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.
"The bulk of these studies have attempted to explain low exercise prevalence in terms of social and environmental barriers. These include, amongst others, poor access to facilities (Matson-Koffman, Brownstein, Neiner, & Greaney, 2005; Varo et al., 2003), low socioeconomic status (Haase et al., 2004; Varo et al., 2003), non-Caucasian race (Kaplan, Lazarus, Cohen, & Leu, 1991), high job strain (Payne, Jones, & Harris, 2005; Van Loon, Tijhuis, Surtees, & Ormel, 2000), subjective " lack of time " "
[Show abstract][Hide abstract] ABSTRACT: A sedentary lifestyle has been cited as one of the main causes of the explosive rise in obesity that starts at an increasingly
younger age(Martinez-Gonzalez, Martinez, Hu, Gibney, & Kearney, 1999). Furthermore, regular exercisers have lower risks for
cardiovascular disease (CVD) and type 2 diabetes than non-exercisers (Albright et al., 2000; Kaplan, Strawbridge, Cohen, &
Hungerford, 1996; Kesaniemi et al., 2001) and the percentage of people at risk because of inactivity is higher than for hypertension,
smoking, and cholesterol (Caspersen, 1987; Stephens & Craig, 1990). Despite these well-documented benefits of exercise, a
large proportion of adults in the Western world do not exercise on a regular basis (Crespo, Keteyian, Heath, & Sempos, 1996;
Haase, Steptoe, Sallis, & Wardle, 2004; Stephens & Craig, 1990). As a consequence, a sedentary lifestyle – and the accompanying
risk for obesity – remains a major threat to health in today’s society. This is reflected in public health recommendations
which unanimously include an encouragement to a more active lifestyle (WHO/FIMS Committee on Physical Activity for Health,
1995; U.S. Department of Health and Human Services, 2005).
"First, we observed modest to strong evidence of heritability for several Echo, ETT and BA function traits, underscoring the contribution of additive genetic effects to interindividual variation in these traits. Our heritability findings confirm prior reports for some of the traits [18,20,22,23,27,28,52], including from our group [14,24]. Second, notwithstanding the modest-to-high heritability, none of the SNP-trait associations we observed achieved genome-wide significance (conservative Bonferroni correction p of 5*10-8). "
[Show abstract][Hide abstract] ABSTRACT: Echocardiographic left ventricular (LV) measurements, exercise responses to standardized treadmill test (ETT) and brachial artery (BA) vascular function are heritable traits that are associated with cardiovascular disease risk. We conducted a genome-wide association study (GWAS) in the community-based Framingham Heart Study.
We estimated multivariable-adjusted residuals for quantitative echocardiography, ETT and BA function traits. Echocardiography residuals were averaged across 4 examinations and included LV mass, diastolic and systolic dimensions, wall thickness, fractional shortening, left atrial and aortic root size. ETT measures (single exam) included systolic blood pressure and heart rate responses during exercise stage 2, and at 3 minutes post-exercise. BA measures (single exam) included vessel diameter, flow-mediated dilation (FMD), and baseline and hyperemic flow responses. Generalized estimating equations (GEE), family-based association tests (FBAT) and variance-components linkage were used to relate multivariable-adjusted trait residuals to 70,987 SNPs (Human 100K GeneChip, Affymetrix) restricted to autosomal SNPs with minor allele frequency > or =0.10, genotype call rate > or =0.80, and Hardy-Weinberg equilibrium p > or = 0.001.
We summarize results from 17 traits in up to 1238 related middle-aged to elderly men and women. Results of all association and linkage analyses are web-posted at http://ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?id=phs000007 webcite. We confirmed modest-to-strong heritabilities (estimates 0.30-0.52) for several Echo, ETT and BA function traits. Overall, p < 10(-5) in either GEE or FBAT models were observed for 21 SNPs (nine for echocardiography, eleven for ETT and one for BA function). The top SNPs associated were (GEE results): LV diastolic dimension, rs1379659 (SLIT2, p = 1.17*10(-7)); LV systolic dimension, rs10504543 (KCNB2, p = 5.18*10(-6)); LV mass, rs10498091 (p = 5.68*10(-6)); Left atrial size, rs1935881 (FAM5C, p = 6.56*10(-6)); exercise heart rate, rs6847149 (NOLA1, p = 2.74*10(-6)); exercise systolic blood pressure, rs2553268 (WRN, p = 6.3*10(-6)); BA baseline flow, rs3814219 (OBFC1, 9.48*10(-7)), and FMD, rs4148686 (CFTR, p = 1.13*10(-5)). Several SNPs are reasonable biological candidates, with some being related to multiple traits suggesting pleiotropy. The peak LOD score was for LV mass (4.38; chromosome 5); the 1.5 LOD support interval included NRG2.
In hypothesis-generating GWAS of echocardiography, ETT and BA vascular function in a moderate-sized community-based sample, we identified several SNPs that are candidates for replication attempts and we provide a web-based GWAS resource for the research community.
"Much of this data comes from the HERITAGE (health, risk factors, exercise training and genetics) Family Study of 130 two-generation families who were assessed in the sedentary state and in response to a standardised 20-week aerobic exercisetraining program (Bouchard et al. 1995). Heritability ranged from 20% to 75% for a number of factors, including maximal oxygen uptake in the sedentary state (Bouchard et al. 1998) and in response to training (Bouchard et al. 1999), oxygen consumption and power output during submaximal exercise (Pe´russe et al. 2001), oxygen uptake at the ventilatory threshold (Gaskill et al. 2001), stroke volume and cardiac output during submaximal exercise (An et al. 2000) and the exercise heart rate response to training (An et al. 2003c). Significant genetic influences have also been identified for measures of skeletal muscle strength and performance , including the response of oxoglutarate dehydrogenase activity to training (Thibault et al. 1986), muscle adaptation to endurance exercise (Hamel et al. 1986), vertical jump height as a measure of explosive power (Maes et al. 1996), various measures of muscle strength and their response to training (Thomis et al. 1998), anaerobic capacity and explosive power (Calvo et al. 2002), average size of type I (slow oxidative) fibres in the sedentary state and maximal activity of energy production enzymes both in the sedentary state and in response to training (Rico-Sanz et al. 2003b). "
[Show abstract][Hide abstract] ABSTRACT: Physical fitness is a complex phenotype influenced by a myriad of environmental and genetic factors, and variation in human physical performance and athletic ability has long been recognised as having a strong heritable component. Recently, the development of technology for rapid DNA sequencing and genotyping has allowed the identification of some of the individual genetic variations that contribute to athletic performance. This review will examine the evidence that has accumulated over the last three decades for a strong genetic influence on human physical performance, with an emphasis on two sets of physical traits, viz. cardiorespiratory and skeletal muscle function, which are particularly important for performance in a variety of sports. We will then review recent studies that have identified individual genetic variants associated with variation in these traits and the polymorphisms that have been directly associated with elite athlete status. Finally, we explore the scientific implications of our rapidly growing understanding of the genetic basis of variation in performance.
Human Genetics 05/2005; 116(5):331-9. DOI:10.1007/s00439-005-1261-8 · 4.82 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.