A Genome Scan for Loci Associated with Aerobic Running Capacity in Rats

Ways, Justin A.; Cicila, George T.; Garrett, Michael R.; Koch, Lauren G.

doi:10.1006/geno.2002.6797

Cited by 32 publications

(45 citation statements)

References 44 publications

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“…Although our sample size was relatively small, our observed effect size was large as there was a 12.9-fold difference in maximal exercise endurance between the two selectively genotyped groups. In addition, the homology of our QTLs with those reported by Ways et al (36) and Bouchard and colleagues (4) further strengthens the validity of our QTLs. As noted in the consensus statement by the Complex Trait Consortium, "there is no single 'gold standard' for the identification of a QTL.…”

Section: Discussionsupporting

confidence: 88%

“…For example, there has been much investigation regarding the role of angiotensin-converting enzyme (ACE) genes (14), mitochondria synthesis genes (38), and the peroxisome proliferatoractivated receptor (PPAR) genes (12) in regulating exercise endurance. These genes (ACE, PPAR, and mitochondrial synthesis) are not found in QTL regions thus far associated with exercise endurance in humans (4,33), rats (36), or mice (present study). Since most investigators agree that the heritable regulation of maximal exercise endurance is likely polygenic, it is probable that genes within and external to the identified QTLs participate in this system.…”

Section: Discussioncontrasting

confidence: 53%

“…Due to the multifactorial nature of exercise endurance control and because the number of genes located in each QTL region is large, candidate gene lists generated from any species are often quite lengthy (see discussion in Refs. 4,32,36). Similarly, a large number of candidate genes that could be involved in the regulation of maximal exercise endurance are located within 15 cM of the QTLs identified in this study; however, discussion of any of these "candidate genes" from the genes located within the identified QTL without further corroborating evidence such as microarray results would be speculative at best.…”

Section: Discussionmentioning

confidence: 71%

“…The treadmill test was stopped when the mouse could not get off the shock grid within 3 s, and exercise endurance was estimated by total time that the mouse ran. This indirect measure of exercise endurance has been used as a phenotype in other rodent genetic studies (1,6,18,26,36), and running speed has been positively correlated with oxygen consumption in mice (13).…”

Section: Estimation Of Exercise Endurancementioning

confidence: 99%

“…Two separate human studies by Bouchard and colleagues (4,33) have identified possible genetic linkages with sedentary aerobic capacity on chromosomes 4,8,11, and 14 in a white population and on chromosomes 1 and 7 in a black population. Ways et al (36) identified a significant QTL linked with aerobic running capacity on rat chromosome 16 and suggestive linkage on chromosome 3. Given the health implications of understanding the genetic regulation of a complex trait such as maximal exercise endurance, it is important that additional research be conducted in species that will allow the use of more powerful genetic tools.…”

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confidence: 99%

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Quantitative trait loci associated with maximal exercise endurance in mice

Lightfoot¹,

Turner²,

Knab³

et al. 2007

Journal of Applied Physiology

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Lightfoot JT, Turner MJ, Knab AK, Jedlicka AE, Oshimura T, Marzec J, Gladwell W, Leamy LJ, Kleeberger SR. Quantitative trait loci associated with maximal exercise endurance in mice. J Appl Physiol 103: 105-110, 2007. First published April 5, 2007 doi:10.1152/japplphysiol.01328.2006.-The role of genetics in the determination of maximal exercise endurance is unclear. Six-to nine-week-old F2 mice (n ϭ 99; 60 female, 39 male), derived from an intercross of two inbred strains that had previously been phenotyped as having high maximal exercise endurance (Balb/cJ) and low maximal exercise endurance (DBA/2J), were treadmill tested to estimate exercise endurance. Selective genotyping of the F2 cohort (n ϭ 12 high exercise endurance; n ϭ 12 low exercise endurance) identified a significant quantitative trait locus (QTL) on chromosome X (53.7 cM, DXMit121) in the entire cohort and a suggestive QTL on chromosome 8 (36.1 cM, D8Mit359) in the female mice. Fine mapping with the entire F2 cohort and additional informative markers confirmed and narrowed the QTLs. The chromosome 8 QTL (EE8 F ) is homologous with two suggestive human QTLs and one significant rat QTL previously linked with exercise endurance. No effect of sex (P ϭ 0.33) or body weight (P ϭ 0.79) on exercise endurance was found in the F 2 cohort. These data indicate that genetic factors in distinct chromosomal regions may affect maximal exercise endurance in the inbred mouse. Whereas multiple genes are located in the identified QTL that could functionally affect exercise endurance, this study serves as a foundation for further investigations delineating the identity of genetic factors influencing maximum exercise endurance. candidate genes; aerobic capacity; genotyping SEVERAL RECENT STUDIES have shown that the maximal exercise endurance of an individual can impact all-cause mortality rates (31), mortality rates from hypertension (7), smoking-related and non-smoking-related cancers (21), and stroke (22). A tremendous amount of research has considered the modifying role of environmental factors on maximal aerobic exercise (e.g., training). It is well accepted that the variation seen in human maximal exercise endurance is due to the influence of genetic factors (3), and current estimations of the contribution of genetics to maximal exercise endurance range from Ϸ51% in humans (3) to 58 -90% in mice (23, 26) to 39% in rats (18).

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Section: Discussionsupporting

confidence: 88%

Section: Discussioncontrasting

confidence: 53%

Section: Discussionmentioning

confidence: 71%

Section: Estimation Of Exercise Endurancementioning

confidence: 99%

mentioning

confidence: 99%

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Quantitative trait loci associated with maximal exercise endurance in mice

Lightfoot¹,

Turner²,

Knab³

et al. 2007

Journal of Applied Physiology

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Genomics and Genetics in the Biology of Adaptation to Exercise

Bouchard¹,

Rankinen²,

Timmons³

2011

Comprehensive Physiology

158

132

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This chapter is devoted to the role of genetic variation and gene-exercise interactions in the biology of adaptation to exercise. There is evidence from genetic epidemiology research that DNA sequence differences contribute to human variation in physical activity level, cardiorespiratory fitness in the untrained state, cardiovascular and metabolic response to acute exercise, and responsiveness to regular exercise. Methodological and technological advances have made it possible to undertake the molecular dissection of the genetic component of complex, multifactorial traits, such as those of interest to exercise biology, in terms of tissue expression profile, genes, and allelic variants. The evidence from animal models and human studies is considered. Data on candidate genes, genome-wide linkage results, genome-wide association findings, expression arrays, and combinations of these approaches are reviewed. Combining transcriptomic and genomic technologies has been shown to be more powerful as evidenced by the development of a recent molecular predictor of the ability to increase VO2max with exercise training. For exercise as a behavior and physiological fitness as a state to be major players in public health policies will require that that the role of human individuality and the influence of DNA sequence differences be understood. Likewise, progress in the use of exercise in therapeutic medicine will depend to a large extent on our ability to identify the favorable responders for given physiological properties to a given exercise regimen.

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