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J H Wilmore

Publications and source records attributed to J H Wilmore.

At least 19 recordsLinked to original sources

Scaling submaximal exercise cardiac output and stroke volume: the HERITAGE Family Study.

This study investigated different methods of scaling submaximal cardiac output (Q) and stroke volume (SV) to best normalize for body size (body surface area [BSA], height [Ht], weight [Wt], and fat-free mass [FFM]). Q and SV were measured at both an absolute (50 W) and a relative power output (60 % of VO2max) in 337 men and 422 women, 17 to 65 years of age. Traditional ratio scaling was examined in addition to allometric scaling, where scaling exponents ( B) were determined for each body size variable (x) that best normalized the physiological outcome variables (y) for body size (y = ax(b)). With ratio scaling, regardless of the body size variable (x = BSA, Ht, Wt, FFM), there was no evidence of a linear relationship between x and y (y = Q or SV). A linear relationship is a necessary condition for appropriate normalization. Further, when ratio-scaled variables (e.g., Q/BSA) were correlated to the body size variable (e.g., BSA) by which they were scaled, significant (p <or= 0.05) relationships still existed for BSA, Ht, Wt, and FFM. Thus, ratio scaling did not meet either criteria for normalizing Q and SV for body size. In contrast, when allometrically-derived scaling exponents were used to normalize Q and SV (e.g., Q/BSA(b)), the resulting scaled values were uncorrelated (i.e., size-independent) with BSA, Ht, Wt, or FFM. These results were independent of age, sex or race. In summary, ratio scaling did not appropriately normalize Q and SV for differences in body size, while allometric scaling did result in size-independent values. Thus, individually-derived allometric exponents should be applied to body size variables to most appropriately adjust Q and SV for body size.

Adolescent↗

Genome-wide scan to identify quantitative trait loci for baseline resting heart rate and its response to endurance exercise training: the HERITAGE Family Study.

Evidence of a genetic component for resting heart rate (RHR) has been found. Quantitative trait loci (QTLs) for baseline RHR have been reported, but not for RHR training response. It is of interest to identify QTLs that may harbor genes influencing RHR variation at baseline and in response to regular exercise training. Here, a multipoint variance components linkage scan using 654 markers was performed to search for QTLs that influence RHR adjusted for several covariates at baseline and in response to 20 weeks of endurance training (post-training minus baseline) in 99 White and 127 Black families in the HERITAGE Family Study. Potentially interesting linkages were revealed on 4 q and 11 p for baseline RHR, and on 1 q and 21 q for RHR training response in Whites. The QTLs on 2 q, 6 q, 7 q, 12 q, 14 q, and 15 q for baseline RHR, and on 3 p, 20 p and 21 q for RHR training response were found in Blacks. Promising linkages (lod scores >or= 1.75, p or= 135/80 mm Hg) subset of 40 White families suggesting a pleiotropic gene for BP and RHR with interactions. In conclusion, among QTLs on 1 q, 2 p, 3 p, 4 q, and 11 p that replicated across subsamples and studies, 11 p is most promising for dense mapping and association studies in HERITAGE and other cohorts.

Black People↗

Quantitative trait loci for maximal exercise capacity phenotypes and their responses to training in the HERITAGE Family Study.

The purpose of this study was to identify regions of the human genome linked to maximal oxygen uptake (VO2max) and maximal power output (MPO), and their response to a standardized 20-wk endurance-training program in sedentary black and white subjects. A total of 509 polymorphic markers covering the 22 autosomes were used in the genome-wide linkage scan. Baseline phenotypes were adjusted for age, sex, and body mass, whereas the training responses were adjusted for age, sex, and the baseline values. Regression-based single- and multipoint linkage analyses were used. In the sedentary state, a total of 351 and 102 sibling pairs were available for whites and blacks, respectively, and 329 and 90 sibling pairs, respectively, for the training response phenotypes. Baseline VO2max showed promising linkage (P < 0.0023) with 11p15.1 (whites), and suggestive evidence of linkage (0.01 > P > 0.0023) was found on 1p31, 7q32, and 7q36 (blacks). Baseline MPO exhibited promising linkage on 10q23 and suggestive evidence of linkage on 13q33 and 18q11-q12 (whites). VO2max training response yielded promising linkages with markers on 1p31 (blacks) and suggestive on 4q27, 7q34, and 13q12 (whites) and on 16q22 and 20q13.1 (blacks). Training-induced changes in MPO showed promising linkages on 5q23 (whites) and suggestive on 1q21, 4p15.1, and 4p13 (whites) and on 1q22 and 13q11 (blacks). In conclusion, the strongest evidence of linkage was found on chromosomal regions 11p15 and 10q23 for VO2 max and MPO in the sedentary state and on chromosomes 1p31 and 5q23 for their responsiveness to training. These chromosomal regions harbor several candidate genes that deserve further investigation.

Adult↗

Sex differences in the relationships of abdominal fat to cardiovascular disease risk among normal-weight white subjects.

The objectives of this study are to investigate the relationships between abdominal fat and risk factors for cardiovascular disease (CVD) among normal-weight (NW) white subjects and to determine how these relationships differ by sex. NW adults (177 males and 258 females) and overweight adults (133 males and 111 females) from the Québec Family Study and the HERITAGE Family Study were retained for this study. Risk factors included systolic and diastolic blood pressures, low-density lipoprotein and high-density lipoprotein cholesterols, triglycerides, and fasting glucose. Only in NW female adults, abdominal visceral fat (AVF) area assessed by computed tomography was significantly correlated with all risk factors, except for fasting glucose, even after age, study cohort, and fat mass were taken into account. NW female subjects with at least one risk factor had a significantly higher AVF than those without risk factors, although the difference was small. Thus, only NW female adults with more AVF tended to have a more adverse CVD risk factor profile.

Abdomen↗

Generalized abdominal visceral fat prediction models for black and white adults aged 17-65 y: the HERITAGE Family Study.

OBJECTIVE: To determine if the relationship between abdominal visceral fat (AVF) and measures of adiposity are different between Black and White subjects and to develop valid field prediction models that accurately identify those individuals with AVF levels associated with high risk for chronic disease. DESIGN: Cross-sectional measurements obtained from 91 Black men, 137 Black women, 227 White men, and 237 White women subjects, ages 17-65 y, who were participants in the HERITAGE Family Study, both at baseline and following 20 weeks of endurance training. MEASUREMENTS: AVF, abdominal subcutaneous fat (ASF), abdominal total fat (ATF), and sagittal diameter (SagD) were measured by computed tomography (CT). Body density was determined by hydrostatic weighing and was used to estimate relative body fat. Arm, waist (WC), and hip circumferences and skinfold thickness measures were taken, and BMI was calculated from weight (kg) and height (m(2)). Since CT abdominal fat variables were skewed, a natural log transformation (Ln) was used to produce a normal distribution. The General Linear Model (GLM) procedure was used to test the relationship between AVF and two different groups of variables-CT and anthropometric. RESULTS: The AVF of White men and women was significantly higher than that of Black men and women, independent of BMI, WHR, WC, and age, and was greater for men than for women. The CT model showed that the combination of SagD, Ln (ASF), age, and race accounted for 84 and 75% of the variance in AVF in men and women, respectively. The anthropometric model provided two valid generalized field AVF prediction equations. The Field-I equation, which included BMI, WHR, age and race, had an r(2) of 0.78 and 0.73 for men and women, respectively. The Field-II equation, which included BMI (women only), WC, age, and race, had an r(2) of 0.78 and 0.72 for men and women, respectively. The field model equations became less accurate as the estimated AVF increased. CONCLUSIONS: (1) At the same age and level of adiposity, Black men and women have less AVF than White men and women. These differences are greater in men than in women. (2) The field regression equations can be generalized to the diverse group of adults studied, both in an untrained and trained state. However, their accuracy decreases with increasing levels of AVF.

Abdomen↗

Associations between cardiorespiratory responses to exercise and the C34T AMPD1 gene polymorphism in the HERITAGE Family Study.

The associations of the C34T polymorphism of the adenosine monophosphate deaminase 1 (AMPD1) gene with cardiorespiratory phenotypes were tested during cycling exercise at absolute and relative power outputs progressing to exhaustion before and after endurance training for 20 wk in the HERITAGE Family Study cohort (n = 779). Since no blacks were mutant homozygotes (TT), only whites were considered for analysis (400 normal homozygotes, CC; 97 heterozygotes, CT; and 6 TT). For sedentary state, cycling at the absolute power output of 50 W resulted in a higher rating of perceived exertion in TT (P < 0.0001). At the relative intensity of 60% of Vo(2 max), stroke volume was lower in TT (P < 0.05). Maximal values for power output, systolic blood pressure, heart rate, Vco(2), and respiratory exchange ratio were lower in TT (P < 0.05). The cardiorespiratory training response at 50 W and at 60% of Vo(2 max) was similar across C34T-AMPD1 genotypes. However, the maximal values for ventilation, Vo(2), and Vco(2) during exercise increased less in TT (P < 0.01). The results indicate that subjects with the TT genotype at the C34T AMPD1 gene have diminished exercise capacity and cardiorespiratory responses to exercise in the sedentary state. Furthermore, the training response of ventilatory phenotypes during maximal exercise is more limited in TT.

AMP Deaminase↗

Post-heparin lipolytic enzyme activities, sex hormones and sex hormone-binding globulin (SHBG) in men and women: The HERITAGE Family Study.

We tested the hypothesis that androgen, estrogen, and sex hormone-binding globulin (SHBG) levels would be significantly related to post-heparin hepatic lipase (HL) and lipoprotein lipase (LPL) activities in a sample of Caucasian men (n = 233) and women (n = 235) aged 17-64 years from the HERITAGE Family Study. Body composition (hydrostatic weighing), abdominal adipose tissue distribution (computed tomography), plasma lipid-lipoprotein and hormone levels, and post-heparin lipases activities were measured. HL activity was significantly higher in males, whereas LPL activity was higher in women (P < 0.005). In women only, HL activity was positively associated with body fat mass (r = 0.17, P < 0.05) and intra-abdominal adipose tissue area (r = 0.18, P < 0.05). Significant associations were also found between fasting insulin and LPL activity (r = -0.16, P < 0.05 and r = -0.18, P < 0.005) as well as HL activity (r = 0.22, P < 0.005, and r = 0.27, P < 0.0001) in men and women, respectively. A positive association between total testosterone and HL activity was noted in men (r = 0.13, P = 0.05). In women, plasma SHBG levels were negatively associated with HL activity (r = -0.48, P < 0.0001), and statistical adjustment for body fat mass, visceral adipose tissue area, and fasting insulin did not attenuate this correlation. In multivariate analyses with models including adiposity variables and measurements of the hormonal profile, insulin, and testosterone levels were both independent positive predictors of HL activity in men. In women, hormone use was a significant positive predictor, and SHBG level a strong negative predictor of HL activity, independent of plasma estradiol and testosterone concentrations. Fasting insulin was the only significant predictor of LPL activity in men (negative association), whereas menstrual status, fasting insulin (negative associations), and plasma SHBG levels (positive association) were all independent predictors of LPL activity in women. These results suggest that the postulated sensitivity of lipolytic enzymes to androgens and estrogens is reflected by a strong negative association between SHBG levels and HL, and a lower magnitude positive association of this hormonal parameter to LPL activity in women. These associations appear to be independent from concomitant variation in total adiposity or body fat distribution.

Adipose Tissue↗

Interactions among the beta2- and beta3- adrenergic receptor genes and total body fat and abdominal fat level in the HERITAGE Family Study.

OBJECTIVE AND SUBJECTS: Interactions between markers in the beta2- and beta3-adrenergic receptor (ADR) genes and total body fat and computerized tomography-measured abdominal fat phenotypes were studied in the HERITAGE Family Study cohort of Black (n=205; 81 males and 124 females) and White (n=415; 198 males and 217 females) subjects before and after an endurance training program. RESULTS: In Black subjects, beta2- and beta3-ADR gene variants showed evidence of interactions on changes in total body fat mass and abdominal fat area (P<0.005 and =0.010, respectively). Black subjects who were carriers of both beta2-ADR Arg16 and beta3-ADR Arg64 alleles had a greater decrease in total fat mass as well as abdominal total and subcutaneous, but not visceral fat areas in response to endurance training than subjects with other genotype combinations (P from 0.011 to 0.047). After correction for multiple tests, the findings remained essentially unchanged for total body fat mass and abdominal fat area, but became nonsignificant for subcutaneous fat area. The changes in abdominal fat correlated positively with the changes in fat mass (P<0.0001). The interactions between beta2 and beta3-ADR gene markers accounted for a maximum of 3% of the variances in the response of total fat mass and abdominal fat area to endurance training in Black subjects but it was not significant in White subjects. CONCLUSION: Interactions between sequence variants in the beta2-beta3-ADR gene contributed to the changes in fat mass and abdominal adiposity in response to endurance training in Black subjects.

Abdomen↗

The agouti-related protein and body fatness in humans.

OBJECTIVE: The objective of this study was to examine the impact of a single nucleotide polymorphism (SNP) (-38C>T) in the promoter of the human agouti-related protein (hAgRP) gene on promoter affinity for transcription factors (TFs) and its possible association with body composition phenotypes. DESIGN: Electrophoretic mobility shift assays for the functional studies and association analyses for the population studies. SUBJECTS AND METHODS: Nuclear extracts were isolated from the mouse hypothalamus cell line GT1-7 and subjected to binding assays using oligonucleotide probes corresponding to the -38C>T region and an antibody for the E12/E47 TFs. Individuals (n = 259) from the HERITAGE Family Study were genotyped for the -38C>T SNP and used in the association studies. RESULTS: Electrophoretic mobility shift and supershift assays confirmed binding of the E12/E47 TF to the -38C>T site in a genotype-dependent manner. The T allele was found exclusively in the black subjects while the genotype with the higher binding affinity, CC, was significantly associated with high BMI, fat mass, and percent body fat in the black subjects of the HERITAGE Family Study. CONCLUSIONS: The E12/E47 TF could play a role in the regulation of hAgRP expression while the population studies suggest that the TT genotype of the -38C>T SNP could play a protective role against the development of obesity in the black population of the HERITAGE Family Study.

Adipose Tissue↗

Familial aggregation of exercise heart rate and blood pressure in response to 20 weeks of endurance training: the HERITAGE family study.

Changes of heart rate (HR) and blood pressure (BP) relative to baseline levels in response to an extended period of endurance training are indices of cardiovascular adaptability. Familial influences were investigated for HR and BP at work rates of 50 W and 60 % of the maximal oxygen uptake (VO2max) in response to 20 weeks of endurance training. A total of 481 participants from 99 sedentary White nuclear families in the HERITAGE Family Study (HERITAGE) were analyzed using a familial correlation model. Each of these training response phenotypes was adjusted for the effects of age, BMI, cigarette smoking, baseline VO2max, and its baseline values in fathers, mothers, sons and daughters, respectively. We found that maximal heritabilities reached 34 % and 29 % for HR training responses at 50 W and 60 % of VO2 max, respectively. The heritability was 22 % for systolic BP (SBP) training response at 50 W, but negligible at 60 % of VO2max. No significant heritabilities were found for diastolic BP (DBP) training responses at either 50 W or 60 % of VO2max. Familial influences for exercise HR and BP training responses were also assessed in a total of 257 participants from 113 Black family units in HERITAGE. However, there was no significant familial resemblance, which may be attributable to the small sample size. In conclusion, HR and SBP training responses during submaximal exercise in Whites were influenced by a modest, but significant, familial component. These observations are therefore in contrast to substantial familial effects (heritability estimates of about 50 %) previously reported for these variables measured at baseline.

Adaptation, Physiological↗

Evidence of major genes for exercise heart rate and blood pressure at baseline and in response to 20 weeks of endurance training: the HERITAGE family study.

Major gene effects on exercise heart rate (HR) and blood pressure (BP) measured at 50 W and 80 % maximal oxygen uptake (VO (2)max) were assessed in 99 White families in the HERITAGE Family Study. Exercise HR and BP were measured both before and after 20 weeks of endurance training. The baseline phenotypes were adjusted for the effects of age and BMI, whereas the training responses (post-training minus baseline) were adjusted for the effects of age, BMI and the corresponding baseline values, within four sex-by-generation groups. Baseline exercise HR at 50 W was under the influence of a major recessive gene and a multifactorial component, which accounted for 30 % and 27 % of the variance, respectively. The training response was found to be under the influence of a major dominant gene, which accounted for 27 % of the variance. These significant major gene effects were independent of the effects of cigarette smoking, baseline VO (2)max, and the resting HR levels. No significant interactions were found between genotype and age, sex, or BMI. No major gene effect was found for exercise BP. Instead, we found the baseline exercise BP at 50 W and 80 % VO (2)max and the training response at 50 W were solely influenced by multifactorial effects, which accounted for about 50 %, 40 % and 20 % of the variance, respectively. No familial resemblance was found for training responses in exercise HR or BP at 80 % VO (2)max. Segregation analysis also was carried out for exercise HR in Whites pooled with a small sample of Blacks in HERITAGE. Similar major effects were found, but the transmission from parents to offspring did not follow Mendelian expectations, suggesting sample heterogeneity. In conclusion, submaximal exercise HR at baseline and in response to endurance training was influenced by putative major genes, with no evidence of interactions with sex, age or BMI, in contrast to a multifactorial etiology for exercise BP.

Black People↗

The hormone-sensitive lipase gene and body composition: the HERITAGE Family Study.

OBJECTIVE: To investigate whether the C-60G polymorphism and other markers in the hormone-sensitive lipase (LIPE) gene are associated with baseline body composition and free-fatty acid (FFA) concentrations measured at rest and during low-intensity exercise in white and black subjects participating in the HERITAGE Family Study. SUBJECTS: Adult sedentary white (245 men and 258 women) and black (91 men and 185 women) subjects. MEASUREMENTS: body mass index (BMI); fat mass (FAT); percentage body fat (%FAT); fat-free mass (FATFR); sum of eight skinfolds (SF8); subcutaneous (ASF), visceral (AVF) and total (ATF) abdominal fat areas assessed by CT scan; plasma FFA concentrations measured at rest (FFAR), at a power output of 50 W (FFA50) and at a relative power output of 60% of VO(2max) (FFA60%); and fasting insulin (INS). STATISTICAL ANALYSIS: Association between the C-60G polymorphism of the LIPE gene and each phenotype was tested separately in men and women using ANCOVA with the effects of age and race as covariates and with further adjustment for FAT for ASF, AVF, ATF, FFAR, FFA50 and FFA60%. Secondly, owing to significant gene-by-race interaction, associations were investigated separately in each of the two race groups. Linkage was tested with the C-60G polymorphism, a dinucleotide repeat polymorphism in the intron 7 of the LIPE gene and two microsatellites markers (D19S178 and D19S903) flanking the LIPE gene. RESULTS: There were no race differences in the allele frequencies of the C-60G polymorphism of the LIPE gene. No association or gene-by-race interaction was observed in men. However, in women, strong gene-by-race interactions were observed for BMI (P=0.0005), FAT (P=0.0007), %FAT (P=0.0003), SF8 (P=0.0001), ASF (P=0.03) and ATF (P=0.01). When the analysis was performed separately in each race, white women carriers of the -60G allele exhibited lower %FAT (P=0.005) and SF8 (P=0.01) than non-carriers, while in black women, the -60G allele was associated with higher BMI (P=0.004), FAT (P=0.009), %FAT (P=0.01) and SF8 (P=0.0009). These associations were no longer significant after adjusting for INS. Evidence of linkage was observed in whites with ATF, FFAR, FFA50 and FFA60%. CONCLUSION: These results suggest that the C-60G polymorphism in the LIPE gene plays a role in determining body composition and that its effect is sex-, race- and insulin-dependent.

Abdomen↗

Is adiposity at normal body weight relevant for cardiovascular disease risk?

OBJECTIVE: To examine the relation between adiposity and risk factors for cardiovascular disease (CVD) in normal weight (NW) individuals. METHODS: Cross-sectional study using the sample of white people, aged from 17 to 60 y from the Québec Family Study and the Heritage Family Study. NW subjects with a body mass index (BMI) between 18.5 and 25 kg/m(2) (181 males and 265 females) and overweight (OW) subjects with a BMI between 25 and 30 kg/m(2) (133 males and 114 females) were retained for this study. NW subjects were divided into quintiles of each adiposity variable, then the quintiles and the OW group were evaluated for the presence of CVD risk factors. Using logistic regression analysis, the odds ratio (OR) for the prevalence of risk factors for each quintile of each adiposity variable and the OW group was estimated relative to the first quintile in NW subjects. Mean values of adiposity variables were compared between the subjects with and without risk factors. In these analyses, age and study cohort effects were taken into account. MEASUREMENTS: Percentage body fat (%fat) and fat mass (FM) measured by underwater weighing were available as adiposity variables. Risk factors included systolic and diastolic blood pressure, LDL and HDL cholesterol, triglycerides and fasting glucose. RESULTS: Wide ranges of values were observed for adiposity variables. HDL cholesterol, triglycerides and fasting glucose in NW males and HDL cholesterol in NW females were significantly correlated with all adiposity variables. For males, higher quintiles of adiposity variables in the NW group and the OW group tended to have higher ORs compared to the first quintiles for the risk factor variables. The fifth quintiles of all adiposity variables had the highest ORs (3.15 for %fat and 3.77 for FM) and they were significantly different from the first quintiles. OW males had ORs similar to those of the fifth quintiles for the risk factor variables. On the other hand, for females, the relatively linear associations were less clear in the NW group. In NW males, the subjects with at least one risk factor had significantly higher %fat and FM than the subjects without risk factors. In NW females, no significant difference was observed for these adiposity variables between the subjects with and without risk factors. CONCLUSION: NW males with elevated adiposity had higher prevalence of risk factors than NW males with less adiposity and the prevalence in the former was rather similar to that seen in OW males. On the other hand, measures of adiposity added little additional information to the BMI classification of NW on CVD risk factors in females.

Adipose Tissue↗

The effect of sex, age and race on estimating percentage body fat from body mass index: The Heritage Family Study.

OBJECTIVE: To study the effects of sex, age and race on the relation between body mass index (BMI) and measured percent body fat (%fat). DESIGN: Cross-sectional validation study of sedentary individuals. SUBJECTS: The Heritage Family Study cohort of 665 black and white men and women who ranged in age from 17 to 65 y. MEASUREMENTS: Body density determined from hydrostatic weighing. Percentage body fat determined with gender and race-specific, two-compartment models. BMI determined from height and weight, and sex and race in dummy coded form. RESULTS: Polynomial regression showed that the relationship between %fat and BMI was quadratic for both men and women. A natural log transformation of BMI adjusted for the non-linearity. Test for homogeneity of log transformed BMI and gender showed that the male-female slopes were within random variance, but the intercepts differed. For the same BMI, the %fat of females was 10.4% higher than that of males. General linear models analysis of the women's data showed that age, race and race-by-BMI interaction were independently related to %fat. The same analysis applied to the men's data showed that %fat was not just a function of BMI, but also age and age-by-BMI interaction. Multiple regression analyses provided models that defined the bias. CONCLUSIONS: These data and results published in the literature show that BMI and %fat relationship are not independent of age and gender. These data showed a race effect for women, but not men. The failure to adjust for these sources of bias resulted in substantial differences in the proportion of subjects defined as obese by measured %fat.

Adipose Tissue↗

Variability in the response of HDL cholesterol to exercise training in the HERITAGE Family Study.

In the HERITAGE Family Study, 675 sedentary, healthy, white and black men and women, aged 17 to 65 years, performed 20 weeks of supervised cycle ergometer exercise at the same relative intensity and weekly volume. As a group, subjects had normal mean baseline lipid levels for North Americans with the exception of below average high density lipoprotein cholesterol (HDL-C) levels. A significant mean increase in plasma HDL-C of 3.6 % was observed; however, there was marked variability in responsiveness to training, ranging from a mean 9.3 % decrease in Quartile 1 of HDL-C response to a mean 18 % increase in Quartile 4 (P < 0.0001 by ANOVA). Parallel changes in HDL(2)-C and HDL(3)-C, apolipoprotein A-I levels, and lipoprotein lipase activity were noted across quartiles. The change in HDL-C across quartiles was inversely related to baseline HDL-C (p < 0.0001) and to changes with training in plasma triglycerides (p = 0.0007). No significant differences in HDL-C response were observed across quartiles by sex, race, age, or increase in VO(2)max with training; however, weak positive associations were observed with age-adjusted education level and with reduction in abdominal fat and increase in VO(2)max at the ventilatory threshold following training. Multivariate regression analysis including baseline variables and training responses only accounted for 15.5 % of the variability in the HDL-C response to training. Thus, marked variability was found in the HDL-C response to the same endurance exercise training stimulus with only a modest amount of the response predictable by identified nongenetic factors.

Adaptation, Physiological↗

Race differences in the response of postheparin plasma lipoprotein lipase and hepatic lipase activities to endurance exercise training in men: results from the HERITAGE Family Study.

Endurance exercise training is known to produce favorable changes in the metabolic profile including reduced plasma triglyceride (TG) and increased high-density lipoprotein (HDL) cholesterol concentrations. These metabolic improvements are likely to contribute to the reduced coronary heart disease (CHD) risk often observed in physically active individuals. However, the physiological mechanisms responsible for such improvements in TG and HDL cholesterol concentrations with endurance exercise are not fully understood. The effect of a 20-week endurance exercise training program on plasma lipoproteins as well as on post-heparin plasma lipoprotein lipase (PH-LPL) and hepatic lipase (PH-HL) activities were therefore examined in a sample of 200 White and 69 Black men who were part of the HERITAGE Family Study. As expected, there were decreases in adiposity and in abdominal fat accumulation following training in both White and Black men. We also found that exercise training was associated with decreases in plasma cholesterol, TG and apolipoprotein B levels, as well as with an increase in HDL cholesterol concentrations in White men. In contrast, Black men showed an increase only in HDL(2) cholesterol over the 20-week period. Higher PH-LPL and lower PH-HL activities were noted in both ethnic groups at follow-up. Whereas in White men improvement of the lipoprotein-lipid profile was related to increased PH-LPL activity, no association between PH-LPL (or PH-HL) and lipoprotein-lipid variables was observed in Black men. Results of the present study suggest that in Whites, the increase in PH-LPL activity in response to endurance exercise training is associated with a better lipoprotein-lipid profile, therefore reducing CHD risk. However, the generally better metabolic profile of Black individuals may minimize further improvement of lipoprotein-lipid concentrations by exercise training.

Adipose Tissue↗

Familial resemblance for glucose and insulin metabolism indices derived from an intravenous glucose tolerance test in Blacks and Whites of the HERITAGE Family Study.

Type 2 diabetes mellitus (T2DM), characterized by hyperglycemia, is a complex disease primarily caused by impairment in insulin sensitivity (SI) and insulin secretion. While a strong genetic component for T2DM is well established, there are few reports on racial differences in the magnitude of the genetic effects of T2DM and indices of glucose and insulin metabolism. We report here on the familial resemblance for traits related to glucose metabolism at pre-exercise training levels in 492 members from 99 sedentary White families and 259 members from 108 Black families participating in the multicenter HERITAGE Family Study. All these traits were obtained from the frequently sampled intravenous glucose tolerance test (IVGTT). They include glucose disappearance index (Kg), an overall index for glucose tolerance, acute insulin response to glucose (AIR(Glucose)) which is an index for insulin secretion, and those derived from the minimal model including SI and the disposition index (DI). DI, derived as the product of SI and AIR(Glucose), is a measure of the activity of the B-cells adjusted for insulin resistance. After adjustment for age, sex, and body mass index, the maximal heritability estimates in Blacks (Whites) are 48+/-14% (25+/-8%) for Kg, 44+/-14% (46+/-8%) for AIR(Glucose), 38+/-12% (44+/-8%) for SI and 32+/-14% (24+/-8%) for DI. Interestingly, Blacks have higher heritability for overall glucose tolerance than Whites but there is no race difference in heritability estimates for insulin sensitivity or insulin secretion.

Adult↗

The Trp64Arg polymorphism of the beta3-adrenergic receptor gene is not associated with training-induced changes in body composition: The HERITAGE Family Study.

OBJECTIVE: To investigate the association between the Trp64Arg polymorphism of the beta3-adrenergic receptor gene and changes in body composition in response to endurance training. RESEARCH METHODS AND PROCEDURES: Adult sedentary white and black subjects participating in the HERITAGE Family Study were measured before and after 20 weeks on endurance training for the body mass index, fat mass, percentage of body fat, fat-free mass, sum of eight skinfolds, and subcutaneous, visceral, and total abdominal fat areas. The association between the Trp64Arg polymorphism and the response phenotypes, computed as the difference between pre- and post-training values, was tested by analysis of covariance separately in men and women. The gene by race interaction term was also tested. RESULTS: No race differences were observed for allelic and genotype frequencies. Training resulted in significant reduction of body fat in both men and women. No association of the Trp64Arg polymorphism was observed with training-induced changes for any of the body composition phenotypes in both men and women. DISCUSSION: These results suggest that the Trp64Arg polymorphism of the beta3-adrenergic receptor gene is not related to changes in body composition in response to exercise training.

Adipose Tissue↗