Medicine & Science in Sports & Exercise:
The Human Gene Map for Performance and Health-Related Fitness Phenotypes: The 2005 Update
RANKINEN, TUOMO1; BRAY, MOLLY S.2; HAGBERG, JAMES M.3; PÉRUSSE, LOUIS4; ROTH, STEPHEN M.3; WOLFARTH, BERND5; BOUCHARD, CLAUDE1
1Human Genomics Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA; 2Children's Nutrition Research Center, Baylor College of Medicine, Houston, TX; 3Department of Kinesiology, College of Health and Human Performance, University of Maryland, College Park, MD; 4Division of Kinesiology, Department of Preventive Medicine, Laval University, Ste-Foy, Québec, CANADA; and 5Preventive and Rehabilitative Sports Medicine, Technical University Munich, Munich, GERMANY
Address for correspondence: Claude Bouchard, PhD, Human Genomics Laboratory, Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA 70808-4124; E-mail: email@example.com.
Submitted for publication April 2006.
Accepted for publication May 2006.
The current review presents the 2005 update of the human gene map for physical performance and health-related fitness phenotypes. It is based on peer-reviewed papers published by the end of 2005. The genes and markers with evidence of association or linkage with a performance or fitness phenotype in sedentary or active people, in adaptation to acute exercise, or for training-induced changes are positioned on the genetic map of all autosomes and the X chromosome. Negative studies are reviewed, but a gene or locus must be supported by at least one positive study before being inserted on the map. By the end of 2000, in the early version of the gene map, 29 loci were depicted. In contrast, the 2005 human gene map for physical performance and health-related phenotypes includes 165 autosomal gene entries and QTL, plus five others on the X chromosome. Moreover, there are 17 mitochondrial genes in which sequence variants have been shown to influence relevant fitness and performance phenotypes. Thus, the map is growing in complexity. Unfortunately, progress is slow in the field of genetics of fitness and performance, primarily because the number of laboratories and scientists focused on the role of genes and sequence variations in exercise-related traits continues to be quite limited.
This paper constitutes the sixth installment in the series on the human gene map for performance and health-related fitness phenotypes published in this journal. It covers the peer-reviewed literature published by the end of December 2005. The search for relevant publications is primarily based on the journals available in MEDLINE, the National Library of Medicine's publication database covering the fields of Life Sciences, biomedicine, and health, using a combination of key words (e.g., exercise, physical activity, performance, training, genetics, genotype, polymorphism, mutation, linkage). Other sources include personal reprint collections of the authors and documents made available to us by colleagues who are publishing in this field. The electronic prepublications, that is, articles that are made available on the Web site of a journal before being published in print, are not included in the current review. The goal of the human gene map for fitness and performance is to review all genetic loci and markers shown to be related to physical performance or health-related fitness phenotypes in at least one study. Negative studies are briefly reviewed for a balanced presentation of the evidence. However, the nonsignificant results are not incorporated in the summary tables.
The physical performance phenotypes for which genetic data are available include cardiorespiratory endurance, elite endurance athlete status, muscle strength, other muscle performance traits, and exercise intolerance of variable degrees. Consistent with the previous reviews, the phenotypes of health-related fitness retained are grouped under the following categories: hemodynamic traits including exercise heart rate, blood pressure and heart morphology; anthropometry and body composition; insulin and glucose metabolism; and blood lipid, lipoprotein, and hemostatic factors. Here, we are not concerned about the effects of specific genes on these phenotypes unless the focus is on exercise, exercise training, athletes, or active people compared against controls or inactive individuals, or exercise intolerance. This is particularly important for the genetic studies that have focused on body mass index, adiposity, fat-free mass, adipose tissue distribution, and various abdominal fat phenotypes. If there were no exercise-related issues in those studies, the papers are not considered here. However, the interested reader can obtain a full summary of these other studies in one of our complementary papers published every year in Obesity Research under the general theme of the status of the human obesity gene map. The interested reader may also consult the following electronic version of this other map (http://obesitygene.pbrc.edu).
The studies incorporated in the review are fully referenced so that the interested reader can access the original papers. Of interest to some could be the early observations made on athletes, particularly Olympic athletes. The results of these case-control studies based on common red blood cell enzymes were essentially negative and are not reviewed in this edition of the map. The interested reader can consult the first installment of the gene map for a complete summary of these early reports (164).
The 2005 synthesis of the human performance and health-related fitness gene map for the autosomes and the X chromosome is summarized in Figure 1. The 2005 update includes 26 additional gene entries and quantitative trait loci (QTL) compared with the 2004 version (255). We have also depicted in Figure 2 the gene loci in the mitochondrial DNA in which sequence variants have been shown to be associated with fitness and performance phenotypes. Table 1 provides a list of all genes or loci, cytogenic locations, and conventional symbols used in this review.
It remains our collective goal to make this publication a useful resource for those who teach undergraduate and graduate students about the role of inheritance on fitness and performance traits and the impact of genetic variation on the health of human beings. It is also our hope that the yearly update of the fitness and performance gene map will be useful to exercise scientists and the sports medicine community.
Several new case-control studies were published in 2005 dealing with endurance performance phenotypes (Table 2). Three studies from Spain included elite cyclists and runners. The first study showed a different pattern of the angiotensin-converting enzyme (ACE) I/D allele distribution with a higher proportion of the D allele in cyclists (65%, N = 50) and controls (57.6%, N = 119) compared with runners (46.3%, N = 27, P < 0.001). A muscle-type creatine kinase gene (CKM) polymorphism showed no significant differences in allele or genotype frequencies between the same athletes and controls (109). The next two papers from the same research group included 104 cyclists and runners. The frequency of the C34T mutation of the adenosine monophosphate deaminase 1 (AMPD1) gene was significantly higher in 100 nonathlete controls (T: 8.5%) than in the athletes (T: 4.3%). However, because there were no genotype-dependent differences in performance traits among the athletes, the authors concluded that the AMPD1 mutation may not significantly affect endurance performance (188). Comparing the same athletes with a group of 100 exeptional unfit controls, Lucia and coworkers found a significant difference in the PPARGC1 (Gly482Ser) genotype distributions between the two groups. The frequency of the minor Ser482 allele was significantly lower in athletes than in the unfit controls (29.1 vs 40.0%) (108).
A group from Finland determined mitochondrial DNA and the alpha 3 actinin (ACTN3) genotypes in national elite endurance (N = 52) and sprint (N = 89) athletes. The frequency of mtDNA haplogroups differed significantly between the two groups, with some haplogroups missing totally in the endurance athletes. Moreover, they found a trend for a higher ACTN3 X/X genotype frequency in the endurance athletes (140). In two cohorts of Ethiopian endurance runners, the investigators did not find a significant distinction for mitochondrial DNA lineages or Y chromosome haplogroups compared with the general Ethiopian population (128,199). Another study investigated two ACE gene polymorphisms in national- and international-level elite runners and nonathlete controls from Kenya. The allele and genotype frequencies did not differ between the athletes and controls (198).
Cross-sectional association studies
Three new studies reported positive findings for endurance-related phenotypes in cross-sectional association studies in 2005 (Table 3). In a study cmprising 29 elite Caucasian wrestlers and 51 age-matched sedentary controls, a significant association between V˙O2max and the ACE I/D genotype was found in both groups, with the D/D subjects having lower values than the I/I homozygotes. No differences were seen in genotype frequencies between the two groups (89). In a cohort of 83 patients with heart failure, peak V˙O2 and exercise time were significantly greater in patients homozygous for the 389R allele of the adrenergic receptor beta 1 (ADRB1) gene compared with the 389G homozygotes. The significant association remained after adjusting for confounding factors (age, treatment with β-blockers, LVEF) (191).
Cam et al. investigated in 88 nonelite male athletes the relationship between the ACE I/D genotype and middle-distance running performance measured by a 2000-m run. The ACE D/D genotype frequency was found to be higher in the superior group than in the poor and mediocre group based on 2000-m performance. However, no genotype-dependent differences were seen for a 60-m sprint in the same cohort (21). Another four studies showed no association between different genetic variants and V˙O2max values in the sedentary state. These studies included NADPH oxidase p22phox gene variants in middle-aged Caucasians, the peroxisome proliferative activated receptor gamma (PPARG) Pro12Ala polymorphism in 139 type 2 diabetic patients, beta-adrenoceptor gene polymorphismsin patients with congestive heart failure, and ACE I/D variation in 18- to 35-yr-old healthy women (2,32,147,183).
Association studies with training response phenotypes
In 2005, two studies analyzed associations between training-induced changes in endurance phenotypes and genetic polymorphisms. The influence of the PPARG Pro12Ala genotype on training-induced changes after 6 months of endurance training was tested in 73 sedentary 50- to 75-yr-old healthy men and women. V˙O2max values increased by almost 20% in average, but the training-induced changes did not differ between the PPARG genotypes (249). Similar findings were reported in 48 healthy subjects who participated in a 10-wk aerobic training program: neither baseline V˙O2max nor V˙O2max training response were associated with the PPARG Pro12Ala and the ACE I/D polymorphisms (143).
No new linkage studies on performance-related phenotypes were published in 2005 (Table 4).
The studies reporting candidate gene associations with muscle strength or anaerobic performance phenotypes are summarized in Table 5. In 2005, six studies reported positive genetic associations with muscle strength-related phenotypes. Williams et al. (250) examined the ACE I/D genotype associations with quadriceps muscle strength in 81 young Caucasian men, 44 of whom completed an 8-wk strength-training program. Baseline isometric strength was significantly associated with ACE genotype (P = 0.026), with I-allele homozygotes showing the lowest strength values. No association was found with changes in strength in response to training.
Peeters and colleagues (149) reported higher isometric grip strength (P = 0.047) and leg-extensor strength (P = 0.07) in 350 predominantly Caucasian older men (> 70 yr) who carried the D1a-T allele of the type I iodothyronine deiodinase (DIO1) gene compared with D1a-C allele homozygotes. Kostek et al. (93) studied 67 older Caucasian men and women before and after a 10-wk unilateral strength-training program for associations between insulin-like growth factor (IGF1) gene polymorphisms and muscle phenotypes. Carriers of the 192 allele of the IGF1 promoter microsatellite showed greater quadriceps-muscle strength gains compared with noncarriers (P = 0.02), with no differences observed for the muscle-quality response to training. Other polymorphisms in the IGF1 gene were not associated with any muscle phenotypes. Nicklas et al. (139) examined associations between several cytokine gene markers and physical function before and after exercise training in older men and women (≥ 60 yr). Stair-climb performance improved in response to training more in A-allele carriers of the A-308G polymorphism in the tumor necrosis factor alpha (TNF) gene compared with G/G homozygotes (P = 0.007).
Clarkson and colleagues (25) reported that one-repetition maximum gains in response to a 12-wk strength-training program were greatest in women homozygous for the X-allele of the (ACTN3) gene compared with the R-allele homozygotes (P < 0.05). In contrast, the X/X women had lower baseline isometric strength than the R/R women (P < 0.05). No association was observed between the ACTN3 R577X polymorphism and muscle phenotypes in men. In an examination of genotypes in the ACTN3 and myosin light-chain kinase (MYLK) genes, Clarkson et al. (26) studied associations with exertional muscle damage in 157 predominantly Caucasian men and women. Subjects performed eccentric contraction of the elbow flexors, with creatine kinase, myoglobin, and isometric strength tested before and after the exercise bout. Although ACTN3 genotype was associated with baseline creatine kinase levels, no associations were observed for any other phenotypes before or after exercise. Polymorphisms in the MYLK gene were associated with baseline muscle strength and with creatine kinase and myoglobin responses and strength loss after the eccentric exercise bout.
In 2005, three studies reported negative genetic associations with muscle strength-related phenotypes. Grundberg et al. (56) reported no association between a TA-repeat polymorphism in the estrogen-receptor alpha (ESR1) gene and several muscle-strength measures in 175 Swedish women (20-39 yr). Walsh and colleagues (245) found no association between muscle strength and an androgen-receptor (AR) gene CAG-repeat polymorphism in two cohorts of older men and women, despite finding significant genotype associations with fat-free mass in the men of both cohorts. Finally, Walston and coworkers (246) examined individual polymorphisms and haplotypes in the interleukin-6 (IL6) gene for association with several muscle-strength measures. They reported no associations for any IL6 genotypes with any strength or related phenotypes in a study of 463 older women (70-79 yr).
In 2005, one investigation provided linkage data relevant to muscle-strength phenotypes (Table 4). Huygens et al. (73) performed a linkage analysis in 367 young Caucasian male siblings from 145 families with markers in the general vicinity of nine genes involved in the myostatin signaling pathway and various measures of muscle strength. Significant linkages were reported on four chromosomal regions with knee muscle-strength measures: chromosome 13q21 (D13S1303), chromosome 12p12-p11 (D12S1042), chromosome 12q12-q13.1 (D12S85), and chromosome 12q23.3-q24.1 (D12S78). These findings represent an expansion of an earlier linkage study reported by the same group in 2004 (71).
HEALTH-RELATED FITNESS PHENOTYPES
In 2005, three groups published results relative to the impact of common genetic variations on exercise-related hemodynamic phenotypes (Table 6). Eisenach and coworkers found that men and women homozygous for the Gly16 allele of the adrenergic receptor beta 2 (ADBR2) gene had larger heart rate responses (60 ± 4 vs 45 ± 4%, P = 0.03) and a higher cardiac output (7.6 ± 0.3 vs 6.5 ± 0.3 L·min−1, P = 0.03) during isometric handgrip exercise than otherwise similar individuals homozygous for the Arg16 allele (38). However, the decrease in systemic vascular resistance during handgrip exercise did not achieve statistical significance between the two homozygous genotype groups (P = 0.09).
Trombetta et al. found in women that the Gly16 and Glu27 genotypes at the ADRB2 gene locus affected the forearm blood flow (FBF), but not conductance, responses to isometric handgrip exercise (225). Whereas all genotype groups increased their FBP during handgrip exercise, women homozygous for both the Gly16 and the Glu27 alleles had a significantly greater FBF increase than those homozygous for the other combinations of these alleles.
Roltsch and coworkers found that the ACE I/D genotype did not significantly influence any hemodynamic responses to submaximal or maximal exercise in a cohort of 77 young healthy women (183). The hemodynamic responses assessed in this study included heart rate, systolic and diastolic BP, cardiac output, stroke volume, total peripheral resistance, and a-V˙O2 difference.
Gene-physical activity interactions
In 2005, two studies assessed the interactive effect of common genetic polymorphisms and physical activity levels on hemodynamic phenotypes (Table 6). Roltsch and coworkers found that the ACE I/D genotype did not interact with habitual level of physical activity, ranging from sedentary to endurance trained, to significantly alter hemodynamic responses (heart rate, systolic and diastolic BP, cardiac output, stroke volume, total peripheral resistance, and a-V˙O2 difference) to submaximal or maximal exercise in young women (183).
Tanriverdi and coworkers found in a group of predominantly male athletes (middle-distance runners, soccer players) that flow-mediated dilation (FMD) was significantly greater in those with the ACE I/I genotype (10.5 ± 1.6%) compared with those with the I/D (8.4 ± 2.3%) or D/D (7.0 ± 1.2%) genotypes (217). No ACE genotype-dependent FMD relationships were evident in the untrained individuals they studied.
Delmonico and coworkers reported that the angiotensinogen (AGT) A-20C genotype affected the resting systolic BP reductions, whereas the angiotensin II receptor type 1 (AGTR1) A1166C genotype affected the resting diastolic BP reductions resulting from 23 wk of resistive training in 52- to 81-yr-old sedentary men and women (34). However, the AGT M235T genotype did not affect the degree to which these men and women reduced their resting systolic or diastolic BP with resistive training (Table 7).
No new linkage studies were published in 2005 (Table 8).
Anthropometry and Body-Composition Phenotypes
In 2005, four studies (10,94,129,143) tested associations between candidate genes and body fat in response to exercise or in interaction with physical activity, and three of them reported positive findings (Table 9). In a 10-yr follow-up study of obese and nonobese Danish men, interactions between leisure-time physical activity and polymorphisms in the uncoupling protein 2 (UCP2) and 3 (UCP3) genes were examined in relation to changes in body mass index (BMI), but no evidence of interaction between the UCP genes and physical activity on the changes in BMI was uncovered (10). The second study (129) examined the interactions between the ACE I/D polymorphism and physical activity on adiposity in adolescent (11-18 yr old) males (N = 535) and females (N = 481). Strong evidence of association was found between the ACE I/D polymorphism and triceps (P = 0.012) and subscapular (P = 0.001) skinfolds, but only in inactive (N = 207) females. The polymorphism accounted for 4.3 and 6.5% of the variance in the triceps and subscapular skinfolds, respectively (129).
Another study involving the ACE I/D polymorphism genotype in more than 3000 adult subjects aged 70-79 yr found higher values of percent body fat and intermuscular thigh fat (assessed by CT scan) in subjects with the I/I genotype compared with those with the I/D or D/D genotype, but the association was observed only among physically active subjects (94). Ostergard and coworkers reported that in a small group of offspring of type 2 diabetics, the Ala12 allele carriers of the PPARG Pro12Ala polymorphism showed a greater weight loss compared with the Pro12Pro homozygotes in response to 10 wk of endurance training (143).
In 2005, one study tested association between candidate genes and bone mineral density (BMD) responses to exercise training. Rabon-Stith and colleagues examined the response of BMD to both aerobic and strength training in 206 total older men and women in relation to two polymorphisms in the vitamin D-receptor gene (VDR) (158). The FokI polymorphism was significantly associated with the femoral neck BMD response to strength training. There was no association between either VDR polymorphism with the BMD response to aerobic training.
No linkage studies pertaining to training-induced changes in body-composition phenotypes (Table 10) were reported in 2005.
Insulin and Glucose Metabolism Phenotypes
Five studies in the past year investigated associations with insulin and glucose metabolism phenotypes in response to exercise (Table 11). The first study investigated associations between the PPARG Pro12Ala polymorphism and improvements in insulin action in response to endurance training in sedentary men (N = 32) and women (N = 41). Subjects underwent an oral glucose-tolerance test before and after 6 months of endurance training. Results showed that decreases in fasting insulin and insulin area under the curve in response to training were about fourfold greater in the Pro12Ala heterozygous men compared with Pro12 homozygous men. No genotype-specific effects of exercise training were found in women (249). The second study evaluated the impact of the PPARG Pro12Ala and the ACE I/D polymorphisms on insulin sensitivity (measured by the hyperinsulinemic euglycemic clamp technique) in response to 10 wk of endurance training in 29 offspring of type 2 diabetic patients and 17 control subjects (143). Improvements in insulin sensitivity were not associated with the PPARG and ACE genotypes.
The third study examined associations between the hepatic lipase (LIPC)-514 C>T polymorphism and changes in insulin sensitivity in response to endurance training in 219 black adults and 443 white adults of the HERITAGE Family Study (219). In the sedentary state, the insulin sensitivity, assessed by an intravenous glucose-tolerance test, did not differ between the LIPC-514 genotypes. However, the training-induced improvements in insulin sensitivity, after adjustment for age, sex, BMI, and baseline values, were found to be greater in both black (P = 0.008) and white (P = 0.002) C/C homozygotes (+1.25 ± 0.2 and +0.22 ± 0.2 μU·min−1·mL−1) than in the T/T homozygotes (+0.27 ± 0.3 and −0.97 ± 0.3 μU·min−1·mL−1). The fourth study examined the effects of the PPARG Pro12Ala polymorphism on changes in glucose homeostasis and body-composition variables in 139 sedentary type 2 diabetic patients who completed 3 months of supervised exercise training (2). Although exercise training resulted in significant improvements in glucose homeostasis and body-composition variables, there were no significant differences between carriers and noncarriers of the Ala allele in response to exercise, except for fasting plasma glucose levels, which showed greater reductions (P = 0.03) in the Ala carriers (−2.02 ± 0.70) than in Pro12Pro homozygotes (−0.86 ± 0.32). In the fifth study, a polymorphism in the adiponectin receptor 1 (ADIPOR1) gene was found to be associated with lower insulin sensitivity in a follow-up study of 45 subjects (average follow-up of 9.8 months) who received diet counselling and increased their physical activity to at least 3 h·wk−1 of sports (211).
The only linkage study pertaining to glucose and insulin metabolism phenotypes reported in 2005 was a genome-wide linkage analysis of prediabetes phenotypes in response to 20 wk of endurance training in subjects from the HERITAGE Family Study (Table 12). Training-induced changes in insulin sensitivity, acute insulin response to glucose, disposition index, and glucose effectiveness were assessed in 441 subjects from 98 white families and 187 subjects from black families, adjusted for the effect of age, sex, BMI, and the respective baseline phenotypic values and tested for linkage with a total of 654 markers (4). In whites, suggestive (P ≤ 0.01 or LOD ≥ 1.17) evidence of linkage with disposition index (a measure of overall glucose homeostasis) was found on chromosomes 1p35.1, 3q25.2, 6p22.1, and 7q21.3. In blacks, suggestive linkages with glucose effectiveness were found on chromosomes 1q44, 2p22.1-p21, 10q23.1-q23.2, 12q13.11-q13.13, and 19q13.33-q13.43.
Blood Lipid and Lipoprotein Phenotypes
Seven new papers were published in 2005 analyzing genetic association or linkage for lipid responses to acute or chronic exercise and/or physical activity (Table 13). Ruano et al. investigated the effect of a promoter region variant (-75G>A) polymorphism in the apolipoprotein A1 gene (APOA1) on high-density lipoprotein (HDL) cholesterol after 6 months of aerobic exercise training (187). Although APOA1 genotype was not associated with either total HDL or subfractions of HDL at baseline or after exercise training, the ratio of large HDL subfraction (HDL3 + HDL4 + HDL5) to small HDL subfraction (HDL1 + HDL2) was significantly different by genotype after exercise training. Homozygotes for the -75G allele had increased amounts of the large HDL subfractions and decreased amounts of the small HDL subfraction compared with carriers of the -75A allele, suggesting that APOA1 genotype is associated with HDL subfraction redistribution after exercise (187).
Halverstadt and colleagues investigated the association between variation in the IL6 gene and HDL-C in elderly men and women undergoing 24 wk of aerobic exercise training (64). Sixty-five subjects were genotyped for the IL6 174G > C variant and measured for total HDL-C as well as HDL-C subfractions before and after training. Although the IL6 174G > C polymorphism not associated with any measure of HDL-C at baseline, this variant was significantly associated with changes in total HDL-C, HDL3-C, integrated HDL4,5-C (as measured by nuclear magnetic resonance spectroscopy), and HDLsize, with homozygotes of the 174C allele having greater increases after exercise training for each of these measures compared with those carrying the 174G allele (64).
The -514C>T polymorphism within the LIPC gene was investigated for association to lipid-related measures before and after exercise in black and white families from the HERITAGE study. Individuals from this study underwent 20 wk of aerobic exercise training and were measured for a lipid panel that included triglycerides (TG), low-density and very-low-density lipoprotein (LDL and VLDL, respectively), HDL, HDL2, HDL3, Apo-A1, and apolipoprotein B (apoB) (219). In addition, the subjects were also measured for postheparin hepatic lipase and lipoprotein-lipase activity. Homozygotes for the -514C allele had significantly higher postheparin hepatic lipase activity at baseline and after exercise training (P < 0.0001 for both) in both black and white subjects compared with those with the T/T genotype. The -514C allele was also associated with lower postheparin lipoprotein lipase in blacks and whites before and after exercise training compared with -514T homozygotes (219). The LIPC -514C>T polymorphism was significantly associated with baseline TG, VLDL, LDL, HDL, ApoA1, and ApoB in whites and with pretraining HDL, HDL3, and ApoA-1 in blacks. The only posttraining variable associated with the LIPC -514C>T variant was the training response measure of apoB in blacks. All other pre- and postexercise lipid measures were unrelated to the -514C>T polymorphism (219).
Two studies assessed the effects of genetic variation in response to diet/lifestyle/behavior interventions that included exercise. Coronary artery disease patients (N = 307) underwent a cardiac rehabilitation intervention that included diet, eduction, psychosocial, and smoking cessation counseling, in addition to twice-weekly aerobic exercise for 16 wk. Three gene variants were measured in these patients: the cholesterol-ester transfer protein (CETP) TaqIB polymorphism, the LIPC -514C>T variant, and the apolipoprotein E (APOE) epsilon variant. Although the cardiac rehabilitation intervention resulted in significant improvements in all measures assessed (total cholesterol (TC), LDL-C, HDL-C, TG, TC/HDL-C, BMI, and exercise capacity), results of this study for genetic association were primarily negative. Of all measures tested, the only significant result was for TC and the CETP TaqIB polymorphism (P < 0.048), with B1/B1 homozygotes experiencing decreased TC levels and B2 carriers having little or no change in TC after the lifestyle/exercise intervention (9). In another study, men and women underwent a diet and physical activity intervention designed to reduce insulin resistance, and the -8503G>A polymorphism within the ADIPOR1 was investigated for association to measures of insulin sensitivity and hepatic lipids (211). The dietary therapy was aimed at reducing fat intake, whereas the physical activity intervention involved a minimum of 3 h·wk−1 of sports participation. After exercise and diet therapy, homozygotes for the -8503G allele had significantly lower hepatic lipid content (as measured by proton magnetic resonance spectroscopy) compared with subjects carrying the -8503A allele (211).
Two linkage studies for lipid-related phenotypes in the context of exercise training were reported in 2005 (Table 12). In a study of black and white families from the HERITAGE Family Study, Feitosa and colleagues reported evidence of QTL on chromosomes 13q and 14q for triglyceride subfractions (low-density lipoprotein (LDL-TG) and HDL-TG) at baseline and after 20 wk of exercise training (43). The highest LOD score reported was for baseline HDL-TG (LOD = 3.8) on 13q12-q14, and suggestive evidence for linkage was found in this same region for LDL-TG training response (LOD = 2.2) in whites only. For baseline LDL-TG in whites, significant or suggestive evidence of linkage was found on 14q31 (LOD = 3.2), 10p14 (LOD = 2.9), and 19p13 (LOD = 2.2). For HDL-TG in whites, suggestive evidence of linkage was found on 12q24 (LOD = 2.7) for baseline measures and on 10q23 (LOD = 2.2) for measures performed after 20 wk of exercise training. No evidence of linkage was found for any measure of total triglycerides, and no linkage was observed in the black families from this study (43).
In a second linkage scan for apoB and LDL-C in the same family sample from the HERITAGE study, suggestive linkages were observed for training responses in LDL-C on 12q14.1 (LOD = 2.1) and in LDL-apoB on 20q13 (LOD = 2.2) (42). Significant or suggestive evidence for linkage was found on 1q41-q44 for baseline measures of LDL-apoB (LOD = 3.7), apoB (LOD = 2.9), and LDL-cholesterol (LOD = 2.1) in blacks. In whites, baseline measures of LDL-chol, LDL-apoB, and apoB were significantly or suggestively linked to chromosomal region 8q24 (LOD = 3.6, 3.3, and 2.5, respectively).
Hemostatic Factors, Inflammation Phenotypes and Plasma Hormone Levels
No new studies were published in 2005.
A significant interaction between physical activity and genotype (P < 0.01) was demonstrated in an analysis of the IGF1 gene on colon cancer outcomes. Homozygotes for a CA repeat polymorphism within the IGF1 gene ("192/192") who reported no habitual physical activity were almost 50% more likely to develop colon cancer (OR = 1.46, 95% CI = 1.08, 2.05), whereas active individuals with the 192/192 genotype experienced decreased risk for colon cancer (OR = 0.57, 95% CI = 0.39, 0.83) compared with active individuals not carrying the 192 allele (209). Similarly, for a single nucleotide polymorphism resulting in an amino acid change from glycine to alanine at codon 32 (Gly32Ala) within the insulin-like growth factor binding protein 3 (IGFBP3) gene, the protective effect of physical activity on colon cancer was only observed in male carriers of the Ala32 allele (P < 0.01) (130).
In a sample of 1577 colon cancer patients (1971 controls) and 794 rectal cancer patients (1001 controls), Slattery and colleagues reported no significant interactions between the Pro12Ala variant in the PPARG gene and energy expenditure (a surrogate of physical activity) in predicting cancer risk (210). In a sample of 4248 elderly white women, Modugno et al. also reported no association between risk for breast cancer and either the catechol-O-methyltransferase (COMT) Val158Met polymorphism or an isoleucine to valine variant at codon 462 in the CYP1A1 gene, a gene also involved in hydroxylation of free estrogen. There was no significant interaction when stratifying by physical activity (walking for exercise) (121).
Nine studies related to exercise intolerance were published in 2005 (Table 14). These studies reported mutations in four nuclear and five mitochondrial genes. Palmieri and coworkers reported a patient with exercise intolerance, lactic acidosis, and hypertrophic cardiomyopathy. A skeletal muscle biopsy revealed presence of ragged-red fibers and multiple deletions of muscle mitochondrial DNA. A mutation screening of muscle-specific adenine nucleotide translocator gene (SLC25A4) revealed a homozygous C to A transversion at nucleotide 368, which changed a highly conserved alanine residue to an aspartic acid at codon 123 (145).
Isackson et al. reported two Caucasian brothers with exercise intolerance and myoadenylate deaminase deficiency (74). Interestingly, neither brother carried the common Q12X nonsense mutation. Instead, they were compound heterozygotes for a K287I mutation in exon 7 and a novel CTTT deletion in intron 2. The K287I mutation is fairly frequent in general population, whereas the intron 2 mutation, which affects the splicing machinery, was found only in these patients. Skeletal muscle mRNA analysis revealed several alternatively spliced AMPD1 transcripts, with either partial or complete deletions of either exon 3 or exons 3 and 4. Moreover, the deletion seems to activate a cryptic splice site that results in an extension of the 5′ end of exon 4 (74).
A Danon disease patient with persistent hyperCKemia, exercise intolerance, and hypertrophic cardiomyopathy but with no muscle weakness or mental impairment was described by Musumeci et al (134). Skeletal muscle samples showed a vacuolar myopathy and a lysosome-associated membrane protein 2 (lamp2) deficiency. The lamp2 protein deficiency was caused by a novel T/C substitution at position 961 in exon 8 of the LAMP2 gene (134). Wang et al. reported an exercise-intolerant patient with severe mitochondrial myoptahy and 92% reduction in skeletal-muscle mitochondrial DNA content. The patient was a compound heterozygote for a T77M and R161K mutations in the thymidine kinase 2 (TK2) gene (247).
Mutations in five mitochondrial DNA genes were reported in exercise-intolerant patients. The only new gene to be introduced in the map was the mitochondrial transfer RNA aspartate (MTTD) gene. An A to G transition at position 7526 was identified in a young girl with pronounced exercise intolerance, decreased anaerobic threshold and V˙O2max, and decreased complex I and IV enzyme activity (202). A heteroplasmic T/C mutation at position 9789 in the mitochondrial cytochrome c oxidase subunit III (MTCO3) gene introducing a S195P change was found in skeletal muscle of a 22-yr-old exercise-intolerant patient (69). Blakely et al. reported a novel mutation in the mitochondrial cytochrome b (MTCYB) gene introducing an Arg318Pro substitution and a severe reduction of both complexes I and III in skeletal muscle (12).
Four new patients were reported carrying an A3302G mutation in the mitochondrial transfer RNA leucine (UUR) (MTTL1) gene. All patients had a mitochondrial myopathy, exercise intolerance, and proximal muscle weakness (70). Finally, Pulkes and colleagues reported a patient with isolated myopathy and exercise intolerance who carried both a C-insertion and a homoplasmic A to C transition at nucleotide position 7472 in the mitochondrial transfer RNA serine (UCN) (MTTS1) gene (156).
One new study on the associations between candidate gene markers and physical activity-related phenotypes was published in 2005 (Table 15). Loos and colleagues reported significant associations between a C/T polymorphism located 2745 base pairs upstream of the melanocortin 4 receptor (MC4R) gene start codon and physical activity phenotypes. Homozygotes for the rare T-allele had significantly lower moderate-to-strenuous physical activity levels and higher inactivity score than the other genotypes (105).
No new linkage studies were published in 2005.
SUMMARY AND CONCLUSIONS
This review provides a compendium of all genes and markers that have been associated with performance and health-related fitness phenotypes in scientific papers published by the end of 2005. Little progress has been made in the last 12 months with respect to the genetic basis of human variation in performance and health-related fitness. Indeed, although a growing number of genes are being identified, only a handful of them have been investigated with a view to assess whether DNA sequence variation in such genes play a role in the biological basis of human individuality.
The 2005 map includes 165 autosomal entries, five X chromosome assignments, and 17 mitochondrial DNA markers. There are 25 more nuclear markers and one more mitochondrial genome marker than in 2004. Given the complexity of the performance- and health-related fitness phenotypes, it should be obvious that we have a long way to go before we have a satisfactory understanding of the role of genetic inheritance on exercise-related traits and in the adaptation to a physically active lifestyle. Given the growing prevalence in obesity, type 2 diabetes, cardiovascular disease, and other chronic diseases associated with physical inactivity, an increased understanding of how the genetic susceptibilities that lead to these diseases may interact with exercise and physical activity interventions is urgently needed.
There is a growing number of genes with at least a minimum of evidence supporting their involvement in fitness- and performance-related phenotypes. This is illustrated by the trends in the number of loci from 2000 to 2005 for the families of phenotypes as defined in this review. Table 16 presents this synthesis for the 10 classes of phenotypes considered here. In each case, the number of genes or markers has increased slowly but steadily since the topic was first reviewed in 2000.
1. Abraham, M. R., L. J. Olson, M. J. Joyner, S. T. Turner, K. C. Beck, and B. D. Johnson. Angiotensin-converting enzyme genotype modulates pulmonary function and exercise capacity in treated patients with congestive stable heart failure. Circulation 106:1794-1799, 2002.
2. Adamo, K. B., R. J. Sigal, K. Williams, G. Kenny, D. Prud'homme, and F. Tesson. Influence of Pro12Ala peroxisome proliferator-activated receptor gamma2 polymorphism on glucose response to exercise training in type 2 diabetes. Diabetologia
3. Alvarez, R., N. Terrados, R. Ortolano, et al. Genetic variation in the renin-angiotensin system and athletic performance. Eur. J. Appl. Physiol. 82:117-120, 2000.
4. An, P., M. Teran-Garcia, T. Rice, T. Rankinen, et al. Genome-wide linkage scans for prediabetes phenotypes in response to 20 weeks of endurance exercise training in non-diabetic whites and blacks: the HERITAGE Family Study. Diabetologia
5. Andreu, A. L., C. Bruno, T. C. Dunne, et al. A nonsense mutation (G15059A) in the cytochrome b gene in a patient with exercise intolerance and myoglobinuria. Ann. Neurol.
45: 127-130, 1999.
6. Andreu, A. L., C. Bruno, S. Shanske, et al. Missense mutation in the mtDNA cytochrome b gene in a patient with myopathy. Neurology
7. Andreu, A. L., M. G. Hanna, H. Reichmann, et al. Exercise intolerance due to mutations in the cytochrome b gene of mitochondrial DNA. N. Engl. J. Med.
8. Andreu, A. L., K. Tanji, C. Bruno, et al. Exercise intolerance due to a nonsense mutation in the mtDNA ND4 gene. Ann. Neurol.
9. Ayyobi, A. F., J. S. Hill, H. O. Molhuizen, and S. A. Lear. Cholesterol ester transfer protein (CETP) Taq1B polymorphism influences the effect of a standardized cardiac rehabilitation program on lipid risk markers. Atherosclerosis
10. Berentzen, T., L. T. Dalgaard, L. Petersen, O. Pedersen, and T. I. Sorensen. Interactions between physical activity and variants of the genes encoding uncoupling proteins -2 and -3 in relation to body weight changes during a 10-y follow-up. Int. J. Obes. (Lond.)
11. Bernstein, M. S., M. C. Costanza, R. W. James, et al. Physical activity may modulate effects of ApoE genotype on lipid profile. Arterioscler. Thromb. Vasc. Biol.
12. Blakely, E. L., A. L. Mitchell, N. Fisher, et al. A mitochondrial cytochrome b mutation causing severe respiratory chain enzyme deficiency in humans and yeast. FEBS J.
13. Blanchet, C., Y. Giguere, D. Prud'homme, M. Dumont, F. Rousseau, and S. Dodin. Association of physical activity and bone: influence of vitamin D receptor genotype. Med. Sci. Sports Exerc.
14. Boer, J. M., J. A. Kuivenhoven, E. J. Feskens, et al. Physical activity modulates the effect of a lipoprotein lipase mutation (D9N) on plasma lipids and lipoproteins. Clin. Genet.
56: 158-163, 1999.
15. Bouchard, C., T. Rankinen, Y. C. Chagnon, et al. Genomic scan for maximal oxygen uptake and its response to training in the HERITAGE Family Study. J. Appl. Physiol.
16. Brull, D., S. Dhamrait, S. Myerson, et al. Bradykinin B2BKR receptor polymorphism and left-ventricular growth response. Lancet
17. Brull, D. J., S. Dhamrait, R. Moulding, et al. The effect of fibrinogen genotype on fibrinogen levels after strenuous physical exercise. Thromb. Haemost.
18. Bruno, C., G. Manfredi, A. L. Andreu, et al. A splice junction mutation in the alpha(M) gene of phosphorylase kinase in a patient with myopathy. Biochem. Biophys. Res. Commun.
19. Bruno, C., F. M. Santorelli, S. Assereto, et al. Progressive exercise intolerance associated with a new muscle-restricted nonsense mutation (G142X) in the mitochondrial cytochrome b gene. Muscle Nerve
20. Buemann, B., B. Schierning, S. Toubro, et al. The association between the val/ala-55 polymorphism of the uncoupling protein 2 gene and exercise efficiency. Int. J. Obes. Relat. Metab. Disord.
21. Cam, F. S., M. Colakoglu, C. Sekuri, S. Colakoglu, C. Sahan, and A. Berdeli. Association between the ACE I/D gene polymorphism and physical performance in a homogeneous non-elite cohort. Can. J. Appl. Physiol.
22. Campos, Y., J. Bautista, E. Gutierrez-Rivas, et al. Clinical heterogeneity in two pedigrees with the 3243 bp tRNA(Leu(UUR)) mutation of mitochondrial DNA. Acta Neurol. Scand.
23. Campos, Y., A. Garcia, A. Lopez, et al. Cosegregation of the mitochondrial DNA A1555G and G4309A mutations results indeafness and mitochondrial myopathy. Muscle Nerve
25: 185-188, 2002.
24. Chagnon, Y. C., T. Rice, L. Perusse, et al. Genomic scan for genes affecting body composition before and after training in Caucasians from HERITAGE. J. Appl. Physiol.
25. Clarkson, P. M., J. M. Devaney, H. Gordish-Dressman, et al. ACTN3 genotype is associated with increases in muscle strength in response to resistance training in women. J. Appl. Physiol.
26. Clarkson, P. M., E. P. Hoffman, E. Zambraski, et al. ACTN3 and MLCK genotype associations with exertional muscle damage. J. Appl. Physiol.
27. Collins, M., S. L. Xenophontos, M. A. Cariolou, et al. The ACE gene and endurance performance during the South African Ironman Triathlons. Med. Sci. Sports Exerc.
28. Comi, G. P., F. Fortunato, S. Lucchiari, et al. Beta-enolase deficiency, a new metabolic myopathy of distal glycolysis. Ann. Neurol. 50:202-207, 2001.
29. Corbalan, M. S. The 27Glu polymorphism of the beta2-adrenergic receptor gene interacts with physical activity influencing obesity risk among female subjects. Clin. Genet.
30. Corella, D., M. Guillen, C. Saiz, et al. Environmental factors modulate the effect of the APOE genetic polymorphism on plasma lipid concentrations: ecogenetic studies in a Mediterranean Spanish population. Metabolism
31. Data, S. A., M. H. Roltsch, B. Hand, R. E. Ferrell, J. J. Park, and M. D. Brown. eNOS T-786C genotype, physical activity, and peak forearm blood flow in females. Med. Sci. Sports Exerc.
32. de Groote, P., N. Lamblin, N. Helbecque, et al. The impact of beta-adrenoreceptor gene polymorphisms on survival in patients with congestive heart failure. Eur. J. Heart Fail.
33. Delanghe, J., M. Langlois, D. Duprez, M. De Buyzere, and D. Clement. Haptoglobin polymorphism and peripheral arterial occlusive disease. Atherosclerosis
34. Delmonico, M. J., R. E. Ferrell, A. Meerasahib, et al. Blood pressure response to strength training may be influenced by angiotensinogen A-20C and angiotensin II type I receptor A1166C genotypes in older men and women. J. Am. Geriatr. Soc.
35. Dengel, D. R., M. D. Brown, R. E. Ferrell, T. H. t Reynolds, and M. A. Supiano. Exercise-induced changes in insulin action are associated with ACE gene polymorphisms in older adults. Physiol. Genomics 11:73-80, 2002.
36. Dhamrait, S. S., L. James, D. J. Brull, et al. Cortical bone resorption during exercise is interleukin-6 genotype-dependent. Eur. J. Appl. Physiol.
37. Dionne, F. T., L. Turcotte, M. C. Thibault, M. R. Boulay, J. S. Skinner, and C. Bouchard. Mitochondrial DNA sequence polymorphism, VO2max, and response to endurance training. Med. Sci. Sports Exerc.
38. Eisenach, J. H., S. A. Barnes, T. L. Pike, et al. Arg16/Gly beta2-adrenergic receptor polymorphism alters the cardiac output response to isometric exercise. J. Appl. Physiol.
39. Eisenach, J. H., A. M. McGuire, R. M. Schwingler, S. T. Turner, and M. J. Joyner. The Arg16/Gly beta2-adrenergic receptor polymorphism is associated with altered cardiovascular responses to isometric exercise. Physiol. Genomics
40. Erbs, S., Y. Baither, A. Linke, et al. Promoter but not exon 7 polymorphism of endothelial nitric oxide synthase affects training-induced correction of endothelial dysfunction. Arterioscler. Thromb. Vasc. Biol.
41. Fatini, C., R. Guazzelli, P. Manetti, et al. RAS genes influence exercise-induced left ventricular hypertrophy: an elite athletes study. Med. Sci. Sports Exerc. 32:1868-1872, 2000.
42. Feitosa, M. F., I. B. Borecki, T. Rankinen, et al. Evidence of QTLs on chromosomes 1q42 and 8q24 for LDL-cholesterol and apoB levels in the HERITAGE family study. J. Lipid Res.
43. Feitosa, M. F., T. Rice, T. Rankinen, et al. Evidence of QTLs on chromosomes 13q and 14q for triglycerides before and after 20 weeks of exercise training: the HERITAGE Family Study. Atherosclerosis
44. Folland, J., B. Leach, T. Little, et al. Angiotensin-converting enzyme genotype affects the response of human skeletal muscle to functional overload. Exp. Physiol.
45. Franks, P. W., I. Barroso, J. Luan, et al. PGC-1alpha genotype modifies the association of volitional energy expenditure with [OV0312]O2max. Med. Sci. Sports Exerc.
46. Franks, P. W., S. Bhattacharyya, J. Luan, et al. Association between physical activity and blood pressure is modified by variants in the G-protein coupled receptor 10. Hypertension 43:224-228, 2004.
47. Friedl, W., F. Krempler, F. Sandhofer, and B. Paulweber. Insertion/deletion polymorphism in the angiotensin-converting-enzyme gene and blood pressure during ergometry in normal males. Clin. Genet.
48. Friedl, W., J. Mair, M. Pichler, B. Paulweber, F. Sandhofer, and B. Puschendorf. Insertion/deletion polymorphism in the angiotensin-converting enzyme gene is associated with atrial natriuretic peptide activity after exercise. Clin. Chim. Acta
49. Garenc, C., L. Perusse, J. Bergeron, et al. Evidence of LPL gene-exercise interaction for body fat and LPL activity: the HERITAGE Family Study. J. Appl. Physiol.
50. Garenc, C., L. Perusse, Y. C. Chagnon, et al. Effects of beta2-adrenergic receptor gene variants on adiposity: the HERITAGE Family Study. Obes. Res. 11:612-618, 2003.
51. Gayagay, G., B. Yu, B. Hambly, et al. Elite endurance athletes and the ACE I allele-the role of genes in athletic performance. Hum. Genet.
52. Geusens, P., C. Vandevyver, J. Vanhoof, J. J. Cassiman, S. Boonen, and J. Raus. Quadriceps and grip strength are related to vitamin D receptor genotype in elderly nonobese women. J. Bone Miner. Res.
53. Gosker, H. R., H. J. Pennings, and A. M. Schols. ACE gene polymorphism in COPD. Am. J. Respir. Crit. Care Med.
54. Grafakou, O., F. A. Hol, K. Otfried Schwab, et al. Exercise intolerance, muscle pain and lactic acidaemia associated with a 7497G(A mutation in the tRNASer(UCN) gene. J. Inherit. Metab. Dis.
55. Grundberg, E., H. Brandstrom, E. L. Ribom, O. Ljunggren, H. Mallmin, and A. Kindmark. Genetic variation in the human vitamin D receptor is associated with muscle strength, fat mass and body weight in Swedish women. Eur. J. Endocrinol.
56. Grundberg, E., E. L. Ribom, H. Brandstrom, O. Ljunggren, H. Mallmin, and A. Kindmark. A TA-repeat polymorphism in the gene for the estrogen receptor alpha does not correlate with muscle strength or body composition in young adult Swedish women. Maturitas
57. Grunig, E., B. Janssen, D. Mereles, et al. Abnormal pulmonary artery pressure response in asymptomatic carriers of primary pulmonary hypertension gene. Circulation
58. Hadjigeorgiou, G. M., N. Kawashima, C. Bruno, et al. Manifesting heterozygotes in a Japanese family with a novel mutation in the muscle-specific phosphoglycerate mutase (PGAM-M) gene. Neuromuscul. Disord.
59. Hagberg, J. M., R. E. Ferrell, D. R. Dengel, and K. R. Wilund. Exercise training-induced blood pressure and plasma lipid improvements in hypertensives may be genotype dependent. Hypertension
60. Hagberg, J. M., R. E. Ferrell, L. I. Katzel, D. R. Dengel, J. D. Sorkin, and A. P. Goldberg. Apolipoprotein E genotype and exercise training-induced increases in plasma high-density lipoprotein (HDL)- and HDL2-cholesterol levels in overweight men. Metabolism 48:943-945, 1999.
61. Hagberg, J. M., R. E. Ferrell, S. D. McCole, K. R. Wilund, and G. E. Moore. VO2max is associated with ACE genotype in postmenopausal women. J. Appl. Physiol.
62. Hagberg, J. M., S. D. McCole, M. D. Brown, et al. ACE insertion/deletion polymorphism and submaximal exercise hemodynamics in postmenopausal women. J. Appl. Physiol. 92:1083-1088, 2002.
63. Halverstadt, A., D. A. Phares, R. E. Ferrell, K. R. Wilund, A. P. Goldberg, and J. M. Hagberg. High-density lipoprotein-cholesterol, its subfractions, and responses to exercise training are dependent on endothelial lipase genotype. Metabolism
64. Halverstadt, A., D. A. Phares, S. Roth, R. E. Ferrell, A. P. Goldberg, and J. M. Hagberg. Interleukin-6 genotype is associated with high-density lipoprotein cholesterol responses to exercise training. Biochim. Biophys. Acta
65. Hanna, M. G., I. P. Nelson, S. Rahman, et al. Cytochrome c oxidase deficiency associated with the first stop-codon point mutation in human mtDNA. Am. J. Hum. Genet.
66. Hao, H., E. Bonilla, G. Manfredi, S. DiMauro, and C. T. Moraes. Segregation patterns of a novel mutation in the mitochondrial tRNA glutamic acid gene associated with myopathy and diabetes mellitus. Am. J. Hum. Genet.
67. Hellerud, C., N. Wramner, A. Erikson, A. Johansson, G. Samuelson, and S. Lindstedt. Glycerol kinase deficiency: follow-up during 20 years, genetics, biochemistry and prognosis. Acta Paediatr.
68. Hopkinson, N. S., A. H. Nickol, J. Payne, et al. Angiotensin converting enzyme genotype and strength in chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med.
69. Horvath, R., B. G. Schoser, J. Muller-Hocker, M. Volpel, M. Jaksch, and H. Lochmuller. Mutations in mtDNA-encoded cytochrome c oxidase subunit genes causing isolated myopathy or severe encephalomyopathy. Neuromuscul. Disord.
70. Hutchison, W. M., D. Thyagarajan, J. Poulton, et al. Clinical and molecular features of encephalomyopathy due to the A3302G mutation in the mitochondrial tRNA(Leu(UUR)) gene. Arch. Neurol.
71. Huygens, W., M. A. Thomis, M. W. Peeters, et al. Linkage of myostatin pathway genes with knee strength in humans. Physiol. Genomics
72. Huygens, W., M. A. Thomis, M. W. Peeters, et al. A quantitative trait locus on 13q14.2 for trunk strength. Twin. Res.
73. Huygens, W., M. A. Thomis, M. W. Peeters, J. Aerssens, R. Vlietinck, and G. P. Beunen. Quantitative trait loci for human muscle strength: linkage analysis of myostatin pathway genes. Physiol. Genomics
74. Isackson, P. J., H. Bujnicki, C. O. Harding, and G. D. Vladutiu. Myoadenylate deaminase deficiency caused by alternative splicing due to a novel intronic mutation in the AMPD1 gene. Mol. Genet. Metab.
75. Ivey, F. M., S. M. Roth, R. E. Ferrell, et al. Effects of age, gender, and myostatin genotype on the hypertrophic response to heavy resistance strength training. J. Gerontol. A Biol. Sci. Med. Sci.
76. Jamshidi, Y., H. E. Montgomery, H. W. Hense, et al. Peroxisome proliferator-activated receptor alpha gene regulates left ventricular growth in response to exercise and hypertension. Circulation
77. Kahara, T., T. Hayakawa, Y. Nagai, A. Shimizu, and T.Takamura. Gln27Glu polymorphism of the beta2 adrenergic receptor gene in healthy Japanese men is associated with the change of fructosamine level caused by exercise. Diabetes Res. Clin. Pract.
78. Kahara, T., T. Takamura, T. Hayakawa, et al. PPARgamma gene polymorphism is associated with exercise-mediated changes of insulin resistance in healthy men. Metabolism
79. Kahara, T., T. Takamura, T. Hayakawa, et al. Prediction of exercise-mediated changes in metabolic markers by gene polymorphism. Diabetes Res. Clin. Pract.
80. Kallio, J., U. Pesonen, K. Kaipio, et al. Altered intracellular processing and release of neuropeptide Y due to leucine 7 to proline 7 polymorphism in the signal peptide of preproneuropeptide Y in humans. Faseb. J.
81. Kallio, J., U. Pesonen, M. K. Karvonen, et al. Enhanced exercise-induced GH secretion in subjects with Pro7 substitution in the prepro-NPY. J. Clin. Endocrinol. Metab.
82. Kanazawa, H., K. Hirata, and J. Yoshikawa. Effects of captopril administration on pulmonary haemodynamics and tissue oxygenation during exercise in ACE gene subtypes in patients with COPD: a preliminary study. Thorax
83. Kanazawa, H., K. Hirata, and J. Yoshikawa. Influence of oxygen administration on pulmonary haemodynamics and tissue oxygenation during exercise in COPD patients with different ACE genotypes. Clin. Physiol. Funct. Imaging
84. Kanazawa, H., T. Okamoto, K. Hirata, and J. Yoshikawa. Deletion polymorphisms in the angiotensin converting enzyme gene are associated with pulmonary hypertension evoked by exercise challenge in patients with chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med.
85. Kanazawa, H., T. Otsuka, K. Hirata, and J. Yoshikawa. Association between the angiotensin-converting enzyme gene polymorphisms and tissue oxygenation during exercise in patients with COPD. Chest
86. Kanazawa, H., Y. Tateishi, and J. Yoshikawa. Acute effects of nifedipine administration in pulmonary haemodynamics and oxygen delivery during exercise in patients with chronic obstructive pulmonary disease: implication of the angiotensin-converting enzyme gene polymorphisms. Clin. Physiol. Funct. Imaging
87. Karadimas, C. L., P. Greenstein, C. M. Sue, et al. Recurrent myoglobinuria due to a nonsense mutation in the COX I gene of mitochondrial DNA. Neurology
88. Karadimas, C. L., L. Salviati, S. Sacconi, et al. Mitochondrial myopathy and ophthalmoplegia in a sporadic patient with the G12315A mutation in mitochondrial DNA. Neuromuscul. Disord.
89. Kasikcioglu, E., A. Kayserilioglu, F. Ciloglu, et al. Angiotensin-converting enzyme gene polymorphism, left ventricular remodeling, and exercise capacity in strength-trained athletes. Heart Vessels
90. Keightley, J. A., R. Anitori, M. D. Burton, F. Quan, N. R. Buist, and N. G. Kennaway. Mitochondrial encephalomyopathy and complex III deficiency associated with a stop-codon mutation in the cytochrome b gene. Am. J. Hum. Genet.
91. Kimura, T., T. Yokoyama, Y. Matsumura, et al. NOS3 genotype-dependent correlation between blood pressure and physical activity. Hypertension 41:355-360, 2003.
92. Kitagawa, I., Y. Kitagawa, T. Nagaya, and S. Tokudome. Interplay of physical activity and vitamin D receptor genepolymorphism on bone mineral density. J. Epidemiol. 11:229-232, 2001.
93. Kostek, M. C., M. J. Delmonico, J. B. Reichel, et al. Muscle strength response to strength training is influenced by insulin-like growth factor 1 genotype in older adults. J. Appl. Physiol.
94. Kritchevsky, S. B., B. J. Nicklas, M. Visser, et al. Angiotensin-converting enzyme insertion/deletion genotype, exercise, and physical decline. JAMA
95. Krizanova, O., J. Koska, M. Vigas, and R. Kvetnansky. Correlation of M235T DNA polymorphism with cardiovascular and endocrine responses during physical exercise in healthy subjects. Physiol. Res.
96. Lahat, H., M. Eldar, E. Levy-Nissenbaum, et al. Autosomal recessive catecholamine- or exercise-induced polymorphic ventricular tachycardia: clinical features and assignment of the disease gene to chromosome 1p13-21. Circulation
97. Lahat, H., E. Pras, T. Olender, et al. A missense mutation in a highly conserved region of CASQ2 is associated with autosomal recessive catecholamine-induced polymorphic ventricular tachycardia in Bedouin families from Israel. Am. J. Hum. Genet.
98. Laitinen, P. J., K. M. Brown, K. Piippo, et al. Mutations of the cardiac ryanodine receptor (RyR2) gene in familial polymorphic ventricular tachycardia. Circulation
99. Lakka, T. A., T. Rankinen, S. J. Weisnagel, et al. Leptin and leptin receptor gene polymorphisms and changes in glucose homeostasis in response to regular exercise in nondiabetic individuals: the HERITAGE family study. Diabetes
100. Lakka, T. A., T. Rankinen, S. J. Weisnagel, et al. A quantitative trait locus on 7q31 for the changes in plasma insulin in response to exercise training: the HERITAGE Family Study. Diabetes
101. Lamantea, E., F. Carrara, C. Mariotti, L. Morandi, V. Tiranti, and M. Zeviani. A novel nonsense mutation (Q352X) in the mitochondrial cytochrome b gene associated with a combined deficiency of complexes I and III. Neuromuscul. Disord.
102. Lanouette, C. M., Y. C. Chagnon, T. Rice, et al. Uncoupling protein 3 gene is associated with body composition changes with training in HERITAGE study. J. Appl. Physiol. 92:1111-1118, 2002.
103. Leon, A. S., K. Togashi, T. Rankinen, et al. Association of apolipoprotein E polymorphism with blood lipids and maximal oxygen uptake in the sedentary state and after exercise training in the HERITAGE family study. Metabolism
104. Lindi, V. I., M. I. Uusitupa, J. Lindstrom, et al. Association of the Pro12Ala polymorphism in the PPAR-gamma2 gene with 3-year incidence of type 2 diabetes and body weight change in the Finnish Diabetes Prevention Study. Diabetes
105. Loos, R. J., T. Rankinen, A. Tremblay, L. Perusse, Y. Chagnon, and C. Bouchard. Melanocortin-4 receptor gene and physical activity in the Quebec Family Study. Int. J. Obes. (Lond)
106. Lorentzon, M., R. Lorentzon, U. H. Lerner, and P. Nordstrom. Calcium sensing receptor gene polymorphism, circulating calcium concentrations and bone mineral density in healthy adolescent girls. Eur. J. Endocrinol.
107. Lorentzon, M., R. Lorentzon, and P. Nordstrom. Vitamin D receptor gene polymorphism is related to bone density, circulating osteocalcin, and parathyroid hormone in healthy adolescent girls. J. Bone Miner. Metab.
108. Lucia, A., F. Gomez-Gallego, I. Barroso, et al. PPARGC1A genotype (Gly482Ser) predicts exceptional endurance capacity in European men. J. Appl. Physiol.
109. Lucia, A., F. Gomez-Gallego, J. L. Chicharro, et al. Is there an association between ACE and CKMM polymorphisms and cycling performance status during 3-week races? Int. J. Sports Med.
110. Macho-Azcarate, T., J. Calabuig, A. Marti, and J. A. Martinez. A maximal effort trial in obese women carrying the beta2-adrenoceptor Gln27Glu polymorphism. J. Physiol. Biochem.
111. Macho-Azcarate, T., A. Marti, J. Calabuig, and J. A. Martinez. Basal fat oxidation and after a peak oxygen consumption test in obese women with a beta2 adrenoceptor gene polymorphism. J. Nutr. Biochem.
112. Macho-Azcarate, T., A. Marti, A. Gonzalez, J. A. Martinez, and J. Ibanez. Gln27Glu polymorphism in the beta2 adrenergic receptor gene and lipid metabolism during exercise in obese women. Int. J. Obes. Relat. Metab. Disord.
113. Mancuso, M., M. Filosto, J. C. Stevens, et al. Mitochondrial myopathy and complex III deficiency in a patient with a newstop-codon mutation (G339X) in the cytochrome b gene. J.Neurol. Sci. 209:61-63, 2003.
114. Martin, M. A., J. C. Rubio, P. del Hoyo, et al. Identification of novel mutations in Spanish patients with muscle carnitine palmitoyltransferase II deficiency. Hum. Mutat.
115. McCole, S. D., M. D. Brown, G. E. Moore, et al. Angiotensinogen M235T polymorphism associates with exercise hemodynamics in postmenopausal women. Physiol. Genomics
116. McCole, S. D., A. R. Shuldiner, M. D. Brown, et al. Beta2- and beta3-adrenergic receptor polymorphisms and exercise hemodynamics in postmenopausal women. J. Appl. Physiol.
117. McFarland, R., R. W. Taylor, P. F. Chinnery, N. Howell, and D. M. Turnbull. A novel sporadic mutation in cytochrome c oxidase subunit II as a cause of rhabdomyolysis. Neuromuscul. Disord.
118. McKenzie, J. A., E. P. Weiss, I. A. Ghiu, et al. Influence of the interleukin-6 -174 G/C gene polymorphism on exercise training-induced changes in glucose tolerance indexes. J. Appl. Physiol.
119. Meirhaeghe, A., N. Helbecque, D. Cottel, and P. Amouyel. Beta2-adrenoceptor gene polymorphism, body weight, and physical activity. Lancet
120. Meirhaeghe, A., J. Luan, P. Selberg-Franks, et al. The effect of the Gly16Arg polymorphism of the beta(2)-adrenergic receptor gene on plasma free fatty acid levels is modulated by physical activity. J. Clin. Endocrinol. Metab.
121. Modugno, F., J. M. Zmuda, D. Potter, et al. Estrogen metabolizing polymorphisms and breast cancer risk among older white women. Breast Cancer Res. Treat.
122. Mongini, T., C. Doriguzzi, I. Bosone, L. Chiado-Piat, E. P. Hoffman, and L. Palmucci. Alpha-sarcoglycan deficiency featuring exercise intolerance and myoglobinuria. Neuropediatrics
123. Montgomery, H., P. Clarkson, M. Barnard, et al. Angiotensin-converting-enzyme gene insertion/deletion polymorphism and response to physical training. Lancet 353:541-545, 1999.
124. Montgomery, H. E., P. Clarkson, C. M. Dollery, et al. Association of angiotensin-converting enzyme gene I/D polymorphism with change in left ventricular mass in response to physical training. Circulation
125. Montgomery, H. E., P. Clarkson, O. M. Nwose, et al. The acute rise in plasma fibrinogen concentration with exercise is influenced by the G-453-A polymorphism of the beta-fibrinogen gene. Arterioscler. Thromb. Vasc. Biol.
126. Montgomery, H. E., R. Marshall, H. Hemingway, et al. Human gene for physical performance. Nature
127. Moore, G. E., A. R. Shuldiner, J. M. Zmuda, R. E. Ferrell, S. D. McCole, and J. M. Hagberg. Obesity gene variant and elite endurance performance. Metabolism
128. Moran, C. N., R. A. Scott, S. M. Adams, et al. Y chromosome haplogroups of elite Ethiopian endurance runners. Hum. Genet.
129. Moran, C. N., C. Vassilopoulos, A. Tsiokanos, et al. Effects of interaction between angiotensin I-converting enzyme polymorphisms and lifestyle on adiposity in adolescent Greeks. Obes. Res.
130. Morimoto, L. M., P. A. Newcomb, E. White, J. Bigler, and J. D. Potter. Insulin-like growth factor polymorphisms and colorectal cancer risk. Cancer Epidemiol. Biomarkers Prev.
131. Mukherjee, M., and K. R. Shetty. Variations in high-density lipoprotein cholesterol in relation to physical activity and Taq 1B polymorphism of the cholesteryl ester transfer protein gene. Clin. Genet.
132. Munoz-Malaga, A., J. Bautista, J. A. Salazar, et al. Lipomatosis, proximal myopathy, and the mitochondrial 8344 mutation. A lipid storage myopathy? Muscle Nerve 23:538-542, 2000.
133. Musumeci, O., A. L. Andreu, S. Shanske, et al. Intragenic inversion of mtDNA: a new type of pathogenic mutation in a patient with mitochondrial myopathy. Am. J. Hum. Genet.
134. Musumeci, O., C. Rodolico, I. Nishino, et al. Asymptomatic hyperCKemia in a case of Danon disease due to a missense mutation in Lamp-2 gene. Neuromuscul. Disord.
135. Myerson, S., H. Hemingway, R. Budget, J. Martin, S. Humphries, and H. Montgomery. Human angiotensin I-converting enzyme gene and endurance performance. J. Appl. Physiol.
136. Myerson, S. G., H. E. Montgomery, M. Whittingham, et al. Left ventricular hypertrophy with exercise and ACE gene insertion/deletion polymorphism: a randomized controlled trial with Losartan. Circulation 103:226-230, 2001.
137. Nakamura, O., T. Ishii, Y. Ando, et al. Potential role of vitamin D receptor gene polymorphism in determining bone phenotype in young male athletes. J. Appl. Physiol.
138. Nazarov, I. B., D. R. Woods, H. E. Montgomery, et al. The angiotensin converting enzyme I/D polymorphism in Russian athletes. Eur. J. Hum. Genet.
139. Nicklas, B. J., J. Mychaleckyj, S. Kritchevsky, et al. Physical function and its response to exercise: associations with cytokine gene variation in older adults with knee osteoarthritis. J. Gerontol. A Biol. Sci. Med. Sci.
140. Niemi, A. K., and K. Majamaa. Mitochondrial DNA and ACTN3 genotypes in Finnish elite endurance and sprint athletes. Eur. J. Hum. Genet.
141. Ortlepp, J. R., J. Metrikat, M. Albrecht, A. von Korff, P. Hanrath, and R. Hoffmann. The vitamin D receptor gene variant and physical activity predicts fasting glucose levels in healthy young men. Diabet. Med.
142. Ortlepp, J. R., J. Metrikat, K. Vesper, et al. The interleukin-6 promoter polymorphism is associated with elevated leukocyte, lymphocyte, and monocyte counts and reduced physical fitness in young healthy smokers. J. Mol. Med.
143. Ostergard, T., J. Ek, Y. Hamid, et al. Influence of the PPAR-gamma2 Pro12Ala and ACE I/D polymorphisms on insulin sensitivity and training effects in healthy offspring of type 2 diabetic subjects. Horm. Metab. Res.
144. Otabe, S., K. Clement, C. Dina, et al. A genetic variation in the 5' flanking region of the UCP3 gene is associated with body mass index in humans in interaction with physical activity. Diabetologia
145. Palmieri, L., S. Alberio, I. Pisano, et al. Complete loss-of-function of the heart/muscle-specific adenine nucleotide translocator is associated with mitochondrial myopathy and cardiomyopathy. Hum. Mol. Genet.
146. Pantoja-Martinez, J., C. Navarro Fernandez-Balbuena, M. Gormaz-Moreno, B. Quintans-Castro, M. A. Esparza-Sanchez, and J. Bonet-Arzo. Myoadenylate deaminase deficiency in a child with myalgias induced by physical exercise. Rev. Neurol.
147. Park, J. Y., R. E. Ferrell, J. J. Park, et al. NADPH oxidase p22phox gene variants are associated with systemic oxidative stress biomarker responses to exercise training. J. Appl. Physiol.
148. Patel, S., D. R. Woods, N. J. Macleod, et al. Angiotensin-converting enzyme genotype and the ventilatory response to exertional hypoxia. Eur. Respir. J. 22:755-760, 2003.
149. Peeters, R. P., A. W. van den Beld, H. van Toor, et al. A polymorphism in type I deiodinase is associated with circulating free insulin-like growth factor I levels and body composition in humans. J. Clin. Endocrinol. Metab.
150. Peters, W. R., J. P. MacMurry, J. Walker, R. J. Giese, Jr., and D. E. Comings. Phenylethanolamine N-methyltransferase G-148A genetic variant and weight loss in obese women. Obes. Res.
151. Phares, D. A., A. A. Halverstadt, A. R. Shuldiner, et al. Association between body fat response to exercise training and multilocus ADR genotypes. Obes. Res.
152. Pisciotta, L., A. Cantafora, A. Piana, et al. Physical activity modulates effects of some genetic polymorphisms affecting cardiovascular risk in men aged over 40 years. Nutr. Metab. Cardiovasc. Dis.
153. Postma, A. V., I. Denjoy, T. M. Hoorntje, et al. Absence of calsequestrin 2 causes severe forms of catecholaminergic polymorphic ventricular tachycardia. Circ. Res.
154. Prior, S. J., J. M. Hagberg, D. A. Phares, et al. Sequence variation in hypoxia-inducible factor 1alpha (HIF1A): association with maximal oxygen consumption. Physiol. Genomics
155. Priori, S. G., C. Napolitano, N. Tiso, et al. Mutations in the cardiac ryanodine receptor gene (hRyR2) underlie catecholaminergic polymorphic ventricular tachycardia. Circulation
156. Pulkes, T., D. Liolitsa, L. H. Eunson, et al. New phenotypic diversity associated with the mitochondrial tRNA(SerUCN) gene mutation. Neuromuscul. Disord.
157. Pulkes, T., A. Siddiqui, J. A. Morgan-Hughes, and M. G. Hanna. A novel mutation in the mitochondrial tRNA(TYr) gene associated with exercise intolerance. Neurology
158. Rabon-Stith, K. M., J. M. Hagberg, D. A. Phares, et al. Vitamin D receptor FokI genotype influences bone mineral density response to strength training, but not aerobic training. Exp. Physiol.
159. Rankinen, T., P. An, L. Perusse, et al. Genome-wide linkage scan for exercise stroke volume and cardiac output in the HERITAGE Family Study. Physiol. Genomics 10:57-62, 2002.
160. Rankinen, T., P. An, T. Rice, et al. Genomic scan for exercise blood pressure in the Health, Risk Factors, Exercise Training and Genetics (HERITAGE) Family Study. Hypertension
161. Rankinen, T., J. Gagnon, L. Perusse, et al. AGT M235T and ACE ID polymorphisms and exercise blood pressure in the HERITAGE Family Study. Am. J. Physiol. Heart Circ. Physiol.
162. Rankinen, T., L. Perusse, I. Borecki, et al. The Na(+)-K(+)-ATPase alpha2 gene and trainability of cardiorespiratory endurance: the HERITAGE family study. J. Appl. Physiol.
163. Rankinen, T., L. Perusse, J. Gagnon, et al. Angiotensin-converting enzyme ID polymorphism and fitness phenotype in the HERITAGE Family Study. J. Appl. Physiol.
164. Rankinen, T., L. Perusse, R. Rauramaa, M. A. Rivera, B. Wolfarth, and C. Bouchard. The human gene map for performance and health-related fitness phenotypes. Med. Sci. Sports Exerc.
165. Rankinen, T., T. Rice, A. Boudreau, et al. Titin is a candidate gene for stroke volume response to endurance training: the HERITAGE Family Study. Physiol. Genomics
166. Rankinen, T., T. Rice, A. S. Leon, et al. G protein beta 3 polymorphism and hemodynamic and body composition phenotypes in the HERITAGE Family Study. Physiol. Genomics
167. Rankinen, T., T. Rice, L. Perusse, et al. NOS3 Glu298Asp genotype and blood pressure response to endurance training: the HERITAGE family study. Hypertension
168. Rauramaa, R., R. Kuhanen, T. A. Lakka, et al. Physical exercise and blood pressure with reference to the angiotensinogen M235T polymorphism. Physiol. Genomics
169. Rauramaa, R., S. Vaisanen, A. Nissinen, et al. Physical activity, fibrinogen plasma level and gene polymorphisms in postmenopausal women. Thromb. Haemost.
170. Rauramaa, R., S. B. Vaisanen, R. Kuhanen, I. Penttila, and C. Bouchard. The RsaI polymorphism in the alpha-fibrinogen gene and response of plasma fibrinogen to physical training-a controlled randomised clinical trial in men. Thromb. Haemost.
171. Remes, T., S. B. Vaisanen, A. Mahonen, et al. Aerobic exercise and bone mineral density in middle-aged finnish men: a controlled randomized trial with reference to androgen receptor, aromatase, and estrogen receptor alpha gene polymorphisms. Bone
172. Rice, T., Y. C. Chagnon, L. Perusse, et al. A genomewide linkage scan for abdominal subcutaneous and visceral fat in black and white families: The HERITAGE Family Study. Diabetes
173. Rice, T., T. Rankinen, Y. C. Chagnon, et al. Genomewide linkage scan of resting blood pressure: HERITAGE Family Study. Health, Risk Factors, Exercise Training, and Genetics. Hypertension
174. Rico-Sanz, J., T. Rankinen, D. R. Joanisse, et al. Associations between cardiorespiratory responses to exercise and the C34T AMPD1 gene polymorphism in the HERITAGE Family Study. Physiol. Genomics
175. Rico-Sanz, J., T. Rankinen, T. Rice, et al. Quantitative trait loci for maximal exercise capacity phenotypes and their responses to training in the HERITAGE Family Study. Physiol. Genomics
176. Riechman, S. E., G. Balasekaran, S. M. Roth, and R. E. Ferrell. Association of interleukin-15 protein and interleukin-15 receptor genetic variation with resistance exercise training responses. J. Appl. Physiol. 97:2214-2219, 2004.
177. Riechman, S. E., T. J. Fabian, P. D. Kroboth, and R. E. Ferrell. Steroid sulfatase gene variation and DHEA responsiveness to resistance exercise in MERET. Physiol. Genomics
178. Rivera, M. A., F. T. Dionne, J. A. Simoneau, et al. Muscle-specific creatine kinase gene polymorphism and VO2max in the HERITAGE Family Study. Med. Sci. Sports Exerc.
179. Rivera, M. A., M. Echegaray, T. Rankinen, et al. Angiogenin gene-race interaction for resting and exercise BP phenotypes: the HERITAGE Family Study. J. Appl. Physiol.
180. Rivera, M. A., M. Echegaray, T. Rankinen, et al. TGF-beta(1) gene-race interactions for resting and exercise blood pressure in the HERITAGE Family Study. J. Appl. Physiol.
181. Rivera, M. A., L. Perusse, J. A. Simoneau, et al. Linkage between a muscle-specific CK gene marker and VO2max in the HERITAGE Family Study. Med. Sci. Sports Exerc. 31:698-701, 1999.
182. Rodas, G., G. Ercilla, C. Javierre, et al. Could the A2A11 human leucocyte antigen locus correlate with maximal aerobic power? Clin. Sci. (Lond.)
183. Roltsch, M. H., M. D. Brown, B. D. Hand, et al. No association between ACE I/D polymorphism and cardiovascular hemodynamics during exercise in young women. Int. J. Sports Med.
184. Roth, S. M., E. J. Metter, M.R. Lee, B. F. Hurley, and R. E. Ferrell. C174T polymorphism in the CNTF receptor gene is associated with fat-free mass in men and women. J. Appl. Physiol.
185. Roth, S. M., M. A. Schrager, R. E. Ferrell, et al. CNTF genotype is associated with muscular strength and quality in humans across the adult age span. J. Appl. Physiol.
186. Roth, S. M., J. M. Zmuda, J. A. Cauley, P. R. Shea, and R. E. Ferrell. Vitamin D receptor genotype is associated with fat-free mass and sarcopenia in elderly men. J. Gerontol. A Biol. Sci. Med. Sci.
187. Ruano, G., R. L. Seip, A. Windemuth, et al. Apolipoprotein A1 genotype affects the change in high density lipoprotein cholesterol subfractions with exercise training. Atherosclerosis
188. Rubio, J. C., M. A. Martin, M. Rabadan, et al. Frequency of the C34T mutation of the AMPD1 gene in world-class endurance athletes: does this mutation impair performance? J. Appl. Physiol.
189. Sakane, N., T. Yoshida, T. Umekawa, A. Kogure, Y. Takakura, and M. Kondo. Effects of Trp64Arg mutation in the beta 3-adrenergic receptor gene on weight loss, body fat distribution, glycemic control, and insulin resistance in obese type 2 diabetic patients. Diabetes Care
190. Salmen, T., A. M. Heikkinen, A. Mahonen, et al. Relation of aromatase gene polymorphism and hormone replacement therapy to serum estradiol levels, bone mineral density, and fracture risk in early postmenopausal women. Ann. Med.
191. Sandilands, A. J., J. Parameshwar, S. Large, M. J. Brown, and K. M. O'Shaughnessy. Confirmation of a role for the 389R(G beta-1 adrenoceptor polymorphism on exercise capacity in heart failure. Heart
192. Sayer, A. A., H. Syddall, S. D. O'Dell, et al. Polymorphism of the IGF2 gene, birth weight and grip strength in adult men. Age Ageing
193. Scanavini, D., F. Bernardi, E. Castoldi, F. Conconi, and G. Mazzoni. Increased frequency of the homozygous II ACE genotype in Italian Olympic endurance athletes. Eur. J. Hum. Genet.
194. Scholte, H. R., R. N. Van Coster, P. C. de Jonge, et al. Myopathy in very-long-chain acyl-CoA dehydrogenase deficiency: clinical and biochemical differences with the fatal cardiac phenotype. Neuromuscul. Disord. 9:313-319, 1999.
195. Schrager, M. A., S. M. Roth, R. E. Ferrell, et al. Insulin-like growth factor-2 (IGF2) genotype, fat-free mass, and muscle performance across the adult life span. J. Appl. Physiol.
196. Schuelke, M., H. Krude, B. Finckh, et al. Septo-optic dysplasia associated with a new mitochondrial cytochrome b mutation. Ann. Neurol.
197. Schwartz, P. J., S. G. Priori, C. Spazzolini, et al. Genotype-phenotype correlation in the long-QT syndrome: gene-specific triggers for life-threatening arrhythmias. Circulation 103:89-95, 2001.
198. Scott, R. A., C. Moran, R. H. Wilson, et al. No association between angiotensin converting enzyme (ACE) gene variation and endurance athlete status in Kenyans. Comp. Biochem. Physiol. A Mol. Integr. Physiol.
199. Scott, R. A., R. H. Wilson, W. H. Goodwin, et al. Mitochondrial DNA lineages of elite Ethiopian athletes. Comp. Biochem. Physiol. B Biochem. Mol. Biol.
200. Seibert, M. J., Q. L. Xue, L. P. Fried, and J. D. Walston. Polymorphic variation in the human myostatin (GDF-8) gene and association with strength measures in the Women's Health and Aging Study II cohort. J. Am. Geriatr. Soc.
201. Selvadurai, H. C., K. O. McKay, C. J. Blimkie, P. J. Cooper, C. M. Mellis, and P. P. Van Asperen. The relationship between genotype and exercise tolerance in children with cystic fibrosis. Am. J. Respir. Crit. Care Med.
202. Seneca, S., N. Goemans, R. Van Coster, et al. A mitochondrial tRNA aspartate mutation causing isolated mitochondrial myopathy. Am. J. Med. Genet. A
203. Sengler, C., A. Heinzmann, S. P. Jerkic, et al. Clara cell protein 16 (CC16) gene polymorphism influences the degree of airway responsiveness in asthmatic children. J. Allergy Clin. Immunol.
204. Senti, M., C. Aubo, R. Elosua, J. Sala, M. Tomas, and J. Marrugat. Effect of physical activity on lipid levels in a population-based sample of men with and without the Arg192 variant of the human paraoxonase gene. Genet. Epidemiol. 18:276-286, 2000.
205. Sherman, J. B., N. Raben, C. Nicastri, et al. Common mutations in the phosphofructokinase-M gene in Ashkenazi Jewish patients with glycogenesis VII-and their population frequency. Am. J. Hum. Genet.
206. Shiwaku, K., A. Nogi, E. Anuurad, et al. Difficulty in losing weight by behavioral intervention for women with Trp64Arg polymorphism of the beta3-adrenergic receptor gene. Int. J. Obes. Relat. Metab. Disord. 27:1028-1036, 2003.
207. Simonen, R. L., T. Rankinen, L. Perusse, et al. A dopamine D2 receptor gene polymorphism and physical activity in two family studies. Physiol. Behav.
208. Simonen, R. L., T. Rankinen, L. Perusse, et al. Genome-wide linkage scan for physical activity levels in the Quebec Family study. Med. Sci. Sports Exerc.
209. Slattery, M. L., K. B. Baumgartner, T. Byers, et al. Genetic, anthropometric, and lifestyle factors associated with IGF-1 and IGFBP-3 levels in Hispanic and non-Hispanic white women. Cancer Causes Control
210. Slattery, M. L., M. A. Murtaugh, C. Sweeney, et al. PPARgamma, energy balance, and associations with colon and rectal cancer. Nutr. Cancer
211. Stefan, N., F. Machicao, H. Staiger, et al. Polymorphisms in the gene encoding adiponectin receptor 1 are associated with insulin resistance and high liver fat. Diabetologia
212. Stefan, N., B. Vozarova, A. Del Parigi, et al. The Gln223Arg polymorphism of the leptin receptor in Pima Indians: influence on energy expenditure, physical activity and lipid metabolism. Int. J. Obes. Relat. Metab. Disord.
213. Sun, G., J. Gagnon, Y. C. Chagnon, et al. Association and linkage between an insulin-like growth factor-1 gene polymorphism and fat free mass in the HERITAGE Family Study. Int. J. Obes. Relat. Metab. Disord.
214. Taggart, R. T., D. Smail, C. Apolito, and G. D. Vladutiu. Novel mutations associated with carnitine palmitoyltransferase II deficiency. Hum. Mutat.
215. Taimela, S., T. Lehtimaki, K. V. Porkka, L. Rasanen, and J. S. Viikari. The effect of physical activity on serum total and low-density lipoprotein cholesterol concentrations varies with apolipoprotein E phenotype in male children and young adults: The Cardiovascular Risk in Young Finns Study. Metabolism
216. Tajima, O., N. Ashizawa, T. Ishii, et al. Interaction of the effects between vitamin D receptor polymorphism and exercise training on bone metabolism. J. Appl. Physiol.
217. Tanriverdi, H., H. Evrengul, S. Tanriverdi, et al. Improved endothelium dependent vasodilation in endurance athletes and its relation with ACE I/D polymorphism. Circ. J.
218. Taroni, F., E. Verderio, F. Dworzak, P. J. Willems, P. Cavadini, and S. DiDonato. Identification of a common mutation in the carnitine palmitoyltransferase II gene in familial recurrent myoglobinuria patients. Nat. Genet. 4:314-320, 1993.
219. Teran-Garcia, M., N. Santoro, T. Rankinen, et al. Hepatic lipase gene variant -514C(T is associated with lipoprotein and insulin sensitivity response to regular exercise: the HERITAGE Family Study. Diabetes
220. Thompson, P. D., G. J. Tsongalis, R. L. Seip, et al. Apolipoprotein E genotype and changes in serum lipids and maximal oxygen uptake with exercise training. Metabolism
221. Tiret, L., O. Poirier, V. Hallet, et al. The Lys198Asn polymorphism in the endothelin-1 gene is associated with blood pressure in overweight people. Hypertension
222. Todorova, B., A. Kubaszek, J. Pihlajamaki, et al. The G-250A promoter polymorphism of the hepatic lipase gene predicts the conversion from impaired glucose tolerance to type 2 diabetes mellitus: the Finnish Diabetes Prevention Study. J. Clin. Endocrinol. Metab.
223. Tomas, M., R. Elosua, M. Senti, et al. Paraoxonase1-192 polymorphism modulates the effects of regular and acute exercise on paraoxonase1 activity. J. Lipid. Res. 43:713-720, 2002.
224. Toscano, A., S. Tsujino, G. Vita, S. Shanske, C. Messina, and S. Dimauro. Molecular basis of muscle phosphoglycerate mutase (PGAM-M) deficiency in the Italian kindred. Muscle Nerve
225. Trombetta, I. C., L. T. Batalha, M. U. Rondon, et al. Gly16 + Glu27 beta2-adrenoceptor polymorphisms cause increased forearm blood flow responses to mental stress and handgrip in humans. J. Appl. Physiol.
226. Tsujino, S., S. Servidei, P. Tonin, S. Shanske, G. Azan, and S. DiMauro. Identification of three novel mutations in non-Ashkenazi Italian patients with muscle phosphofructokinase deficiency. Am. J. Hum. Genet.
227. Tsujino, S., S. Shanske, A. K. Brownell, R. G. Haller, and S. DiMauro. Molecular genetic studies of muscle lactate dehydrogenase deficiency in white patients. Ann. Neurol.
228. Tsujino, S., S. Shanske, and S. DiMauro. Molecular genetic heterogeneity of myophosphorylase deficiency (McArdle's disease). N. Engl. J. Med.
229. Tsujino, S., S. Shanske, and S. DiMauro. Molecular genetic heterogeneity of phosphoglycerate kinase (PGK) deficiency. Muscle Nerve 3:S45-S49, 1995.
230. Tsujino, S., S. Shanske, S. Sakoda, G. Fenichel, and S. DiMauro. The molecular genetic basis of muscle phosphoglycerate mutase (PGAM) deficiency. Am. J. Hum. Genet.
231. Tsuritani, I., K. S. Brooke-Wavell, S. S. Mastana, P. R. Jones, A. E. Hardman, and Y. Yamada. Does vitamin D receptor polymorphism influence the response of bone to brisk walking in postmenopausal women? Horm. Res.
232. Turgut, G., S. Turgut, O. Genc, A. Atalay, and E. O. Atalay. The angiotensin converting enzyme I/D polymorphism in Turkish athletes and sedentary controls. Acta Medica (Hradec Kralove)
233. Tworoger, S. S., J. Chubak, E. J. Aiello, et al. The effect of CYP19 and COMT polymorphisms on exercise-induced fat loss in postmenopausal women. Obes. Res.
234. Vaisanen, S. B., S. E. Humphries, L. A. Luong, I. Penttila, C. Bouchard, and R. Rauramaa. Regular exercise, plasminogen activator inhibitor-1 (PAI-1) activity and the 4G/5G promoter polymorphism in the PAI-1 gene. Thromb. Haemost.
235. Van Pottelbergh, I., S. Goemaere, L. Nuytinck, A. De Paepe, and J. M. Kaufman. Association of the type I collagen alpha1 Sp1 polymorphism, bone density and upper limb muscle strength in community-dwelling elderly men. Osteoporos. Int.
236. van Rossum, E. F., P. G. Voorhoeve, S. J. te Velde, et al. The ER22/23EK polymorphism in the glucocorticoid receptor gene is associated with a beneficial body composition and muscle strength in young adults. J. Clin. Endocrinol. Metab.
237. Vermeer, S., A. Verrips, M. A. Willemsen, H. J. ter Laak, I. B. Ginjaar, and B. C. Hamel. Novel mutations in three patients with LGMD2C with phenotypic differences. Pediatr. Neurol.
238. Vissing, J., M. B. Salamon, P. Arlien-Soborg, et al. A new mitochondrial tRNA(Met) gene mutation in a patient with dystrophic muscle and exercise intolerance. Neurology
239. Vives-Bauza, C., J. Gamez, M. Roig, et al. Exercise intolerance resulting from a muscle-restricted mutation in the mitochondrial tRNA(Leu (CUN)) gene. Ann. Med.
240. Vladutiu, G. D., M. J. Bennett, N. M. Fisher, et al. Phenotypic variability among first-degree relatives with carnitine palmitoyltransferase II deficiency. Muscle Nerve 26:492-498, 2002.
241. Vladutiu, G. D., M. J. Bennett, D. Smail, L. J. Wong, R. T. Taggart, and H. B. Lindsley. A variable myopathy associated with heterozygosity for the R503C mutation in the carnitine palmitoyltransferase II gene. Mol. Genet. Metab.
242. Vorgerd, M., J. Karitzky, M. Ristow, et al. Muscle phosphofructokinase deficiency in two generations. J. Neurol. Sci.
243. Wagoner, L. E., L. L. Craft, B. Singh, et al. Polymorphisms of the beta(2)-adrenergic receptor determine exercise capacity in patients with heart failure. Circ. Res.
244. Wagoner, L. E., L. L. Craft, P. Zengel, et al. Polymorphisms of the beta1-adrenergic receptor predict exercise capacity in heart failure. Am. Heart. J.
245. Walsh, S., J. M. Zmuda, J. A. Cauley, et al. Androgen receptor CAG repeat polymorphism is associated with fat-free mass in men. J. Appl. Physiol.
246. Walston, J., D. E. Arking, D. Fallin, et al. IL-6 gene variation is not associated with increased serum levels of IL-6, muscle, weakness, or frailty in older women. Exp. Gerontol.
247. Wang, L., A. Limongelli, M. R. Vila, F. Carrara, M. Zeviani, and S. Eriksson. Molecular insight into mitochondrial DNA depletion syndrome in two patients with novel mutations in the deoxyguanosine kinase and thymidine kinase 2 genes. Mol. Genet. Metab.
248. Wang, Q., M. E. Curran, I. Splawski, et al. Positional cloning of a novel potassium channel gene: KVLQT1 mutations cause cardiac arrhythmias. Nat. Genet.
249. Weiss, E. P., O. Kulaputana, I. A. Ghiu, et al. Endurance training-induced changes in the insulin response to oral glucose are associated with the peroxisome proliferator-activated receptor-gamma2 Pro12Ala genotype in men but not in women. Metabolism
250. Williams, A. G., S. H. Day, J. P. Folland, P. Gohlke, S. Dhamrait, and H. E. Montgomery. Circulating angiotensin converting enzyme activity is correlated with muscle strength. Med. Sci. Sports Exerc.
251. Williams, A. G., S. S. Dhamrait, P. T. Wootton, et al. Bradykinin receptor gene variant and human physical performance. J. Appl. Physiol. 96:938-942, 2004.
252. Williams, A. G., M. P. Rayson, M. Jubb, et al. The ACE gene and muscle performance. Nature
253. Wilund, K. R., R. E. Ferrell, D. A. Phares, A. P. Goldberg, and J. M. Hagberg. Changes in high-density lipoprotein-cholesterol subfractions with exercise training may be dependent on cholesteryl ester transfer protein (CETP) genotype. Metabolism
254. Winnicki, M., V. Accurso, M. Hoffmann, et al. Physical activity and angiotensin-converting enzyme gene polymorphism in mild hypertensives. Am. J. Med. Genet. A 125:38-44, 2004.
255. Wolfarth, B., M. S. Bray, J. M. Hagberg, et al. The human gene map for performance and health-related fitness phenotypes: the 2004 update. Med. Sci. Sports Exerc.
256. Wolfarth, B., M. A. Rivera, J. M. Oppert, et al. A polymorphism in the alpha2a-adrenoceptor gene and endurance athlete status. Med. Sci. Sports Exerc.
257. Woo, S. K., and H. S. Kang. Apolipoprotein C-III SstI genotypes modulate exercise-induced hypotriglyceridemia. Med. Sci. Sports Exerc.
258. Woods, D., M. Hickman, Y. Jamshidi, et al. Elite swimmers and the D allele of the ACE I/D polymorphism. Hum. Genet.
259. Woods, D., G. Onambele, R. Woledge, et al. Angiotensin-I converting enzyme genotype-dependent benefit from hormone replacement therapy in isometric muscle strength and bone mineral density. J. Clin. Endocrinol. Metab.
260. Woods, D. R., M. World, M. P. Rayson, et al. Endurance enhancement related to the human angiotensin I-converting enzyme I-D polymorphism is not due to differences in the cardiorespiratory response to training. Eur. J. Appl. Physiol.
261. Yang, N., D. G. MacArthur, J. P. Gulbin, et al. ACTN3 genotype is associated with human elite athletic performance. Am. J. Hum. Genet.
262. Zhang, B., T. Sakai, S. Miura, et al. Association of angiotensin-converting-enzyme gene polymorphism with the depressor response to mild exercise therapy in patients with mild to moderate essential hypertension. Clin. Genet. 62:328-333, 2002.
263. Zhao, B., S. M. Moochhala, S. Tham, et al. Relationship between angiotensin-converting enzyme ID polymorphism and VO(2max) of Chinese males. Life Sci.
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Molecular BiologyAssociation of a PPARD polymorphism with human physical performanceMolecular Biology
Journal of Sports SciencesThe human genome and sport, including epigenetics and athleticogenomics: A brief look at a rapidly changing fieldJournal of Sports Sciences
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Exercise and Sport Sciences ReviewsNhlh2: A Basic Helix-Loop-Helix Transcription Factor Controlling Physical ActivityExercise and Sport Sciences Reviews
Medicine & Science in Sports & ExerciseMitochondrial Haplogroups Associated with Elite Kenyan Athlete StatusMedicine & Science in Sports & Exercise
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CANDIDATE GENES; QUANTITATIVE TRAIT LOCI; LINKAGE; GENETIC VARIANTS; MITOCHONDRIAL GENOME; NUCLEAR GENOME; GENETICS
©2006The American College of Sports Medicine
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