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Biomedical subjects

J N Roemmich

Publications and source records attributed to J N Roemmich.

At least 19 recordsLinked to original sources
PubMed2006

Relationship between sex of parent and child on weight loss and maintenance in a family-based obesity treatment program.

OBJECTIVE: To determine if the sex of the participating parent/child pair is a contributing factor in initial weight loss and maintenance within a family-based obesity treatment program. DESIGN: A 2-year family-based obesity treatment program targeting one overweight parent and one overweight child. SUBJECTS: One overweight parent (body mass index (BMI) > or = 25) and child (> or = 85th BMI percentile) from 164 families. MEASUREMENTS: Parameters of body weight, including height, weight, BMI, z-BMI, percent overweight (BOV) at baseline and at 6-, 12- and 24-month follow-up time points. RESULTS: Children within the opposite-sex dyads had greater weight loss (P < 0.01) at 6- and 12-month time points compared with children in the same-sex dyads. Parents within opposite-sex dyads had significantly greater weight loss at 24 months (P < 0.05) compared with those in the same-sex dyads. When individual dyads were examined, the change in child z-BMI after 6 months was greater for the mother-son dyad as compared to the mother-daughter and father-son (P < 0.05). For parent z-BMI, the mother-daughter dyad consistently exhibited the poorest results. At 6- and 12-month time points, parents in the mother-daughter dyad lost significantly less weight than parents in all other dyads (P < 0.05), and at 24 months, parents in the mother-daughter dyad lost less weight than parents in the opposite-sex dyads (P < 0.05). CONCLUSION: These data reveal that child-parent sex interactions can strongly influence the outcome of obesity treatment when both parent and child are the target for weight loss. The reasons that underlie this effect remain to be determined.

Adult↗
PubMed2002

Pubertal alterations in growth and body composition. VI. Pubertal insulin resistance: relation to adiposity, body fat distribution and hormone release.

OBJECTIVE: To investigate the independent influence of alterations in fat mass, body fat distribution and hormone release on pubertal increases in fasting serum insulin concentrations and on insulin resistance assessed by the homeostasis model (HOMA). DESIGN AND SUBJECTS: Cross-sectional investigation of pre- (n=11, n=8), mid- (n=10, n=11), and late-pubertal (n=10, n=11) boys and girls with normal body weight and growth velocity. MEASUREMENTS: Body composition (by a four-compartment model), abdominal fat distribution and mid-thigh interfascicular plus intermuscle (extramyocellular) fat (by magnetic resonance imaging), total body subcutaneous fat (by skinfolds), mean nocturnal growth hormone (GH) release and 06:00 h samples of serum insulin, sex steroids, leptin and insulin-like growth factor-I (IGF-I). RESULTS: Pubertal insulin resistance was suggested by greater (P<0.001) fasting serum insulin concentrations in the late-pubertal than pre- and mid-pubertal groups while serum glucose concentrations were unchanged and greater (P<0.001) HOMA values in late-pubertal than pre- and mid-pubertal youth. From univariate correlation fat mass was most related to HOMA (r=0.59, P<0.001). Two hierarchical regression models were developed to predict HOMA. In one approach, subject differences in sex, pubertal maturation, height and weight were held constant by adding these variables as a block in the first step of the model (r(2)=0.36). Sequential addition of fat mass (FM) increased r(2) (r(2)((inc)remental)=0.08, r(2)=0.44, P<0.05) as did the subsequent addition of a block of fat distribution variables (extramyocellular fat, abdominal visceral fat, and sum of skinfolds; r(2)(inc)=0.11, r(2)=0.55, P<0.05). Sequential addition of a block of hormone variables (serum IGF-I and log((10)) leptin concentrations; r(2)(inc)=0.04, P>0.05) did not reliably improve r(2) beyond the physical characteristic and adiposity variables. In a second model, differences in sex and pubertal maturation were again held constant (r(2)=0.25), but body size differences were accounted for using percentage fat data. Sequential addition of percentage body fat (r(2)((inc)remental)=0.11, r(2)=0.36, P<0.05), then a block of fat distribution variables (percentage extramyocellular fat, percentage abdominal visceral fat, and percentage abdominal subcutaneous fat; r(2)(inc)=0.08, r(2)=0.44, P=0.058), and then a block of serum IGF-I and log((10)) leptin concentrations (r(2)(inc)=0.07, r(2)=0.51, P<0.05) increased r(2). Mean nocturnal GH release was not related to HOMA (r=-0.04, P=0.75) and therefore was not included in the hierarchical regression models. CONCLUSION: Increases in insulin resistance at puberty were most related to FM. Accumulation of fat in the abdominal visceral, subcutaneous and muscular compartments may increase insulin resistance at puberty beyond that due to total body fat. Serum concentrations of leptin and IGF-I may further modulate HOMA beyond the effects of adiposity and fat distribution. However, the results are limited by the cross-sectional design and the use of HOMA rather than a criterion measure of insulin resistance.

Adipose Tissue↗
PubMed2001

Consequences of sport training during puberty.

Growth at puberty depends on one's genetic potential, nutritional status and a series of hormones. Energy expenditure may modify the effects of these three factors on the linear growth rate and the relative proportions of fat-free and fat mass. Participation in sports where weight control is not required does not seem to affect pubertal timing or alter linear growth rate. The growth and maturation of athletes in weight control sports have the additional burden of energy output greater than intake; however, in only a minority the energy deficit is great enough to slow growth and maturation. Studies focusing on male wrestlers and female gymnasts are reviewed. In the wrestlers the hormonal picture is consistent with mild-to-moderate GH resistance and perhaps mild maturational delay, especially in the lower weight classes. The deficits in lean body mass and fat mass "catch-up" quickly following the end of training and competitive season. The situation with the gymnasts is somewhat different, the goal being to develop muscular strength within a shorter and lighter physique. Marked under-nutrition can keep these adolescents pre-pubertal for many years of training and competition. Whether subsequent growth is disproportionate or not remains indeterminate, but the marked delay in the onset of estrogen action can permanently cause the skeleton to be under-mineralized. In conclusion, most athletes continue to track along the centiles of their genetic potential. To define the mechanisms of growth and maturational delay one must longitudinally study children in weight-control sports.

Adolescent↗
PubMed2001

Behavioral therapy in the treatment of pediatric obesity.

This article was designed to make a strong case for the importance of studying behavior and using behavioral therapy in the treatment of pediatric obesity. Behavioral treatments have been the most studied approaches to pediatric obesity, with great success. Six studies that provided long-term results are presented, and ideas for translating behavioral therapy into common pediatric practice are presented. Additional progress is needed to incorporate new findings in learning and behavioral neuroscience into clinical interventions and to integrate behavioral therapy with pharmacologic interventions and genetic predispositions and new advances in nutrition and exercise science.

Behavior Therapy↗
PubMed2001

Alterations in body composition and fat distribution in growth hormone-deficient prepubertal children during growth hormone therapy.

Growth hormone (GH) deficiency in children results in increased body fat, reduced fat-free mass (FFM) including muscle (protein) and bone, and abdominal obesity. Thus, proper GH secretion likely has major developmental influences on later health risks including cardiovascular diseases and osteoporosis. However, the in vivo control of the development of the body composition and fat distribution by GH has not yet been accurately investigated using children with GH deficiency as a model. We determined the effect of GH therapy (GH replacement, n = 3; GH + physiologic cortisol and thyroxine replacement, n = 3) on body composition, the proportional composition of the FFM, and body fat distribution in GH-deficient prepubertal children compared with healthy control children (n = 6) not treated with GH. The GH-deficient and control children were initially matched for gender, bone age, and weight. As assessed by a 4-compartment model, GH therapy reduced percent body fat during the first 3 months of therapy but not thereafter. This change was primarily due to FFM, which increased 3-fold more in the GH-deficient group and accounted for 91.5% of the increase in body weight. Fat mass increased in the controls but was unchanged in the GH-deficient group. Therapy temporarily increased the proportional contribution of water to the FFM, decreased the proportion of mineral, and slightly increased the proportion of protein. Using magnetic resonance imaging (MRI), abdominal visceral fat was reduced in the GH-deficient group and unchanged in the controls. Abdominal subcutaneous fat measured in the same image was not changed. The abdominal and suprailiac skinfold thicknesses also were not decreased in the GH-deficient group. In conclusion, within 1 to 3 months, GH therapy accelerates lean tissue accrual, especially the water and protein components, but has a smaller effect on reducing fat mass. GH therapy has site-specific effects on reducing abdominal adiposity.

Abdomen↗
PubMed2001

Reducing sedentary behavior: role in modifying physical activity.

Decreased physical activity is associated with the increased incidence of obesity. Behavioral economic research demonstrates that reducing sedentary behaviors in children increases physical activity. Understanding how people choose physical or sedentary activities can aid in developing public health initiatives that increase access to physical activity, while reducing access to sedentary behaviors.

Adult↗
PubMed2001

How much activity do youth get? A quantitative review of heart-rate measured activity.

OBJECTIVE: Recommendations for adult physical activity have shifted from 20 to 60 minutes of continuous vigorous activity 3 to 5 times a week to accumulation of 30 minutes of moderate to vigorous physical activity most days of the week. Variations of these guidelines also have been suggested for children, based on the idea of accumulating moderate to vigorous physical activity throughout the day, rather than attaining vigorous physical activity in continuous blocks. The goal of this study was to assess accumulated amounts of physical activity at different intensities in children. METHODS: We reviewed 26 studies (n = 1883) in youth aged 3 to 17 years that used heart-rate recording to measure physical activity in children to determine accumulated daily activity. Included were studies that provided time being active for at least 2 heart rate intensities at or above 120 beats/minute. Descriptive characteristics of the study groups were determined, and the influence of age, gender, and hours and days of observation on the slope of activity time as a function of percentage of heart rate reserve (HRR) was determined using hierarchical linear regression. RESULTS: Youth attained 128.0 +/- 45.6, 47.1 +/- 14.9, 29.3 +/- 13.7, and 14.7 +/- 6.0 minutes/day between 20% to 40%, 40% to 50%, 50% to 60%, and greater than 60% HRR, respectively. Age was a significant predictor of the intercept and slope of the physical activity and %HRR relationship. CONCLUSION: Youth of all ages attain >60 minutes/day of low-intensity physical activity and approximately 30 minutes/day of activity at traditional cardiovascular fitness training levels of 50% or more of HRR. Recommendations for youth activity are discussed.

Activities of Daily Living↗
PubMed2000

Growth and pubertal development in children and adolescents: effects of diet and physical activity.

The longitudinal growth of an individual child is a dynamic statement of the general health of that child. Measurements should be performed often and accurately to detect alterations from physiologic growth. Although any single point on the growth chart is not very informative, when several growth points are plotted over time, it should become apparent whether that individual's growth is average, a variant of the norm, or pathologic. Somatic growth and maturation are influenced by several factors that act independently or in concert to modify an individual's genetic growth potential. Linear growth within the first 2 y of life generally decelerates but then remains relatively constant throughout childhood until the onset of the pubertal growth spurt. Because of the wide variation among individuals in the timing of the pubertal growth spurt, there is a wide range of physiologic variations in normal growth. Nutritional status and heavy exercise training are only 2 of the major influences on the linear growth of children. In the United States, nutritional deficits result from self-induced restriction of energy intake. That single factor, added to the marked energy expenditure of training and competition for some sports, and in concert with the self-selection of certain body types, makes it difficult to identify the individual factors responsible for the slow linear growth of some adolescent athletes, for example, those who partake in gymnastics, dance, or wrestling.

Adolescent↗
PubMed2000

Alterations in growth and body composition during puberty. IV. Energy intake estimated by the youth-adolescent food-frequency questionnaire: validation by the doubly labeled water method.

BACKGROUND: Estimates of energy intake are required for an understanding of growth and disease; however, few methods of energy intake in children have been validated. OBJECTIVE: Our objective was to validate energy intake estimated by the Youth-Adolescent Food-Frequency Questionnaire (YAQ) against the criterion total energy expenditure (TEE) by doubly labeled water (DLW). DESIGN: Twenty-three boys and 27 girls (8.6-16.2 y of age) completed the YAQ and TEE measurements in 1 y. RESULTS: Energy intake by the YAQ (10. 03 +/- 3.12 MJ) and energy expenditure by DLW (9.84 +/- 1.79 MJ) were similar (P: = 0.91) with large lower (-6.30 MJ) and upper (6.67 MJ) +/-2 SD limits of agreement. When within-subject CVs of repeated measures of the DLW and YAQ methods were used, 25 of the 50 subjects were deemed to have misreported their energy intake. The discrepancy in energy intake (YAQ - TEE) was related to body weight (r = -0.25, P: = 0.077) and percentage body fat (r = -0.24, P: = 0.09) but not to age (r = -0.07, P: = 0.63) or the time between measures. From logistic regression, fatter boys were more likely to underreport energy intake than were fatter girls. CONCLUSION: The YAQ provides an accurate estimation of mean energy intake for a group but not for an individual.

Adolescent↗
PubMed2000

Pubertal alterations in growth and body composition. V. Energy expenditure, adiposity, and fat distribution.

We determined whether activity energy expenditure (AEE, from doubly labeled water and indirect calorimetry) or physical activity [7-day physical activity recall (PAR)] was more related to adiposity and the validity of PAR estimated total energy expenditure (TEE(PAR)) in prepubertal and pubertal boys (n = 14 and 15) and girls (n = 13 and 18). AEE, but not physical activity hours, was inversely related to fat mass (FM) after accounting for the fat-free mass, maturation, and age (partial r = -0.35, P < or = 0.01). From forward stepwise regression, pubertal maturation, AEE, and gender predicted FM (r(2) = 0.36). Abdominal visceral fat and subcutaneous fat were not related to AEE or activity hours after partial correlation with FM, maturation, and age. When assuming one metabolic equivalent (MET) equals 1 kcal. kg body wt(-1). h(-1), TEE(PAR) underestimated TEE from doubly labeled water (TEE bias) by 555 kcal/day +/- 2 SD limits of agreement of 913 kcal/day. The measured basal metabolic rate (BMR) was >1 kcal. kg body wt(-1). h(-1) and remained so until 16 yr of age. TEE bias was reduced when setting 1 MET equal to the measured (bias = 60 +/- 51 kcal/day) or predicted (bias = 53 +/- 50 kcal/day) BMR but was not consistent for an individual child (+/- 2 SD limits of agreement of 784 and 764 kcal/day, respectively) or across all maturation groups. After BMR was corrected, TEE bias remained greatest in the prepubertal girls. In conclusion, in children and adolescents, FM is more strongly related to AEE than activity time, and AEE, pubertal maturation, and gender explain 36% of the variance in FM. PAR should not be used to determine TEE of individual children and adolescents in a research setting but may have utility in large population-based pediatric studies, if an appropriate MET value is used to convert physical activity data to TEE data.

Adipose Tissue↗
PubMed2000

Gender and sexual maturation-dependent contrasts in the neuroregulation of growth hormone secretion in prepubertal and late adolescent males and females--a general clinical research center-based study.

Although numerous studies have delineated an impact of gender on the neuroendocrine control of GH secretion in the adult, few investigations have defined the nature and extent of sex differences before puberty. This deficit reflects jointly the sensitivity limitations of earlier GH assays and the paucity of intensive sampling protocols in healthy children. Here we have applied a chemiluminescence-based GH assay (sensitivity, 0.005 microg/L) to study GH release in blood sampled every 10 min for 12 h from 1800-0600 h in 58 healthy children. Males and females were evaluated in prepuberty (n = 17 boys; n = 11 girls) and late adolescence (n = 13 males; n = 17 females). We quantitated the principal regulated facets of GH release by 1) deconvolution analysis to assess basal vs. pulsatile GH secretion, 2) approximate entropy to compute the regularity of GH release patterns, and 3) cosine regression analysis to evaluate the overnight rhythmic release of GH. Gender by maturation analysis of variance revealed a mean 2.3-fold increase in the integrated serum GH concentration between prepuberty and late adolescence (P < 10(-6)). Deconvolution analysis disclosed that 91-97% of total GH secretion was pulsatile. Pulsatile, but not basal, GH release showed marked sexual maturation dependence (P < 10(-5)). Pulsatile GH release rose in adolescents due to a 2.25-fold greater GH secretory burst mass (P = 0.00011), which reflected joint 1.5-fold increases in GH secretory pulse amplitude and duration (P < 0.01). Pulse-mass enhancement across puberty was gender independent, but mechanistically specific, as GH pulse frequency, intersecretory burst interval, and half-life were invariant of pubertal status. The approximate entropy statistic identified more disorderly GH secretion patterns in adolescent females compared with prepubertal children and adolescent males (P = 0.00074). Cosinor analysis unmasked elevated overnight rhythms in GH secretory burst mass and interburst intervals in late adolescents of both genders compared with prepubertal boys (for burst mass) or girls (for interburst intervals). Linear regression analysis disclosed strong correlations among 1) the plasma insulin-like growth factor I concentration and GH secretory burst mass (P < 10(-3)), 2) the GH pulse mass and the serum testosterone concentration (P = 10(-3)), 3) the irregularity (entropy) of GH secretory patterns and the serum estradiol concentration (P < 10(-4)), and 4) the basal GH secretion rate and the serum estradiol concentration (P = 10(-2)). In summary, healthy prepubertal children and late adolescent boys and girls manifest distinctive mechanisms controlling GH release, as appraised for all three of the pulsatile, entropic, and 12-h rhythmic modes of GH neuroregulation. The major maturational contrast in the pulsatile mode of GH secretion is amplified secretory burst mass in adolescents due to jointly heightened GH pulse amplitude and duration. The dominant gender distinction lies in the reduced orderliness of GH release patterns in late adolescent girls. Overnight rhythms in GH secretory burst mass and interburst intervals enlarge in both sexes at adolescence, thus signaling enhanced coupling between the rhythmic and pulsatile control of GH release at this time. At the extrema of pubertal development, sex steroid hormones are associated differentially with specific facets of GH release, e.g. an elevated basal GH secretion rate (estrogen), greater irregularity of GH release patterns (estrogen), and amplified GH secretory burst mass and higher plasma insulin-like growth factor I concentrations (testosterone). Accordingly, we postulate that sex steroids supervise selectively each of the dominant facets of GH neurosecretory control across human puberty.

Adolescent↗
PubMed1999

Role of leptin during childhood growth and development.

Leptin, the product of the ob/ob gene in rodents, regulates energy balance and fertility. Two genetic models, the ob/ob mouse (deletion of leptin protein) and the db/db mouse (deletion of leptin receptor) have markedly augmented research in obesity. Human obesity is more closely linked to leptin resistance than to the absence of leptin. Serum leptin concentrations reflect the size of the subcutaneous fat depot better than total fat mass or abdominal visceral fat. At the initiation of puberty there is a divergence in circulating leptin concentrations between boys and girls. In boys, leptin concentrations increase and then markedly decrease to prepubertal concentration levels. In girls there are only increasing concentrations. The authors believe these patterns are relevant to the markedly different alterations in the regional distribution of body fat that occurs in boys and girls at puberty.

Adipose Tissue↗
PubMed1998

Gender differences in leptin levels during puberty are related to the subcutaneous fat depot and sex steroids.

Little is known about the influence of adiposity and hormone release on leptin levels in children and adolescents. We utilized criterion methods to examine the relationships among sex steroids, body composition (4 compartment), abdominal visceral and subcutaneous fat (magnetic resonance imagery), total subcutaneous fat (sum of 9 skinfolds), energy expenditure (doubly labeled water), aerobic fitness, and serum leptin levels in prepubertal and pubertal boys (n = 16; n = 13) and girls (n = 12; n = 15). The sum of skinfolds accounted for more variance in leptin levels of all girls [coefficient of determination (R2) = 0.70, P < 0.001] and all boys (R2 = 0.60, P < 0.001) than the total fat mass (girls, R2 = 0.52, P < 0.001; boys, R2 = 0.23, P < 0.001). Total energy expenditure, corrected for the influence of fat-free mass, correlated inversely with leptin (R2 = 0.18, P = 0.02). Gender differences in leptin disappeared when corrected for sex steroid levels or the combination of adiposity and energy expenditure. In multiple regression, the sum of skinfolds and free testosterone and estrogen levels accounted for 74% of the variance in leptin levels. We conclude that serum leptin levels are positively related to subcutaneous adiposity but negatively related to androgen levels. Energy expenditure may be negatively related to leptin levels by reduction of the adiposity, or a common genetic factor may influence both the activity and serum leptin levels.

Abdomen↗
PubMed1998

Alterations in growth and body composition during puberty: III. Influence of maturation, gender, body composition, fat distribution, aerobic fitness, and energy expenditure on nocturnal growth hormone release.

We examined the relationships among gender, sexual maturation, four-compartment model estimates of body composition, body fat distribution (magnetic resonance imaging for abdominal visceral fat and anthropometrics), aerobic fitness, basal and total energy expenditure, and overnight GH release in an ultrasensitive chemiluminescence assay in healthy prepubertal and pubertal boys (n = 18 and 11, respectively) and girls (n = 12 and 18, respectively). Blood samples were withdrawn every 10 min from 1800-0600 h to determine the area under the serum GH-time curve (AUC), sum of the GH peak heights (sigma GH peak heights), and the mean nadir GH concentration. GH release was greater in the pubertal than prepubertal subjects due to an increase in sigma GH peak heights (43.8 +/- 3.6 vs. 24.1 +/- 3.5 ng.mL-1, P = 0.0002) and mean nadir (1.7 +/- 0.2 vs. 0.7 +/- 0.2 ng.mL-1, P = 0.0002), but not peak number (4.3 +/- 0.2 vs. 4.5 +/- 0.2). The girls had a greater sigma GH peak heights (39.0 +/- 3.5 vs. 28.8 +/- 3.6 ng.mL-1, P = 0.05) and mean nadir concentration (1.4 +/- 0.2 vs. 0.9 +/- 0.2 ng.mL-1, P = 0.05) than the boys. Significant inverse relationships existed between sigma GH peak heights (r = -0.35, P = 0.06) or mean nadir (r = -0.39, P = 0.04) and four-compartment percent body fat for all boys but not for all girls or when combining all subjects. For all girls, significant inverse relationships existed between sigma GH peak heights (r = -0.39, P = 0.03) or mean nadir (r = -0.37, P = 0.04) and waist/hip ratio. Similar inverse relationships in all boys or all subjects were not significant. Forward stepwise regression analysis determined that bone age (i.e. maturation, primary factor) and gender were the significant predictors of AUC, sigma GH peak heights, and mean nadir. The influence of maturation reflects rising sex steroid concentrations, and the gender differences appear to be because of differences in estradiol concentrations rather than to body composition or body fat distribution.

Adipose Tissue↗
PubMed1997

Exercise and growth hormone: does one affect the other?

The release of growth hormone (GH) is sensitive to many pharmacologic and physiologic stimuli, including exercise. Although the role of the increased amount of GH released during exercise is not fully understood, it most likely contributes to metabolic fuel adaptations during exercise, and tissue repair after the exercise session. The GH response to exercise is altered by many factors, including sex steroid concentrations, fitness level, and the intensity of previous exercise sessions. For both endurance and resistance exercise, greater activation of anaerobic glycolysis and lactate formation increases the amount of GH released. Whether an endurance exercise session or an endurance exercise training regimen influences the total amount of GH released during a 24-hour period is not clear; this may depend on the gender of the person, the intensity of the exercise, and the duration of exercise training. The influence of a single session of resistance exercise or resistance training on 24-hour GH secretion has not been studied. Preexercise diet modulation (especially modulation of fat intake) may also influence the release of GH during endurance exercise. Studies that measure the 12- to 24-hour GH response to resistance exercise after the ingestion of various macronutrient diets have not been completed.

Adaptation, Physiological↗
PubMed1997

Weight loss and wrestling training: effects on nutrition, growth, maturation, body composition, and strength.

Adolescent wrestlers (n = 9, 15.4 yr) and recreationally active control adolescent males (n = 7, 15.7 yr) were measured before, at the end (late season), and 3.5-4 mo after a wrestling season to assess the influence of dietary restriction on growth, maturation, body composition, protein nutrition, and muscular strength. Controls consumed adequate amounts of energy, carbohydrate (CHO), protein, and fat, and demonstrated normal gains in weight, fat mass (FM) and fat-free mass (FFM). Wrestlers consumed a high-CHO (61 +/- 2% kcal), low-fat (24 +/- 2% kcal) diet during the season but did not consume adequate energy (24.7 +/- 3.5 kcal.kg-1.day-1) or protein (0.9 g.kg-1.day-1). Deficient dietary intake reduced prealbumin levels (26.0 +/- 1.9 vs. 20.2 +/- 0.9 mg/dl) and slowed the accrual of lean arm and thigh cross-sectional muscle areas (AXSECT, TXSECT, respectively). For wrestlers, dietary deficiency also decreased weight (60.3 +/- 3.5 to 58.0 +/- 3.3 kg), relative fat (9.9 +/- 0.5 to 8.0 +/- 0.7%), and FM (6.0 +/- 0.5 to 4.7 +/- 0.6 kg). Postseason, wrestlers and controls consumed similar diets, and wrestlers had significant increases in prealbumin, AXSECT, and TXSECT. Wrestlers also increased their weight (6.1 +/- 0.6 kg), FFM (3.0 +/- 0.6 kg), and FM (3.2 +/- 0.5 kg) postseason. Rates of bone maturation and segmental growth were not different between the groups. The wrestlers had reductions in elbow and knee strength from preseason to late season but increases postseason. Lean tissue changes were associated with the changes in strength and power (r = 0.72-0.91, P < 0.001). After covariance for FFM or limb-specific cross section, few significant changes remained. In conclusion, dietary restriction reduced protein nutrition and muscular performance but produced little effect on linear growth and maturation. Prealbumin levels and the rate of lean tissue accrual were positively related (r = 0.43, P < or = 0.05).

Adolescent↗
PubMed1997

Weight loss and wrestling training: effects on growth-related hormones.

Adolescent wrestlers (n = 9, 15.4 yr) and recreationally active control males (n = 7, 15.7 yr) were measured before, at the end of, and 3.5-4 mo after a competitive wrestling season to assess the influence of dietary restriction on growth-related hormones. Wrestlers had significant elevations preseason to late season for morning serum concentrations (mean of 8 serial samples) of growth hormone (GH; 2.9 +/- 0.7 vs. 6.5 +/- 1.4 ng/ml) and sex hormone-binding globulin (SHBG; 16.1 +/- 2.3 vs. 27.9 +/- 6.9 nmol/l) and significant reductions in GH-binding protein (GHBP; 178 +/- 19 vs. 109 +/- 17 pmol/l), insulin-like growth factor I (IGF-I; 332 +/- 30 vs. 267 +/- 34 ng/ml), testosterone (T; 4.9 +/- 0.4 vs. 3.6 +/- 0.4 ng/ml), and free testosterone (Free-T; 22.4 +/- 3.6 vs. 15.7 +/- 2.8 pg/ml). Wrestlers had significant postseason reductions in GH (3.44 +/- 1.30 ng/ml) and SHBG (10.43 +/- 4.13 nmol/l) but elevations in GHBP (66.7 +/- 23.8 pmol/l), IGF-I (72.9 +/- 25.1 ng/ml), T (2.10 +/- 0.46 ng/ml), and Free-T (9.76 +/- 3.01 pg/ml). Concentrations of luteinizing hormone (LH), estradiol, prolactin, cortisol, insulin, and thyroid hormones did not differ because of exercise-dietary practices of wrestlers. In-season elevations in GH, with concomitant reductions in GHBP and IGF-I, that were reversed during the postseason suggest a reduction in GH receptor number and partial GH resistance during the season. Nonelevated LH with reduced T levels suggests a central hypothalamic-pituitary-gonadal (H-P-G) axis impairment. In conclusion, undernutrition may lead to altered H-P-G and GH-IGF-I axes function in adolescent wrestlers. However, only the wrestlers' late-season Free-T concentrations were outside the normal range, and the hormone axis impairments were quickly reversed. The present data do not address hormonal axis responses to several years of wrestling and weight loss.

Diet↗
PubMed1997

Alterations in growth and body composition during puberty. I. Comparing multicompartment body composition models.

A four-compartment (4C) model of body composition was used as a criterion to determine the accuracy of three-compartment (3C) and two-compartment (2C) models to estimate percent body fat (%BF) in prepubertal and pubertal boys (genital I & II, n = 17; genital III & IV, n = 7) and girls (breast I & II, n = 8; breast III & IV, n = 15). The 3C water-density (3C-H2O) and 3C mineral-density models, dual-energy X-ray absorptiometry, the Lohman age-adjusted equations, the Slaughter et al. skinfold equations, and the Houtkooper et al. and Boileau bioelectrical impedance equations were evaluated. Agreement with the 4C model increased with the number of compartments (i.e., body water, bone mineral) measured. Except for the 3C-H2O model, the limits of agreement were large and did not perform well for individuals. The mean %BF by dual-energy X-ray absorptiometry (23.6%) was greater than that of the criterion 4C method (21.7%). For the field methods, the Slaughter et al. skinfold equations performed better than did the Houtkooper et al. and Boileau bioimpedance equations. The hydration of the fat-free mass decreased (genital I & II = 75.7%, genital III & IV = 74.8%, breast I & II = 75.5%, breast III & IV = 74.4%) and the mineral content increased (genital I & II = 4.9%, genital III & IV = 5.0%, breast I & II = 5.1%, breast III & IV = 5.7%) with maturation. The density of the fat-free mass also increased (genital I & II = 1.084 g/ml, genital III & IV = 1.087 g/ml, breast I & II = 1.086 g/ml, breast III & IV = 1.091 g/ml) with maturation. All of the models reduced the %BF overprediction of the Siri 2C model, but only the 4C and 3C-H2O models should be used as criterion methods for body composition validation in children and adolescents.

Adipose Tissue↗