Selected Contribution: Variation and heritability for  the adaptational response to exercise  in genetically heterogeneous rats

Troxell, Michael Lee; Britton, Steven L.; Koch, Lauren G.

doi:10.1152/japplphysiol.00851.2002

Cited by 24 publications

(26 citation statements)

References 27 publications

(42 reference statements)

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“…To our knowledge, a standardized or commonly accepted method of progressive overload, which takes into account these key considerations, is currently unavailable. Previous investigations that have described a progressive overload have typically done so by increasing a combination of treadmill speed, incline, and exercise duration (Powers et al 1990;Criswell et al 1993;Mokelke et al 1997;Eddington et al 1998;Fiebig et al 1998;Demirel et al 1999;Noble et al 1999;Braga et al 2000;González et al 2000;Machida et al 2000;Jew and Moore 2002;Troxell et al 2003;Jafari et al 2005;Peres et al 2005;Ghanbari-Niaki 2006;Mueller and Hasser 2006;Yang et al 2006;Ghanbari-Niaki et al 2007;Leandro et al 2007;Mueller 2007;Harris et al 2008;Vichaiwong et al 2009;Eynan et al 2010). However, the descriptions of the increases in intensity or duration have often not been implemented in a systematic or standardized way, and as such a dose-response relationship cannot be discerned.…”

Section: Discussionmentioning

confidence: 99%

A prospective evaluation of non-interval- and interval-based exercise training progressions in rodents

Jendzjowsky

DeLorey

2011

Appl. Physiol. Nutr. Metab.

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Non-interval and interval training progressions were used to determine (i) the mean rate at which treadmill speed could be incremented daily using a non-interval training progression to train rats to run continuously at different intensities and (ii) the number of training days required for rats to run continuously at different exercise intensities with non-interval- and interval-based training progressions to establish methods of progressive overload for rodent exercise training studies. Rats were randomly assigned to mild-intensity (n = 5, 20 m·min(-1), 5% grade), moderate-intensity (n = 5, 30 m·min(-1), 5% grade), and heavy-intensity non-interval groups (n = 5, 40 m·min(-1), 5% grade) or a heavy-intensity interval (n = 5, 40 m·min(-1), 5% grade) group and ran 5 days·week(-1) for 6 weeks. Non-interval training involved a daily increase of treadmill speed, whereas interval training involved a daily increase of interval time, until the animal could run continuously at a prescribed intensity. In mild-, moderate-, and heavy-intensity non-interval-trained rats, treadmill speed was increased by 0.6 ± 0.7 m·min(-1)·day(-1), 0.6 ± 0.2 m·min(-1)·day(-1), and 0.8 ± 0.1 m·min(-1)·day(-1), respectively. Target training intensity and duration were obtained following 0.4 ± 0.5 days, 17 ± 3 days, and 23 ± 3 training days (p < 0.05) in mild-, moderate-, and heavy-intensity groups, respectively. In contrast, interval-trained rodents required 11 ± 1 training days. These data demonstrate that rodents will tolerate an increase in treadmill speed of ∼0.7 ± 0.1 m·min(-1)·day(-1) and that this progression enables rats to run continuously at moderate and heavy intensities with 3-4 weeks of progressive overload. Interval training significantly reduces the number of training days required to attain a target intensity.

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Section: Discussionmentioning

confidence: 99%

A prospective evaluation of non-interval- and interval-based exercise training progressions in rodents

Jendzjowsky

DeLorey

2011

Appl. Physiol. Nutr. Metab.

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“…In 2002, we initiated a large-scale bidirectional selection experiment for the response to exercise training in a laboratory rat population with wide genetic heterogeneity (N:NIH outcrossed stock) (27). A base population (n ϭ 152) was tested for maximal treadmill running capacity before and after receiving the same amount of a moderate standardized treadmill training stimulus over an 8-wk period (3 exercise sessions per week) (61). On average, training produced a 140-m gain in maximal running capacity with interindividual variation ranging in magnitude from Ϫ339 to ϩ627 m. Ten male and ten female rats that represented the extreme ends for training response (Ͼ1 SD) were bred at each successive generation to develop low response to training (LRT) and high response to training (HRT) selected lines.…”

Section: Continuedmentioning

confidence: 99%

A transcriptional map of the impact of endurance exercise training on skeletal muscle phenotype

Keller

Vollaard

Gustafsson

et al. 2011

Journal of Applied Physiology

213

218

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The molecular pathways that are activated and contribute to physiological remodeling of skeletal muscle in response to endurance exercise have not been fully characterized. We previously reported that ∼800 gene transcripts are regulated following 6 wk of supervised endurance training in young sedentary males, referred to as the training-responsive transcriptome (TRT) (Timmons JA et al. J Appl Physiol 108: 1487-1496, 2010). Here we utilized this database together with data on biological variation in muscle adaptation to aerobic endurance training in both humans and a novel out-bred rodent model to study the potential regulatory molecules that coordinate this complex network of genes. We identified three DNA sequences representing RUNX1, SOX9, and PAX3 transcription factor binding sites as overrepresented in the TRT. In turn, miRNA profiling indicated that several miRNAs targeting RUNX1, SOX9, and PAX3 were downregulated by endurance training. The TRT was then examined by contrasting subjects who demonstrated the least vs. the greatest improvement in aerobic capacity (low vs. high responders), and at least 100 of the 800 TRT genes were differentially regulated, thus suggesting regulation of these genes may be important for improving aerobic capacity. In high responders, proangiogenic and tissue developmental networks emerged as key candidates for coordinating tissue aerobic adaptation. Beyond RNA-level validation there were several DNA variants that associated with maximal aerobic capacity (Vo(₂max)) trainability in the HERITAGE Family Study but these did not pass conservative Bonferroni adjustment. In addition, in a rat model selected across 10 generations for high aerobic training responsiveness, we found that both the TRT and a homologous subset of the human high responder genes were regulated to a greater degree in high responder rodent skeletal muscle. This analysis provides a comprehensive map of the transcriptomic features important for aerobic exercise-induced improvements in maximal oxygen consumption.

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“…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). Large differences were reported for training responses across several inbred strains of rats, and these strain differences persisted whether training was performed at the same relative or absolute workload (30,63).…”

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confidence: 99%

“…In contrast, less is known about the change in exercise capacity with training across inbred strains of rodents (30,42,63). Large differences were reported for training responses across several inbred strains of rats, and these strain differences persisted whether training was performed at the same relative or absolute workload (30,63). Using a mouse model of exercise training, Massett and Berk (42) reported that the change in exercise capacity with training varied significantly across inbred (B6, Balb/cJ, and FVB) and hybrid mouse strains.…”

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confidence: 99%

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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Selected Contribution: Variation and heritability for the adaptational response to exercise in genetically heterogeneous rats

Cited by 24 publications

References 27 publications

A prospective evaluation of non-interval- and interval-based exercise training progressions in rodents

A prospective evaluation of non-interval- and interval-based exercise training progressions in rodents

A transcriptional map of the impact of endurance exercise training on skeletal muscle phenotype

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

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