Publications

There is evidence from human twin and family studies as well as mouse and rat selection experiments that there are considerable interindividual differences in the response of cardiorespiratory fitness (CRF) and other cardiometabolic traits to a given exercise programme dose. We developed this consensus statement on exercise response variability following a symposium dedicated to this topic. There is strong evidence from both animal and human studies that exercise training doses lead to variable responses. A genetic component contributes to exercise training response variability. In this consensus statement, we (1) briefly review the literature on exercise response variability and the various sources of variations in CRF response to an exercise programme, (2) introduce the key research designs and corresponding statistical models with an emphasis on randomised controlled designs with or without multiple pretests and post-tests, crossover designs and repeated measures designs, (3) discuss advantages and disadvantages of multiple methods of categorising exercise response levels—a topic that is of particular interest for personalised exercise medicine and (4) outline approaches that may identify determinants and modifiers of CRF exercise response. We also summarise gaps in knowledge and recommend future research to better understand exercise response variability.

No abstract is provided for this article.

Objectives: Examine the reproducibility of plasma lipid and lipoprotein measurements in the HERITAGE Family Study. Design and Methods: In a sample of 379 subjects (191 men and 188 women), reproducibility was determined for lipids, lipoproteins (done on two occasions) and post-heparin lipase assays using an Intracenter Quality Control study by generating split samples from an additional 60 subjects (35 men and 25 women), which were assayed in a blind fashion by the lipid core laboratory. Reproducibility was estimated using intraclass correlation coefficients (ICC) for the selected variables. Analytical error (ANER) and coefficient of variation (CV) were also calculated. Day-to-day variation for 10 variables including plasma cholesterol and triglycerides (TG), HDL-cholesterol and its subfractions HDL2-cholesterol and HDL3-cholesterol, LDL-cholesterol and VLDL-cholesterol, as well as apoprotein (apo) A-I, apo B, and LDL-apo B were assessed. Results: In the HERITAGE study, all lipid and lipoprotein variables had ICC above 0.79. Plasma VLDL-cholesterol (31%) and TG (23%) levels, which are well known to be highly variable from one day to another, had CVs greater than 20%. Other variables had CVs lower than 10% except for HDL2-cholesterol which reached 16%. In the intracenter reliability sub-study, the measurement errors were found to be low except for HDL2-cholesterol. For the lipases, the reproducibility of repeated samples was very high, with ICC over 0.95. The within-assay CV corresponded to 2.1 and 5.3% for hepatic lipase (HL) and lipoprotein lipase (LPL), respectively, whereas the between-assay CV reached 8–12% for HL and about 15% for LPL. Due to the complexity of these two assays, the results are considered to be quite satisfactory. Conclusions: The reproducibility of plasma lipid and lipoprotein measurements, as well as of post-heparin lipase activities, is good in the multicenter HERITAGE Family Study. In addition, the well-documented gender difference in the plasma lipoprotein profile was confirmed in the present study, women having lower fasting triglyceride and LDL-cholesterol levels than men as well as reduced cholesterol/HDL-cholesterol and increased HDL2-cholesterol/HDL3-cholesterol ratios compared to men. Results of the present study support the notion that the higher LPL and low HL activities found in women compared to men are important factors contributing to explain gender difference in the lipoprotein profile. However, additional factors not examined in the present study are involved beyond the contribution of post-heparin lipase to the sex dimorphism in plasma lipoprotein levels.

Objective : It is commonly recognized that genetic, environmental, behavioral, and social factors are involved in the development of obesity. The family environment may play a key role in shaping children's eating behaviors. The purpose of this study was to estimate the degree of familial resemblance in eating behavioral traits (cognitive dietary restraint, disinhibition, and susceptibility to hunger). Research Methods and Procedures : Eating behavioral traits were assessed with the Three‐Factor Eating Questionnaire in 282 men and 402 women (202 families) from the Quebec Family Study. Familial resemblance for each trait (adjusted for age, sex, and BMI) was investigated using a familial correlation model. Results : The pattern of familial correlation showed significant spouse correlation for the three eating behavior phenotypes, as well as significant parent‐offspring and sibling correlations for disinhibition and susceptibility to hunger. According to the most parsimonious model, generalized heritability estimates (including genetic and shared familial environmental effects) reached 6%, 18%, and 28% for cognitive dietary restraint, disinhibition, and susceptibility to hunger, respectively. Discussion : These results suggest that there is a significant familial component to eating behavioral traits but that the additive genetic component appears to be small, with generalized heritability estimates ranging from 6% to 28%. Thus, non‐familial environmental factors and gene‐gene and gene‐environmental interactions seem to be the major determinants of the eating/behavioral traits.

The small, dense LDL phenotype is associated with an increased cardiovascular disease risk. A genome-wide scan performed on 236 nuclear families of the Quebec Family Study (QFS) revealed a quantitative trait locus affecting LDL peak particle diameter (LDL-PPD) and density on the 1p31 region. This region contains the low-density lipoprotein receptor-related protein 8 (LRP8) gene. LRP8, a receptor for apolipoprotein (apo) E, modulates apoE levels, thus contributing to plasma cholesterol and triglyceride (TG) concentrations. We investigate the effects of LRP8 polymorphisms on LDL-PPD, on the relative proportion of small LDL (<255Å) and the absolute concentration of cholesterol among the small LDL particles. LRP8 rs5174 was associated with LDL-PPD and estimated cholesterol concentrations in the small LDL particles adjusted for the effects of age and sex (p =0.008, p =0.04, respectively). LRP8 rs3820198 was associated with total and LDL-cholesterol levels as well as with apoB concentrations adjusted for the effects of age and sex (p =0.005, p =0.004 and p =0.01, respectively) but not with LDL size-related variables. These results suggest that LRP8 gene polymorphisms influence plasma cholesterol levels as well as size and composition of LDL particles.

PURPOSE: We examined the hypothesis of association between the ACE insertion/deletion genotype and endurance performance level in Mexican marathon runners. METHODS: DNA samples were available from 256 (men n = 166; women n = 90) marathon runners who had completed at least two 42 Km road races. Cases; CAS (n=88; men=63; women=25) were finishers in the top 3rd %ile, while controls; CON (n=168; men=103; women=65) were those in the lowest 3rd %ile of their respective age and gender. The DNA sequence variation was detected by the tetra-primer ARMS-PCR procedure. Genotypes were determined by PCR product size. RESULTS: The three expected ACE genotypes were observed in both groups (CON: DD = 20%. ID = 41%, II = 39%; and CAS: DD = 28%, ID =41%, II = 31%). These genotype frequencies were in Hardy-Weinberg equilibrium (X2 P>0.05) and were not significantly (X2 P>0.05) different between genders or groups. Allelic frequencies (CON; D = 0.41%, I = 0.59% and CAS; D = 0.48, I = 0.51) were not significantly (X2 P>0.05) different between groups or genders. Comparing genotype frequencies by I or D allele carrier status revealed no statistically significant (X2 P≥0.05) differences. CONCLUSIONS: We found no support for the hypothesis of association between the ACE I/D polymorphism and endurance performance level status in our homogeneous cohort of Mexican marathon runners.

There is evidence linking intrauterine growth retardation with increased cardiovascular risk and diabetes mellitus (DM) later in life. However, little is known about the association between malnutrition during the first year of life and metabolic abnormalities in adulthood. The objective of this study was to assess the effect of documented malnutrition during the first year of life on glucose tolerance, plasma insulin, lipid profile, and blood pressure in early adulthood, as well as to assess the interaction between body mass index (BMI) and malnutrition on these variables. A study group of young men with a documented history of malnutrition during their first year of life was recruited from 4 pediatric hospitals in Mexico City and compared with a control group. Subjects included were 52 men, aged 20.2 ± 3.6 years, with a mean birth weight of 3.0 ± 0.7 kg and documented malnutrition in their first year of life; controls were 50 men, aged 23.3 ± 1.8 years, with a mean birth weight of 3.2 ± 0.5 kg. Insulin and glucose concentrations, fasting and in response to an oral glucose load, plasma lipids, blood pressure, and an insulin sensitivity index (ISI) were measured. The areas under the curves of glucose (AUCG) and insulin (AUCI) were significantly higher in cases ( P = .012 and < .002, respectively), independent of birth weight, BMI, or age. BMI was significantly associated with fasting plasma insulin (FPI), AUCI, ISI, triglyceride, and high-density lipoprotein (HDL)-cholesterol concentrations in cases, but not in controls. These data suggest that early malnutrition in extrauterine life, independently of birth weight, has an adverse effect on insulin metabolism and glucose tolerance in young men, and it worsens as body mass increases even within the normal range of BMI. Therefore, it is advisable to prevent obesity in individuals exposed to early malnutrition.

No abstract is provided for this article.

No abstract is provided for this article.

No abstract is provided for this article.

No abstract is provided for this article.