Biomedical subjects

Claude Bouchard

Publications and source records attributed to Claude Bouchard.

At least 91 records · Page 5Linked to original sources

PubMed2003

Estimated daily energy expenditure and blood lipids in adolescents: the Québec Family Study.

PURPOSE: To examine the association between estimated daily energy expenditure and blood lipids in a sample of adolescents. METHODS: The sample consisted of 415 males and 356 females aged 10-19 years, mainly French Canadian, recruited from the greater Quebec City area through the media as part of Phase I of the Quebec Family Study. Estimates of daily energy expenditure (DEE) were obtained with a 3-day physical activity record. Blood lipids were measured by standard procedures. The sample was stratified into three activity groups (least active, less than 25th percentile of DEE; moderately active, 25-74th percentile of DEE; and most active, 75th percentile or greater of DEE), and also by clinical cutpoints for blood lipids. Analysis of covariance, controlling for age and fatness, was conducted to compare blood lipids within gender across activity groups. Logistic regression analysis, controlling for age and fatness, was used to estimate the relative risk of being classified with an undesirable level of a blood lipid parameter on the basis of the DEE. RESULTS: Total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels were not significantly different across activity groups in males or females. High-density lipoprotein cholesterol (HDL-C) was significantly different across activity groups in males (p <.05) and females (p <.05), but the pattern of variation was different between genders. In males, the TC/HDL-C and LDL-C/HDL-C ratios decreased between the moderately active and most active groups (p <.05). Significant differences remained when subcutaneous fatness was considered as a covariate. The results from logistic regression analysis indicated that the odds ratios for low HDL-C levels was significant only in low DEE girls (odds ratio 2.83) compared with high DEE girls. CONCLUSIONS: The results suggest that increased energy expenditure and physical activity are associated with higher levels of HDL-C in adolescents of both sexes.

Adolescent↗

PubMed2003

The peroxisome proliferator-activated receptor alpha L162V mutation is associated with reduced adiposity.

OBJECTIVE: To determine the contribution of the peroxisome proliferator-activated receptor alpha (PPARalpha) L162V mutation to the variation of several indexes of body fatness obtained from healthy adults who participated in the Quebec Family Study. RESEARCH METHODS AND PROCEDURES: The PPARalpha L162V mutation was determined by a mismatch polymerase chain reaction method. Adiposity phenotypes were obtained by standardized anthropometric measurements, underwater weighing technique, and computed tomography. RESULTS: For all adiposity phenotypes, subjects carrying the V162 allele had lower values compared with L162 homozygotes (HMZs) [BMI (kg/m(2)): 27.8 +/- 7.6 vs. 26.0 +/- 5.6, p < 0.05; percentage body fat: 28.5 +/- 10.7 vs. 25.7 +/- 10.1, p < 0.05; waist circumference (cm): 89.0 +/- 18.1 vs. 85.7 +/- 15.8, p = 0.07; total computed tomography abdominal fat areas (cm(2)): 406 +/- 221 vs. 359 +/- 192, p = 0.15; means +/- SD for L162 HMZs vs. V162 carriers, respectively]. Differences in cross-sectional abdominal adipose tissue areas and waist circumference were abolished after adjustment for total body fat mass. Similar trends were observed when results were analyzed by gender, although associations seemed stronger in women. The odds ratio of having a BMI above 30 kg/m(2) reached 1.77 (1.02; 3.07, 95% confidence intervals) for L162 HMZs. This risk could be considered marginal on an individual basis, but because 85% of the subjects are affected by this small risk, the impact on the population is important. DISCUSSION: The PPARalpha V162 allele is associated with reduced adiposity and has a substantial population-attributable risk.

Abdomen↗

PubMed2003

The human obesity gene map: the 2002 update.

This is the ninth update of the human obesity gene map, incorporating published results through October 2002 and continuing the previous format. Evidence from single-gene mutation obesity cases, Mendelian disorders exhibiting obesity as a clinical feature, quantitative trait loci (QTLs) from human genome-wide scans and various animal crossbreeding experiments, and association and linkage studies with candidate genes and other markers is reviewed. For the first time, transgenic and knockout murine models exhibiting obesity as a phenotype are incorporated (N = 38). As of October 2002, 33 Mendelian syndromes relevant to human obesity have been mapped to a genomic region, and the causal genes or strong candidates have been identified for 23 of these syndromes. QTLs reported from animal models currently number 168; there are 68 human QTLs for obesity phenotypes from genome-wide scans. Additionally, significant linkage peaks with candidate genes have been identified in targeted studies. Seven genomic regions harbor QTLs replicated among two to five studies. Attempts to relate DNA sequence variation in specific genes to obesity phenotypes continue to grow, with 222 studies reporting positive associations with 71 candidate genes. Fifteen such candidate genes are supported by at least five positive studies. The obesity gene map shows putative loci on all chromosomes except Y. More than 300 genes, markers, and chromosomal regions have been associated or linked with human obesity phenotypes. The electronic version of the map with links to useful sites can be found at http://obesitygene.pbrc.edu.

Animals↗

PubMed2003

Effects of beta2-adrenergic receptor gene variants on adiposity: the HERITAGE Family Study.

We investigated whether the Arg16Gly and Gln27Glu polymorphisms of the beta2-adrenergic receptor gene were associated with body-fat and fat-distribution phenotypes measured before and in response to a 20-week endurance-training program. BMI, fat mass (FAT), percentage of body fat (%FAT), sum of eight skinfolds (SF8), and abdominal fat areas assessed by computed tomography were measured in adult sedentary white and black participants of the HERITAGE Family Study. Evidence of gene-by-obesity interaction was found in whites for several adiposity phenotypes measured before training. Analyses performed separately in nonobese and obese subjects revealed that obese men carrying the Glu27 allele have lower fat accumulation (BMI, FAT, and %FAT) than noncarriers. Among white obese women, Gly16Gly homozygotes had a lower fat accumulation (BMI, FAT, and SF8) than Arg16Gly and Arg16Arg carriers. In response to endurance training, white women with the Arg16Arg genotype exhibited a greater reduction in BMI, FAT, and %FAT. Results observed in blacks were mostly negative. These results suggest that polymorphisms in the beta2-adrenergic receptor gene influence the amount of body fat in white obese men (Gln27Glu) and women (Arg16Gly), as well as the changes in adiposity in response to endurance training in white women (Arg16Gly).

Adipose Tissue↗

PubMed2003

Greater than predicted decrease in energy expenditure during exercise after body weight loss in obese men.

This study was performed retrospectively to investigate whether exercise energy expenditure (EE) measured during a standardized treadmill protocol (4.5 km/h at 0% grade) falls below predicted values after body weight loss in obese men. A reference equation was established to predict net exercise EE in a control sample of 83 obese individuals (27 kg/m(2)< or = body mass index <45 kg/m(2)), using age, fat mass and fat-free mass as independent variables. This equation was then used to predict net exercise EE in another group of 11 obese men before and after a 15-week drug-based weight loss programme that was coupled with energy restriction [-2929 kJ/day (-700 kcal/day)]. Body weight and body composition were determined by hydrodensitometry. Net exercise EE, insulin, leptin, 3,3',5-tri-iodothyronine and free thyroxine were measured after an overnight fast at baseline and 2-4 weeks after the end of the programme, when subjects were weight stable. Body weight was significantly reduced (-11%; P <0.01) at the end of the weight loss programme. At baseline, measured net exercise EE was similar to that predicted from the regression equation [19.6 and 19.8 kJ/min (4.69 and 4.74 kcal/min) respectively; not significant]. However, after the end of the intervention, measured net exercise EE was significantly below the predicted value [15.5 and 17.3 kJ/min (3.71 and 4.14 kcal/min) respectively; P <0.01]. The difference between the predicted and the measured fall in net exercise EE was significantly associated with changes in leptin concentration ( r =0.79, P <0.01), even after correction for changes in fat mass and insulin. These observations suggest that net exercise EE falls below predicted values after body weight loss. In addition, this greater than predicted decrease in net exercise EE was associated with changes in leptin.

Adult↗

PubMed2003

[Genetics of obesity and metabolic complications in the Quebec Family Study].

Considerable progress has been accomplished over the past 10 years in the understanding of the genetic basis of obesity and its related metabolic complications. It is now well established that obesity aggregates within families and that genes are partly responsible for this familial aggregation. The number of genes potentially involved in obesity continues to grow. This review summarizes the evidence accumulated so for regarding the contribution of genetic factors in obesity and the number of gene and loci linked to obesity in the Quebec Family Study.

Cohort Studies↗

PubMed2003

Lack of pleiotropic genetic effects between adiposity and sex hormone-binding globulin concentrations before and after 20 weeks of exercise training: the HERITAGE family study.

The relationship between sex hormone-binding globulin (SHBG) concentrations and body fat accumulation and distribution is governed by complex dynamic factors, which may involve common genetic and/or environmental factors. The current study investigated the genetic and environmental basis for the correlation between SHBG and body fat. Several measures of adiposity were investigated including body mass index (BMI) and a trunk to extremity skinfold thickness ratio (TER) assessed by anthropometry, body composition measured by hydrostatic weighing (total body fat mass [FM], fat-free mass [FFM], and percent body fat [%BF]), and abdominal fat measured by computerized tomography scanning (abdominal visceral fat [AVF]). The study comprised 501 white subjects from 99 families and 277 black subjects from 117 families participating in the HERITAGE Family Study. Familial correlations between traits and their cosegregation were investigated both at baseline and in response to endurance exercise training. Significant inverse phenotypic correlations were detected in both races between SHBG and adiposity measures at baseline and also in response to training. Significant cross-trait familial resemblance was found between SHBG and both BMI and FFM at baseline that accounted for 11% and 4% of maximal heritability, respectively, in white families. However, a joint segregation analysis of the traits failed to implicate shared genetic effects. Specifically, neither a pleiotropic major locus nor pleiotropic polygenic effects were detected between SHBG and BMI or FFM. A maximal cross-trait heritability of 45% was obtained for SHBG and TER at baseline in black families. However, no firm conclusions as to the etiology of this relationship could be drawn because of the limitations of small sample size. For the training response phenotypes, there was no significant cross-trait correlation between SHBG and any adiposity measures studied here, suggesting that their correlation may have an environmental basis. Therefore, this study fails to support the hypothesis of genetic pleiotropy between SHBG concentrations and body fat phenotypes, and suggests an environmental basis for the correlation, ie, SHBG concentrations are genetically independent of body composition and abdominal adiposity phenotypes.

Adipose Tissue↗

PubMed2003

Impact of abdominal visceral fat, growth hormone, fitness, and insulin on lipids and lipoproteins in older adults.

We examined the relationship between abdominal visceral fat (AVF) and plasma concentrations of lipids and lipoproteins in 19 females (F) (not on estrogen) and 31 males (M) over the age of 60 (age = 66.8 years). In addition, the effects of growth hormone (GH) release, fitness (Vo(2) peak), insulin, and glucose concentrations (both fasting and in response to an oral glucose tolerance test) on lipids were examined. Subjects were categorized by low (L) and high (H) AVF (L < 130 cm(2), H > 130 cm(2)), fat mass (FM) (above or below median value), and AVF corrected for fat mass. Factorial analysis of variance (ANOVA) showed that when subjects were divided by AVF and FM, similar results were observed with H > L (P <.05) for very-low-density lipoprotein-cholesterol (VLDL-C), triglycerides (TG), VLDL-TG, apolipoprotein (apo)-B, apo-B VLDL, cholesterol (Chol)/high-density lipoprotein (HDL), LDL/HDL, apoB/A1 and L > H for HDL, HDL(2), HDL(3), apo A1, and LDL/apo-B LDL. Gender differences were also observed with F > M for Chol, LDL, HDL, and HDL(2). When AVF was corrected for FM, these gender differences were still present. After correcting for FM, differences remained between H and L AVF groups for VLDL, TG, VLDL-TG, apo-B, apo-B LDL, apo-B VLDL, apoB/A1 (P <.05). Twenty-four hour integrated GH concentration (IGHC) was inversely related to VLDL, TG, VLDL TG, LDL TG, apoB, apoB VLDL, apoB LDL, Chol/HDL, LDL/HDL, and apoB/A1 in F, but not M (P <.05). Vo(2) peak was directly related to Chol, LDL, HDL(3), and apoB LDL with stronger relationships observed in F. Fasting insulin was related to lipids and lipoproteins in both men and women. These data suggest that, in older adults, elevated levels of AVF, FM, and AVF corrected for FM are associated with unfavorable lipid-lipoprotein profiles and extend similar findings reported in younger males and females with elevated AVF. These data also support previous findings indicating that AVF is a primary determinant of GH release.

Abdomen↗

PubMed2003

Genomic scan of glucose and insulin metabolism phenotypes: the HERITAGE Family Study.

Genetic factors play a role in the regulation of glucose metabolism-related traits such as insulin sensitivity (S(I)), insulin secretion, and glucose effectiveness (S(G)). Several genomic scans have been performed to localize genes involved in glucose metabolism-related traits. However, few of these studies have been performed with phenotypes derived from the frequently sampled intravenous glucose tolerance test (IVGTT) using the minimal modeling (MINMOD) approach. Here, we report on such a scan for glucose metabolism-related traits derived from MINMOD analysis of IVGTT data in 322 sibling pairs from 95 sedentary white families and 75 sibling pairs from 49 sedentary black families from the HERITAGE Family Study. In addition to S(I) and S(G), we also considered acute insulin response to a glucose challenge (AIR(Glucose)), which is an index for insulin secretion, and disposition index (DI, product of S(I) and AIR(Glucose)), which is a measure of the activity of pancreatic beta cells corrected for insulin resistance. These traits were adjusted for age, sex, and body mass index (BMI) in each of 8 sex-by-generation-by-race groups, and then standardized residuals were used as the phenotypes in the linkage analyses. Analyses were with the multipoint variance components linkage method, as implemented in the computer program SEGPATH, using 509 markers. Several regions with promising linkages (LOD score >/= 1.75, P </=.0023) were detected. They include five regions (1q41 and 8p23.2 for S(I), 4q32.1 and 10p15.3 for AIR(Glucose), and 13q32.1 for DI) in whites and 2 regions (9p11.2 for S(G) and 10q26.11 for S(I)) in blacks. Three of these regions (4q32.1, 9p11.2, 10p15.3) are likely to harbor genes that influence interindividual variation in glucose metabolism-related traits as they replicate findings from other studies. Fine mapping and association studies of candidate genes within these genomic regions are warranted.

Adolescent↗

PubMed2003

Calcium intake, body composition, and lipoprotein-lipid concentrations in adults.

BACKGROUND: Recent data suggest that variations in calcium intake may influence lipid metabolism and body composition. OBJECTIVE: The association between daily calcium intake and body composition and plasma lipoprotein-lipid concentrations was studied cross-sectionally in adults from phase 2 of the Québec Family Study. DESIGN: Adults aged 20-65 y (235 men, 235 women) were studied. Subjects who consumed vitamin or mineral supplements were excluded. Subjects were divided into 3 groups on the basis of their daily calcium intake: groups A (< 600 mg), B (600-1000 mg), and C (> 1000 mg). RESULTS: Daily calcium intake was negatively correlated with plasma LDL cholesterol, total cholesterol, and total:HDL cholesterol in women and men after adjustment for variations in body fat mass and waist circumference (P < 0.05). In women, a significantly greater ratio of total to HDL cholesterol (P < 0.05) was observed in group A than in group C after correction for body fat mass and waist circumference. In women, body weight, percentage body fat, fat mass, body mass index, waist circumference, and total abdominal adipose tissue area measured by computed tomography were significantly greater (P < 0.05) in group A than in groups B and C, even after adjustments for confounding variables. Comparable trends were observed in men, but not after adjustment for the same covariates. CONCLUSION: A low daily calcium intake is associated with greater adiposity, particularly in women. In both sexes, a high calcium intake is associated with a plasma lipoprotein-lipid profile predictive of a lower risk of coronary heart disease risk compared with a low calcium intake.

Abdomen↗

PubMed2003

Increased abdominal obesity, insulin and glucose levels in nondiabetic subjects with a T29C polymorphism of the transforming growth factor-beta1 gene.

BACKGROUND: In humans, a T-->C transition at nucleotide 29 in the region encoding the signal peptide sequence of the transforming growth factor (TGF)-beta(1), which results in a Leu-->Pro substitution at codon 10, has been associated with myocardial infarction. AIMS/METHODS: In the present study, we genotyped 284 unrelated, nondiabetic Swedish men born in 1944 to assess the impact of the Leu10Pro variant on obesity, including abdominal obesity, and estimates of insulin, glucose and lipid metabolism as well as blood pressure. RESULTS: The frequency of the Pro10 variant was 38.9% (95% CI 32.2-46.0%), and the distribution of genotypes was in Hardy-Weinberg equilibrium. Data analysis showed that heterozygotes had significantly higher body mass index compared to homozygous carriers to the Leu10 variant. In addition, homozygous carriers of the Leu10 variant had significantly lower abdominal sagittal diameter than both Leu10Pro and Pro10Pro carriers. We also found that heterozygotes had significantly higher fasting insulin values as well as higher HOMA insulin-resistance index in comparison to homozygous carriers of the Leu10. Fasting glucose levels were significantly higher in subjects with the Pro10Pro variant compared to subjects with either the Leu10Leu or Leu10Pro variant. CONCLUSION: These findings suggest that the Pro10 allele in the TGF-beta(1) gene pathway might contribute to prevalent diseases such as obesity and type 2 diabetes mellitus.

Abdomen↗

PubMed2003

Long-term adiposity changes are related to a glucocorticoid receptor polymorphism in young females.

Male and female preadolescents and adolescents who participated in phase 1 of the Québec Family Study, and who were retested about 12 yr later, were recruited and subdivided on the basis of a genetic variant within the intron 2 of the glucocorticoid receptor (GRL IVS2-BclI). The increase in sc adiposity over the 12-yr follow-up period in the 4.5/2.3 genotype female subgroup was more than twice that observed in the 4.5/4.5 and the 2.3/2.3 genotype subgroups (P < 0.01). The statistical significance of this difference was essentially unchanged after adjusting for changes, over time, in percent dietary energy as fat, alcohol consumption, and participation in vigorous physical activity. In male subjects, the same trend was found, but it did not reach statistical significance. In conclusion, this study suggests that a significant interaction effect exists between variation in the glucocorticoid receptor gene and body fat gain in female subjects experiencing the transition between adolescence and adulthood. Further research will, however, be necessary to characterize the lifestyle factors promoting fat accumulation, over time, among genetically susceptible individuals.

Adipose Tissue↗

PubMed2003

Genome-wide linkage scan for the metabolic syndrome in the HERITAGE Family Study.

The metabolic syndrome involves multiple and interactive effects of genes and environmental factors. To identify chromosomal regions encoding genes possibly predisposing to the metabolic syndrome, we performed a genome-wide scan with 456 white and 217 black participants from 204 nuclear families of the HERITAGE Family Study, using regression-based, single- and multipoint linkage analyses on 509 markers. A principal component analysis was performed on 7 metabolic syndrome-related phenotypes. Two principal components, PC1 and PC2 (55% of the variance), were used as metabolic syndrome phenotypes. ANOVA was used to quantify the familial aggregation of PC1 and PC2. Family membership contributed significantly (P < 0.0023) to the variance in PC1 (r(2) = 0.38 in whites; r(2) = 0.55 in blacks) and PC2 (r(2) = 0.51; r(2) = 0.48). In whites, promising evidence for linkage (P < 0.0023) was found for PC1 (2 markers on 10p11.2) and PC2 (a marker on 19q13.4). Suggestive evidence of linkage (0.01 > P > 0.0023) appeared for PC1 (1q41 and 9p13.1) and PC2 (2p22.3). In blacks, promising linkage was found for PC2 on 1p34.1, and suggestive linkage was found on 7q31.3 and 9q21.1. The genome-wide scan revealed evidence for quantitative trait loci on chromosomal regions that have been previously linked with individual cardiovascular disease and type 2 diabetes risk factors. Some of these chromosomal regions harbor promising potential candidate genes.

Adolescent↗

PubMed2003

Genome-wide linkage scan for physical activity levels in the Quebec Family study.

PURPOSE AND METHODS: It is commonly recognized that there is familial aggregation for physical activity level. However, the genes and sequence variants responsible for the familial clustering have not been investigated. We performed a genome-wide linkage scan based on 432 markers typed in 767 subjects from 207 families of the Quebec Family study with the aim of identifying loci affecting physical activity levels. Four physical activity level phenotypes were used. RESULTS: Promising evidence of linkage (P < 0.0023) was found for physical inactivity on chromosome 2p22-p16. Suggestive linkages (0.0023<P < 0.01) were found for inactivity (7p11.2, 20q13.1), total physical activity (13q22-q31), moderate to strenuous physical activity (4q28.2, 7p11.2, 9q31.1, 13q22-q31), and time spent in physical activity (11p15 and 15q13.3). CONCLUSION: This study identified several chromosomal regions harboring genes that may contribute to the propensity to be physically active or sedentary.

Adult↗

PubMed2003

The human gene map for performance and health-related fitness phenotypes: the 2002 update.

This review presents the 2002 update of the human gene map for physical performance and health-related phenotypes. It is based on peer-reviewed papers published by the end of 2002 and includes association studies with candidate genes, genome-wide scans with polymorphic markers, and single gene defects causing exercise intolerance to variable degrees. The genes and markers with evidence of association or linkage with a performance or fitness phenotype in sedentary or active people, in adaptation to acute exercise, or for training-induced changes are positioned on the genetic map of all autosomes and the X chromosome. Negative studies are reviewed, but a gene or locus must be supported by at least one positive study before being inserted on the map. By the end of 2000, 29 loci were depicted on the map. The 2001 map includes 71 loci on the autosomes and two on the X chromosome. In contrast, the 2002 human gene map for physical performance and health-related phenotypes includes 90 gene entries and QTL, plus two on the X chromosome. To all these loci, one must add 14 mitochondrial genes in which sequence variants have been shown to influence relevant fitness and performance phenotypes.

Anthropometry↗

PubMed2003

Familial resemblance for muscle phenotypes in the HERITAGE Family Study.

INTRODUCTION/PURPOSE: We hypothesized that skeletal muscle histological and biochemical phenotypes aggregate within families. METHODS: Nineteen families (78 Caucasians) from the HERITAGE Family Study participated in the study. Proportions and areas of Type I, IIA, and IIX muscle fibers, capillary density, and maximal enzyme activities were determined in biopsy samples from the vastus lateralis obtained in the sedentary state and after a 20-wk endurance-training program. RESULTS: In the sedentary state, there was evidence for familial resemblance for Type I fiber area (P = 0.007), number of capillaries around Type I and Type IIA fibers (P = 0.04), and Type I and IIA fiber areas per capillary (P = 0.01 and P = 0.04, respectively). Significant familial aggregation (0.05>P > 0.0001) was observed for maximal activities of enzymes of the energy production pathways. With regard to the training response, significant familial aggregation (0.05 > P < 0.0001) was observed for maximal activities of enzymes of the energy production pathways. CONCLUSION: These data provide evidence of familial aggregation for enzyme activities of the main energy metabolism pathways of the skeletal muscle in the sedentary state and in response to regular exercise.

Adaptation, Physiological↗

PubMed2003

Targeting the metabolic syndrome with exercise: evidence from the HERITAGE Family Study.

PURPOSE: To determine the efficacy of exercise training in treating the metabolic syndrome. METHODS: The sample included 621 black and white participants from the HERITAGE Family Study, identified as sedentary and apparently healthy (no chronic disease or injury). The metabolic syndrome was defined as having three or more risk factors according to the guidelines of the National Cholesterol Education Program, including elevated waist circumference, blood pressure, triglycerides, blood glucose, and low HDL cholesterol. The presence of the metabolic syndrome and component risk factors were determined before and after 20 wk of supervised aerobic exercise training. RESULTS: The prevalence of the metabolic syndrome was 16.9% in this sample (105/621) of apparently healthy participants. Of the 105 participants with the metabolic syndrome at baseline, 30.5% (32 participants) were no longer classified as having the metabolic syndrome after the exercise training. Among the 32 participants who improved their metabolic profile, 43% decreased triglycerides, 16% improved HDL cholesterol, 38% decreased blood pressure, 9% improved fasting plasma glucose, and 28% decreased their waist circumference. There were no sex or race differences in the efficacy of exercise in treating the metabolic syndrome: 32.7% of men, 28.0% of women, 29.7% of black, and 30.9% of white participants with the metabolic syndrome were no longer classified as having the syndrome after training. CONCLUSION: Aerobic exercise training in patients with the metabolic syndrome can be useful as a treatment strategy and provides support for a role for physical activity in the prevention of chronic disease.

Adult↗

PubMed2003

Heart rate versus %VO2max: age, sex, race, initial fitness, and training response--HERITAGE.

PURPOSE: In the HERITAGE Family Study, heart rate (HR) associated with various percentages of maximal oxygen intake (VO2max) was used to prescribe exercise intensity. When fitness improved, HR at the same power output (PO) decreased, and PO was increased to produce the prescribed HR. Although we assumed that subjects were again working at the same %VO2max, there were no studies with a large heterogeneous population to determine whether this was correct. METHODS: Therefore, 653 subjects with complete data were classified by age, sex, race, initial VO2max, and VO2max response after 20 wk of training. RESULTS: All groups had a significant increase in VO2max and a significant decrease in HR at the same absolute PO after training but no difference in HR at the same relative intensity. CONCLUSIONS: Training does not affect HR at a given %VO2max in a heterogeneous population of men and women, blacks and whites aged 17-65 yr with different initial VO2max values and different responses to training.

Adolescent↗