Quantitative trait loci associated with maximal exercise endurance in mice

Lightfoot, J. Timothy; Turner, Michael J.; Knab, Amy Kleinfehn; Jedlicka, Anne; Oshimura, Tomohiro; Marzec, Jacqui; Gladwell, Wesley; Leamy, Larry J.; Kleeberger, Steven R.

doi:10.1152/japplphysiol.01328.2006

Cited by 26 publications

(33 citation statements)

References 39 publications

(53 reference statements)

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“…A significant QTL was identified on chromosome 16 (D16Rat17), and two suggestive QTL localized to chromosomes 3 (D3Rat56) and 16 (D16Rat55). The two QTL on rat chromosome 16 are homologous to regions of mouse chromosome 8, overlapping with QTL reported in the present study (pretraining work) and by Lightfoot et al (37) (Supplemental Fig. S1).…”

Section: Discussionsupporting

confidence: 90%

“…In addition, the finding that there is some overlap of QTL for intrinsic exercise capacity in independent crosses (present study and Ref. 37) as well as the agreement across mouse, rat, and human studies for exercise and exercise training QTL (Supplemental Fig. S1) support the validity of the QTL identified in the present study (1).…”

Section: Discussionsupporting

confidence: 84%

“…Previous studies in mice, rats, and humans demonstrated that intrinsic exercise capacity is determined, in part, by genetic factors (13,37,53,65). In the present study, 1 The online version of this article contains supplemental material.…”

Section: Discussionmentioning

confidence: 49%

“…2; Table 2). These QTL are designated as endurance exercise QTL 3 and 4 (Eeq3 and Eeq4), respectively, because QTL for a similar phenotype in mice have been designated as Eeq1 and Eeq2 (37). Suggestive QTL were identified on chromosomes 1, 2, 3, and 8, with the QTL on chromosome 8 surpassing a LOD score of 3.0.…”

Section: Exercise Capacity In Parental Strains and (Fvbmentioning

confidence: 99%

“…Using a similar protocol, Lightfoot et al (36) also found that B6 mice had relatively low intrinsic exercise capacity, whereas Balb/cJ mice had high intrinsic exercise capacity. Given these strain-dependent differences, quantitative trait locus (QTL) mapping has been used to identify QTL for intrinsic exercise capacity in rats and mice (37,65). In contrast, less is known about the change in exercise capacity with training across inbred strains of rodents (30,42,63).…”

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confidence: 99%

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Quantitative trait loci for exercise training responses in FVB/NJ and C57BL/6J mice

Massett

Fan

Berk

2009

Physiological Genomics

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Massett MP, Fan R, Berk BC. Quantitative trait loci for exercise training responses in FVB/NJ and C57BL/6J mice. Physiol Genomics 40: 15-22, 2009. First published September 29, 2009 doi:10.1152/physiolgenomics.00116.2009.-The genetic factors determining the magnitude of the response to exercise training are poorly understood. The aim of this study was to identify quantitative trait loci (QTL) associated with adaptation to exercise training in a cross between FVB/NJ (FVB) and C57BL/6J (B6) mice. Mice completed an exercise performance test before and after a 4-wk treadmill running program, and changes in exercise capacity, expressed as work (kg ⅐ m), were calculated. Changes in work in F2 mice averaged 1.51 Ϯ 0.08 kg ⅐ m (94.3 Ϯ 7.3%), with a range of Ϫ1.67 to ϩ4.55 kg ⅐ m. All F2 mice (n ϭ 188) were genotyped at 20-cM intervals with 103 single nucleotide polymorphisms (SNPs), and genomewide linkage scans were performed for pretraining, posttraining, and change in work. Significant QTL for pretraining work were located on chromosomes 14 at 4.0 cM [3.72 logarithm of odds (LOD)] and 19 at 34.4 cM (3.63 LOD). For posttraining work significant QTL were located on chromosomes 3 at 60 cM (4.66 LOD) and 14 at 26 cM (4.99 LOD). Suggestive QTL for changes in work were found on chromosomes 11 at 44.6 cM (2.30 LOD) and 14 at 36 cM (2.25 LOD). When pretraining work was used as a covariate, a potential QTL for change in work was identified on chromosome 6 at 68 cM (3.56 LOD). These data indicate that one or more QTL determine exercise capacity and training responses in mice. Furthermore, these data suggest that the genes that determine pretraining work and training responses may differ. treadmill running; genetic factors LOW EXERCISE CAPACITY or cardiorespiratory fitness is comparable to elevated systolic blood pressure, obesity, diabetes, and smoking as a risk factor and predictor of future disease (33,47). Improving cardiorespiratory fitness through increased physical activity can significantly reduce the risk of all-cause mortality (8), regardless of the level of initial fitness (22). However, there is a high degree of individual variation in the responses to exercise training. For example, there are some individuals who might not show an increase in maximal oxygen consumption (V O 2max ) in response to endurance training (9, 12). Consequently, identifying the genetic factors modulating the adaptations to exercise may provide insight into individual differences in responses to training. However, the genetic factors determining the magnitude of the response to exercise are poorly understood.Initial studies investigating the genetic basis for exercise capacity and training responses focused on familial resemblance and heritability of performance phenotypes. Results from cross-sectional, twin, and prospective studies indicate that the heritability for training-induced changes in V O 2max and submaximal power output ranges from 25% to 50% (11). Heritability estimates from family studies also vary between 25% and 50%, depending...

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 49%

Section: Exercise Capacity In Parental Strains and (Fvbmentioning

confidence: 99%

mentioning

confidence: 99%

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Quantitative trait loci for exercise training responses in FVB/NJ and C57BL/6J mice

Massett

Fan

Berk

2009

Physiological Genomics

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Genomics and Genetics in the Biology of Adaptation to Exercise

Bouchard¹,

Rankinen²,

Timmons³

2011

Comprehensive Physiology

149

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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