Spectrum of aerobic endurance running performance in eleven inbred strains of rats

Barbato, John C.; Koch, Lauren G.; Darvish, Ahmad; Cicila, George T.; Metting, Patricia J.; Britton, Steven L.

doi:10.1152/jappl.1998.85.2.530

Cited by 88 publications

(82 citation statements)

References 18 publications

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“…When exhaustion was determined, defined as an inability to maintain running speed despite repeated contact with the electric grid, each mouse was immediately removed from the treadmill and returned to its home cage. Maximal exercise capacity was estimated from each run to exhaustion trial with three parameters: the duration of the run (in min), the distance run (in m), and vertical work performed (in kg ⅐ m) (2,42). In our laboratory, this protocol yields a within-mouse coefficient of variation for work of 10 Ϯ 1% for two tests conducted within 72 h by the same individual (M. P.…”

Section: Animalsmentioning

confidence: 99%

“…Strain-dependent differences in intrinsic or pretraining exercise capacity measured during a graded treadmill test have been reported for inbred mice and rats (2,34,36,62). In a screen of several inbred mouse strains, Lerman et al (34) reported that maximal speed achieved during a graded treadmill test was highest in FVB/NJ (FVB) mice and lowest in C57BL/6J (B6) mice.…”

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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: Animalsmentioning

confidence: 99%

mentioning

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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“…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%

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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“…6,40 After retrograde perfusion for 15 minutes at 80 mm Hg, anterograde perfusion was initiated at a preload of 15 mm Hg and an afterload of 70 mm Hg for the duration of each study.…”

Section: Isolated Heart Studiesmentioning

confidence: 99%

Mechanisms for Aldosterone and Spironolactone-Induced Positive Inotropic Actions in the Rat Heart

et al. 2004

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Abstract-Previously, we reported that aldosterone and spironolactone have inotropic effects in the isolated perfused heart.To address the mechanisms underlying these inotropic effects, we examined the effects of aldosterone and spironolactone on isolated cardiac myocyte shortening, intracellular calcium ( ). Collectively, these data strongly suggest that the inotropic actions of aldosterone and spironolactone are caused by different mechanisms of action. Aldosterone appeared to increase inotropy primarily through increased cytosolic pH, whereas spironolactone increased myosin ATPase calcium sensitivity and diastolic calcium concentration. Key Words: mineralocorticoid Ⅲ cardiac function Ⅲ heart failure Ⅲ calcium T he Randomized ALdactone Evaluation Study (RALES) demonstrated significant reductions in morbidity and mortality when spironolactone, the aldosterone mineralocorticoid receptor antagonist, was included in the treatment of heart failure. 1 This study, along with many translational reports, strongly developed the concept that aldosterone may play an important, deleterious effect in human congestive heart failure. [2][3][4][5] In addition, we have previously observed that aldosterone has rapid, inotropic effects in the isolated perfused rat heart; 6 however, rapid, inotropic effects were observed as early as the 1960s. 7,8 This rapid, inotropic effect of aldosterone almost certainly occurs through nongenomic mechanism(s).Nongenomic actions of aldosterone were first identified by Wehling et al in smooth muscle cells. 9 -12 These actions were classified as nongenomic because of their speed, lack of inhibition by spironolactone, and independence from new protein synthesis. Based on these characteristics, nongenomic effects of aldosterone have been reported from a number of laboratories in renal epithelial cells, 13 vascular smooth muscle cells, 14,15 skeletal muscle cells, 16 and colonic. The molecular basis of these nongenomic effects of aldosterone actions have been ascribed to changes in intracellular pH (pHi), [17][18][19] 20 -25 Although it has been observed that aldosterone does have rapid effects on protein kinase C activity in cultured cardiac cells, 26 and that aldosterone has rapid effects on cardiac sodiumhydrogen exchange, 27 the molecular mechanism of the rapid inotropic effect of aldosterone is still unclear.The spironolactone issue is less well defined and perhaps of greater interest because of the favorable results of the RALES trial. 1 We previously observed that substantial inotropy could be observed with levels of spironolactone that were comparable to those achieved with this agent in standard clinical practice. Moreover, the inotropic effect of spironolactone was found to be additive to that of aldosterone when both agents were administered together. These studies strongly suggest that although aldosterone and spironolactone are similar in structure, they have independent mechanism(s) of actions. Therefore, the objective of the present study was

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Spectrum of aerobic endurance running performance in eleven inbred strains of rats

Cited by 88 publications

References 18 publications

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

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

Quantitative trait loci associated with maximal exercise endurance in mice

Mechanisms for Aldosterone and Spironolactone-Induced Positive Inotropic Actions in the Rat Heart

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