and 240 min (33-35).


Plasma concentrations of glucose, insulin, lipids, leptin, adiponectin, and high sensitive C-reactive protein (hs-CRP) were measured as previously described (41). Nonbone LBM and fat mass (FM) were measured by dual-energy x-ray absorptiometry (QDR 11.2; Hologic, Bedford, MA) (33,34,40).

Abdominal, hepatic, and intramyocellular fat contents were measured by MRI and MRS using a Philips Achieva 1.5-T whole-body clinical scanner software release 1.5 (Philips Healthcare, Best, The Netherlands) as previously described in detail (33,40,42). The MR image of abdominal fat, i.e., visceral (intra-abdominal) and subcutaneous (peripheral) fat content was acquired in a single transversal slice at the level of the umbilicus (33,40,42). MRI data are expressed as cross-sectional area (cm2).

A PRESS single-voxel technique was used to obtain the liver MR spectra as previously described in detail (42). Data were analyzed using the scanner software, and results are expressed as total lipid/water peak area ratio (%). Hepatic fat was considered normal if the MRS lipid peak/water peak was <5.6% and high if the MRS lipid peak/water peak was >5.6% (37).

A PRESS chemical shift imaging technique was used for measuring IMCL in the soleus muscle (42). Data were analyzed using jMRUI v3.0 (26) with the AMARES algorithm to obtain the peak areas as described by Szczepaniak et al. (36). IMCL is expressed as the relationship between the areas of the IMCL and water peaks, respectively (%).


Rates of glucose production and glycerol turnover (an indicator of lipolysis) were calculated under approximate steady-state conditions from the average isotopic enrichments obtained for [13C1]glucose and [2H5]glycerol, respectively, in the samples obtained at −30, −20, −10, and 0 min (33-35).

During the same period, the gluconeogenic contribution to glucose was determined using 2H2O and the average 2H enrichments of carbons 1, 3, 4, 5, and 6 of glucose (7).

Peripheral insulin sensitivity (the sensitivity of glucose disposition to insulin) was calculated by applying the minimal model to SLIVGTT data (2,33-35).

Hepatic insulin sensitivity was calculated in the fasting state by the hepatic insulin sensitivity index: 1000/[GPR (µmol·kg−1 LBM·min−1) × fasting plasma insulin (μU·mL−1)], where 1000 is a constant that results in numbers between 1 and 10, as described by Matsuda and DeFronzo (22).

Statistical methods.

Power calculations were based on data from our previous study on the effects of an aerobic exercise program (41,42). Thus, 12 subjects would be sufficient to detect changes of the same magnitude as those found in response to the aerobic exercise program with a power of 0.8 and a type 2 error of 0.05. Data are presented as mean ± SE. Differences between values obtained on the two study occasions were tested by paired t-test. Generalized estimating equations (SPSS 17.0, Chicago, IL) were used to assess the effects of gender and the interaction between the effect of the exercise program and gender. Correlation analysis was used to test potential relationships between measures of insulin sensitivity (hepatic and peripheral) and body fat distribution (visceral, hepatic, and IMCL). A P < 0.05 was considered statistically significant.


Exercise Compliance and Strength Improvement

The participants completed 96% ± 1% of the total 24 exercise sessions (range = 22-24 exercises). Strength increased for upper body muscles (represented by biceps, triceps, and chest) as well as lower body muscles (represented by quadriceps and hamstrings; Table 3).

Peak torque measures (N·m) were performed in the leg extensor muscles at 180° using a Biodex instrument (data were available for nine subjects). As shown in Table 3, peak torque increased for both legs. Muscle mass in the left and right legs was obtained by DXA, and the peak torque per gram of leg muscle was calculated before and after exercise as a surrogate measure of muscle quality. Peak torque per gram of leg muscle in the right leg increased from 0.0093 to 0.0115 N·mg−1 (P = 0.008) and that in the left leg increased from 0.0108 to 0.0119 N·mg−1 (P = 0.06), indicating that, at least in the leg muscle, not only strength and muscle mass but also muscle quality increased.

Energy Intake

Average daily energy intakes during the 7-d prestudy diet period were not different at baseline (2911 ± 170 kcal·d−1) and after exercise (2853 ± 158 kcal·d−1). The macronutrient distribution of the intake corresponded to the designed (31% ± 1% CHO, 54% ± 1% fat, and 15% ± 1% protein) on both study occasions.

Effect of Resistance Exercise on Body Composition

Total body composition (dual-energy x-ray absorptiometry).

Total body weight increased (P < 0.01; Table 1). This increase was primarily accounted for (∼80%) by an increase in LBM (2.1 ± 0.5 kg, P < 0.01), whereas total body FM did not change. Bone mineral density was slightly higher postexercise (0.015 g·cm−2, i.e., 1.4%, P < 0.01; Table 1). There was no difference between males and females. Our data for both boys and girls were all within the 97th to 3rd percentile (7/12 were close to the 50th percentile) reported in Mexican males and females of corresponding age (21).

Abdominal fat distribution (MRI).

Visceral fat content did not change significantly, whereas a minor increase (5% ± 2%, P < 0.05) in subcutaneous fat was observed.

Hepatic fat content (MRS)

This did not change significantly. Of 12 adolescents, 7 (58%) had high liver fat content (lipid peak/water peak > 5.6%) (37). In these seven participants, hepatic fat content averaged 13.9% ± 4.3% at baseline and 14.2% ± 4.5% postexercise (NS). In the five participants with a lipid/water peak < 5.6%, hepatic fat content was 2.7% ± 0.7% at baseline and 2.7% ± 0.9% postexercise (NS).

Intramyocellular fat content (MRS).

This did not change significantly.

Effect of Resistance Exercise on Insulin Sensitivity, Glucose, and Lipid Metabolism.

Fasting glucose and insulin concentrations

Fasting glucose and insulin concentrations did not change (Table 4).

Biochemical measurements at baseline and postexercise (mean ± SE).

Peripheral insulin sensitivity.

The average peripheral insulin sensitivity did not change significantly. In 8/12 adolescents, peripheral insulin sensitivity increased, whereas it decreased to the same extent in 4/12 participants (Fig. 1).

Peripheral insulin sensitivity, calculated by the minimal model applied to SLIVGTT data (SI), and hepatic insulin sensitivity, measured by hepatic insulin sensitivity index (HISI), at baseline and postexercise (mean ± SE). Baseline is depicted by black bars, postexercise by gray bars. Different from baseline: *P < 0.05, **P < 0.01.

Hepatic insulin sensitivity.

Hepatic insulin sensitivity increased by 24% ± 9% (P < 0.05; Fig. 1).

Neither peripheral nor hepatic insulin sensitivity was significantly correlated with visceral, hepatic, or intramyocellular fat content.

Glucose production from gluconeogenesis and glycogenolysis.

GPR decreased by 8% ± 1% (P < 0.01) accounted for by a 12% ± 5% decrease in glycogenolysis (P < 0.05). Gluconeogenesis remained unchanged (Fig. 2).

GPR, consisting of gluconeogenesis (GNG; solid part of the bar) and glycogenolysis (GLY; hatched part of the bar), at baseline (black bars) and postexercise (gray bars; mean ± SE). Significant differences in GPR are depicted above the bars. Significant difference in GLY is depicted inside the bar. Different from baseline: *P < 0.05, **P < 0.01.


The exercise program did not have any effect on total glycerol Ra (baseline: 225 ± 15 μmol·min−1; postexercise: 248 ± 24 μmol·min−1) or blood lipids (Table 4).

Effect of Resistance Exercise on Adiponectin, Leptin, and Hs-CRP

Concentrations of leptin, adiponectin, and hs-CRP did not change (Table 4). For comparison, baseline values previously published in lean adolescents of the same age and Tanner stage are included in Table 4 (41).

Effect of Gender

The females had lower weight, height, and LBM (all P < 0.05) than the males, although their fat percent and leptin concentrations were higher (both P < 0.05). No other variable differed between genders at baseline. Except for a greater increase in LBM in the males, effects of the exercise program did not differ between genders.


The results of the present study demonstrate that this 12-wk controlled resistance exercise program increased strength, LBM, and hepatic insulin sensitivity and slightly reduced glucose production in obese Hispanic adolescents. In contrast, the program had no effect on total body, visceral, hepatic, and intramyocellular fat or peripheral insulin sensitivity.

Although increased muscle mass and hepatic insulin sensitivity are important results of the resistance exercise program, aerobic exercise seems to have more extensive effects. We demonstrated in a similar group of obese adolescents that the same volume of aerobic exercise significantly reduced total, visceral, and hepatic fat content and increased both peripheral and hepatic insulin sensitivity (41,42). These findings are in agreement with other studies in adults and children (12,13,28,45). In contrast, the effect of resistance exercise is less clear (4,6,8,15,24,32,39). Although most studies reported increased strength and LBM (muscle mass) in response to resistance exercise (6,15,24,32,39), only a few studies found effects on body fat (4,24,32). Similarly, its influence on insulin sensitivity was inconsistent. Some studies reported improved insulin sensitivity (6,15,16,32), whereas others found no metabolic effects of resistance exercise (4,8,39). The methods used in the referenced studies (unlabeled frequent sample intravenous glucose tolerance test (FSIVGTT), unlabeled clamp, oral glucose tolerance test, and homeostatic model assessment-insulin resistance (HOMA-IR)) provide a measure of whole-body (i.e., peripheral + hepatic) insulin sensitivity. Using the SLIVGTT and the Hepatic Insulin Sensitivity Index enabled us to determine peripheral and hepatic insulin sensitivity separately.

The increase in body weight resulting from the exercise program was almost completely explained by the increase in LBM. Theoretically, one would expect that increased LBM (muscle mass), i.e., increased insulin sensitive tissue mass would result in increased insulin sensitivity, primarily peripherally. The increase in LBM resulting from our program might have been insufficient to achieve this effect. Neither LBM at baseline and postexercise nor exercise-induced change in LBM correlated with peripheral or hepatic insulin sensitivity (data not shown). This is in agreement with the referenced studies, where changes in whole-body insulin sensitivity (or lack thereof) were independent of changes in LBM (6,15,16,32,39). In addition, muscular strength alone has been shown to be a positive predictor for insulin sensitivity (5). It has been suggested that resistance training might increase insulin sensitivity as a result of qualitative changes within the muscle (6,15). Brooks et al. (6) and Holten et al. (15) conducted muscle biopsies in adults with type 2 diabetes participating in a whole-body (6) or one-leg resistance exercise program (15). Brooks et al. (6) demonstrated increased muscle quality (strength/unit of muscle mass) and increased areas of type I and type II fibers. The increase in type I fiber area correlated significantly with the decrease in insulin resistance. Holten et al. (15) showed increased insulin activity and Glut 4 protein but no effect on markers of oxidative capacity in skeletal muscle. Because muscle biopsies cannot be performed in healthy children and adolescents for ethical reasons, we were not able to pursue potential cellular mechanisms. We did calculate peak torque per gram of leg muscle from the DXA and Biodex analyses as a surrogate measure of muscle quality. We found an increase in this value for the right leg and a value that approached significance (P = 0.06) for the left. These values did not correlate with insulin sensitivity.

A failure to increase lipid oxidation during fasting might lead to intramyocellular fat deposition in obese individuals, subsequently contributing to patterns of insulin resistance (17). Exercise could potentially improve fat oxidation, which might lead to reduced intramyocellular fat content. Indeed, Koopman et al. (19) demonstrated a decrease in intramyocellular fat directly after a resistance exercise session. However, 120 min after the exercise session, the inramyocellular fat content had returned to preexercise levels, indicating only a short-term effect (19). To our knowledge, there are no published data on the effects of a resistance exercise program on intramyocellular fat content. We measured intramyocellular fat at baseline and after the exercise program using MRS but found no changes.

Resistance exercise significantly increased fasting hepatic insulin sensitivity. The mechanism for this effect is not clear. Hepatic fat content measured by MRS did not change in response to the program and did not correlate with hepatic insulin sensitivity. Thus, the improvements in hepatic insulin sensitivity could not be explained by any reduction in hepatic fat accumulation. This finding indicates that liver lipid content is not a reliable predictor of hepatic insulin resistance. Heled et al. (14) reported that aerobic exercise training (treadmill) increased hepatic insulin sensitivity because of the ameliorated insulin signaling response and inhibited phosphoenolpyrurate carboxykinase (PEPCK) activity in the hepatocyte of diabetes-prone fat sand rats. Because we could not perform liver biopsies in our healthy adolescents, hepatocellular mechanisms could not be investigated. Although none of the more metabolically active fat deposits (visceral, hepatic, and intramyocellular) changed in response to our resistance exercise program, we observed a small increase in subcutaneous abdominal fat. This finding might be of importance. It has been speculated that defective differentiation of subcutaneous fat might lead to defective fat storage in this compartment with subsequent overflow of fat into visceral, hepatic, and intramyocellular fat deposits (9,38). Increased subcutaneous abdominal fat without changes in visceral fat was also reported by Treuth et al. (39) in response to a 5-month resistance exercise program in prepubertal girls.

Our study population consists of Hispanic adolescents; thus, the studies by Davis et al. (8), Shaibi et al. (32), and Ventura et al. (43) in a similar population are of particular interest. In a first study, overweight adolescent Latino boys performed a resistance exercise program, two times at 1 h·wk−1 for 16 wk (32). Insulin sensitivity increased by 45%. LBM also increased and body fat percent (but not FM) decreased. In a later study, overweight adolescent Latino boys and girls were subjected to the same resistance exercise program with an additional diet component aiming at reducing sugar and increasing fiber intake (8). Surprisingly, in that study, insulin sensitivity and body composition were completely unaffected. The investigators speculated that the diet intervention might have canceled out the effect of the exercise. However, a post hoc analysis of the response to the diet intervention showed no difference among a control group, a diet-alone group, and the diet + strength training group (43).

A weakness of our study might be that we did not include a nonexercising control group. However, it would be ethically questionable to subject healthy adolescents to comparatively invasive metabolic studies without any intervention. Muscle mass and strength increases until adulthood (3). Because our participants were postpubertal and, thus, had passed their growth peak, it is unlikely that growth and maturation explain the increase in strength and muscle mass that was observed during the relatively short 12-wk exercise program. For the same reason, pubertal effects on insulin sensitivity are very unlikely.

Resistance exercise resulted in a small decrease (8%) in glucose production due to a decrease (12%) in glycogenolysis, whereas gluconeogenesis remained unchanged. Most likely, the decrease in glucose production has limited clinical relevance in our normoglycemic adolescents with normal glucose tolerance. However, in diabetic adolescents, increased glucose production might result in hyperglycemia (10). Thus, one might speculate that in these individuals, resistance exercise could be a tool to reduce glucose production and, subsequently, hyperglycemia. The association between decreased glycogenolysis and increased hepatic insulin sensitivity confirms that glycogenolysis is more sensitive to insulin than gluconeogenesis, as suggested by Gastaldelli et al. (11).

Baseline leptin and hs-CRP concentrations were significantly higher compared with a previously studied group of lean adolescents of the same age (41). The higher CRP concentrations indicate a low-grade whole-body inflammation in obese adolescents. Data regarding the effect of resistance exercise on adiponectin, leptin, and hs-CRP concentrations are limited (6,18). Brooks et al. (6) found that adiponectin increased and CRP decreased in response to resistance exercise, whereas Klimcakova et al. (18) reported unchanged adiponectin and hs-CRP but decreased leptin concentration. We observed no exercise-induced changes in these parameters.

In conclusion, resistance exercise might be an attractive alternative to aerobic exercise for obese adolescents. Increased strength, LBM, and hepatic insulin sensitivity are important findings. However, the more comprehensive effects of aerobic exercise involving metabolic parameters, body composition, and body fat distribution might have a greater potential to prevent obesity-related illnesses (41,42). Thus, a program combining resistance and aerobic exercise might be a viable strategy to achieve the positive effects of both types of exercise.

This work is a publication of the US Department of Agriculture/Agricultural Research Service, Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX. The contents of this publication do not necessarily reflect the views or policies of the US Department of Agriculture nor does mention of trade names, commercial products, or organizations imply endorsement from the US government.

The study was supported by National Institute of Child Health and Human Development grant RO1 HD044609, by Baylor General Clinical Research Center grant MO1-RR-00188-34, and US Department of Agriculture Cooperative Agreement 6250-51000-046.

The authors have nothing to disclose.

The results of the present study do not constitute endorsement by the American College of Sports Medicine.

The authors thank all research participants for their time and commitment; Dr. Morey Haymond, Dr. Luisa Rodriguez, research nurses Amy Pontius, Cindy Bryant, Linda Peasant, and Shawn Asphall, research coordinator Janette Gonzalez, dietitian Ann McMeans, exercise physiologists Tomas Green, Cynthia Newberry, Ashley Albright, Veronica Victorian, and Jennifer Watts, and the General Clinical Research Center staff at Texas Children's Hospital for their invaluable help in conducting these studies. The authors thank Susan Sharma, Marcia Ekworomadu, Shaji Chacko, and Dan Donaldson for excellent technical assistance.


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