Our goal is to make this publication a useful resource for those who have to teach the role of the inheritance on fitness and performance traits, and the impact of genetic variation among human beings. It is our hope that the yearly update of the fitness and performance gene map is found useful to the exercise scientists and the sports medicine community.
The case-control studies reporting statistically significant differences in allele and genotype frequencies between endurance athletes and sedentary controls are summarized in Table 2. Yang and coworkers (181) investigated the frequency of a common nonsense mutation in the skeletal muscle alpha 3 actinin (ACTN3) gene in a cohort of 429 international class athletes representing 14 different sports and 436 unrelated controls. In 107 elite sprint and power athletes, they found a significantly lower frequency of the XX genotype (homozygotes for the stop-codon allele) as compared with the controls. In addition, they found the allele frequencies in sprint and endurance athletes deviating in opposite directions with significantly different values between the sprint and endurance groups for male and female athletes, respectively.
Significant results from nine cross-sectional association studies with sequence variations in six different genes were published in 2003 (Table 3). In 400 white subjects from the HERITAGE Family Study, an association was found between the rating of perceived exertion (RPE) during a submaximal-to-maximal exercise test and a C/T transition in the gene encoding the adenosine monophosphate deaminase (AMPD1). In the sedentary state, homozygotes for the rare T allele, which results in a truncated gene product, reported significantly higher RPE during steady-state submaximal exercise at 50 W than the C/C homozygotes and the C/T heterozygotes (129). Franks et al. (33) investigated the associations between a Gly482Ser polymorphism of the peroxisome proliferative activated receptor gamma coactivator 1 alpha (PPARGC1A) gene and physical activity energy expenditure (PAEE) and V̇O2max. PAEE was measured using a 4-d heart rate monitoring and individual resting and exercise oxygen consumption-heart rate relationship, whereas the V̇O2max was predicted from the heart rate and oxygen consumption data measured during submaximal exercise test. Neither PAEE nor predicted V̇O 2max per se was associated with the PPARGC1A polymorphism. However, the correlation between PAEE and predicted V̇O 2max was stronger among the Ser482Ser homozygotes than in the carriers of the 482Gly allele.
The studies reporting associations between strength or anaerobic performance phenotypes with different candidate genes are summarized in Table 5. In 2003, four studies reported data related to strength phenotypes. In the Baltimore Longitudinal Study on Aging cohort, a C174T polymorphism in the ciliary neurotrophic factor receptor (CNTFR) gene was associated with age, race, height, and physical activity-adjusted eccentric slow- and fast-velocity knee extensor peak torque both in men and in women. Carriers of the 174T allele also had a greater nonosseous total and lower limb fat-free mass as compared with the C174C homozygotes. Consequently, the associations between the CNTFR genotype and knee extensor peak torque phenotypes disappeared after further adjustment for fat-free mass, suggesting that the genotype-related differences in lower-limb strength were explained by the differences in muscle mass (135). Frederiksen and coworkers (35) found no associations between ACE I/D genotype and several measured and self-reported strength abilities in elderly Danish twins. In addition, in elderly men aged 71–86 yr, a (TTTA)n-repeat polymorphism in the aromatase enzyme gene (CYP19A1) showed no association with grip strength (166). Likewise, an IL6 C-174G polymorphism was not associated with grip strength or leg extension strength in elderly Italian subjects (8).
During 2003, two studies reported significant associations between hemodynamic traits measured during acute exercise and candidate gene polymorphisms (Table 6). Kanazawa and coworkers (61,62) reported two studies on the associations between pulmonary hemodynamics during exercise and the ACE I/D polymorphism in patients with COPD. One study investigated the effects of ACE inhibitor captopril on pulmonary arterial pressure and pulmonary vascular resistance (61), whereas the other study addressed the impact of supplementary oxygen administration on the same traits (62). In both reports, the D/D homozygotes showed significantly higher pulmonary artery pressure and pulmonary vascular resistance after acute exercise than patients with one or two copies of the I allele. The ACE I/D polymorphism was not associated with maximal exercise heart rate in patients with chronic ischemic heart failure (2).
The number of studies addressing the question of genotype—fitness and genotype—physical activity interactions on health-related fitness phenotypes has increased, and in 2003, two studies were published dealing with hemodynamic phenotypes (Table 6). Data and coworkers (25) measured resting heart rate and blood pressures as well as forearm blood flow before and after arm arterial occlusion in healthy sedentary and endurance-trained women. Statistically significant interactions were observed between physical activity status and the NOS3 T-786C polymorphism on baseline forearm blood flow (FBF; P = 0.03 for interaction) and forearm vascular resistance (FVR; P = 0.0003 for interaction). Among the sedentary women, the carriers of the −786C allele had lower baseline FBF and higher FVR as compared with the TT homozygotes, whereas in physically active women the TT homozygotes showed lower FBF and higher FVR (25).
The effects of exercise training on acetylcholine-induced changes in average peak velocity (APV) of coronary or mammary arteries was investigated in 67 patients with coronary artery disease (Table 7). Exercise training improved significantly APV. However, the training response was significantly blunted in the carriers of the NOS3 −786C allele as compared to the patients who were homozygotes for the −786T allele (30). In the HERITAGE Family Study, training-induced changes in maximal exercise diastolic blood pressure was associated with the AMPD1 C34T polymorphism: the CC homozygotes showed a greater reduction in maximal DBP than the TT homozygotes (129). Resting blood pressure responses to endurance training did not differ between the PPARG Pro12Ala genotypes in healthy Japanese males (57).
In 2003, the first follow-up study of a quantitative trait locus (QTL) from the HERITAGE Family Study was published (120). A QTL for submaximal exercise stroke volume and cardiac output training responses on chromosome 2q31–q32 was investigated further by dense microsatellite mapping (Table 8). The evidence of linkage was greatly enhanced with additional markers and the maximum linkage was detected with markers in or near the gene encoding titin (TTN). Transmission disequilibrium test with the same dense microsatellite marker set provided evidence of association with one of the markers in the TTN gene (120).
No new genes or mutations were reported in 2003.
The first study related to bone phenotypes investigated the relationship between a G-174C polymorphism in the promotor of the IL6 gene and exercise-induced femoral cortical bone resorption in 130 young (19.5 ± 0.2 yr) male army recruits (28). The subjects underwent a 10-wk exercise-training program comprising a mixture of upper- and lower-body strength-endurance exercise of graded workload. Exercise-induced changes in proximal right femoral cross-sectional cortical area, after adjustment for pretraining values, were strongly genotype-dependent with the GG homozygotes losing 6.8% cortical area, GC gaining 5.5% and CC gaining 17.3% (P = 0.007 for linear trend). These genotype-mediated changes persisted throughout the different scans of the femur but were less important in the distal area. The authors concluded that the IL6 gene was an important regulator of the bone remodeling in humans (28).
The second study investigated associations between polymorphisms of the androgen receptor (AR), CYP19A1 and estrogen receptor 1 (ESR1) genes and bone mineral density (BMD) measured in 140 middle-aged Finnish men participating in a 4-yr randomized controlled exercise intervention trial (126). The men in the intervention group (N = 70) were prescribed aerobic exercise, 45–60 min per session, five times a week, whereas the men in the reference group were advised to make their personal choice as to whether or not engage in physical exercise. The lumbar spine BMD values were significantly different among the ESR1 genotypes in the exercise group (P = 0.007), with no significant changes observed in subjects homozygotes (pp) for the mutation (two copies of the PvuII restriction site), whereas increases of 6% and 5%, were observed in subjects with the PP and Pp genotypes, respectively. There were no associations between the AR and CYP19A1 polymorphisms and the BMD responses to the intervention (126).
The third study was aimed at investigating the impact of a polymorphism in the phenylethanolamine N-methyltransferase (PNMT) gene on weight loss induced by a combination of pharmacological treatment (sibutramine) and monthly health-education classes (108). The PNMT gene encodes the rate-limiting enzyme of the conversion of nor-epinephrine to epinephrine and is thus considered as a candidate gene of sibutramine-induced weight loss because this drug acts as an inhibitor of the reuptake of norepinephrine in the neurons. In that study, 149 obese women participated in a 6-month weight loss trial that included daily intake of a dose of 15 mg of sibutramine and a monthly 1-h behavior modification seminar that encouraged participants to eat low-fat foods, increase the consumption of vegetables and fruits, and to exercise daily. Estimates of physical activity were obtained from self-reported daily activity records. A G to A transition in the promotor (position −148) of the PNMT gene was genotyped and tested for association with the response to the intervention. A comparison of the genetic distribution of the G-148A PNMT genotypes between subjects categorized into tertitles of percentage weight loss revealed a significant (P < 0.002) association with greater weight loss in the A/A and G/G homozygotes as compared to the heterozygote G/A subjects. A regression model that included PNMT homozygosity versus heterozygosity and dietary and physical activity variables revealed that the PNMT gene, in addition to total caloric, fat, and fiber intakes, was a significant predictor of percentage of weight loss at 6 months.
Finally, the third study investigated the impact of a common vitamin D receptor (VDR) gene polymorphism (BsmI) on fasting serum glucose levels in 1539 active aircrew members of the armed forces (102). The BsmI VDR gene polymorphism was considered because vitamin D modulates insulin receptor gene expression and because of previous associations reported between this polymorphism and Type 2 diabetes. Physical activity was assessed based on the average time per week spent on sports activity over the year, and subjects were categorized into low (≤3 h) and high (>3 h) physical activity groups. The authors found that subjects of the low physical activity group with the BB genotype had higher levels of fasting glucose (5.61 ± 0.49 mmol·L−1) than subjects with the Bb (5.44 ± 0.44 mmol·L−1) or bb (5.38 ± 0.44 mmol·L−1) genotypes (P < 0.001). This association was not observed in subjects within the high physical activity group. The results suggest that the BsmI VDR polymorphism is associated with the control of glucose homeostasis in young men with low physical activity level (102).
The previous three updates of the Human Fitness Gene Map have summarized the available information on several risk factors for chronic diseases. In 2003, the first studies were published on the genotype-physical activity interactions on the actual risk of chronic diseases.
In the San Luis Valley Diabetes Study, 397 Hispanics and 569 non-Hispanic Whites were followed for 14 yr. During the follow-up, 91 coronary heart disease (CHD) events were recorded. The frequency of the T/T genotype of the LIPC C–480T polymorphism was higher among the CHD cases, and the CHD-free survival during the follow-up among the T/T homozygotes was significantly worse than in the C/C homozygotes and the C/T heterozygotes. A multivariate analysis revealed a significant interaction between the LIPC C-480T genotype and physical activity level on the CHD risk. The increased CHD risk associated with the T/T genotype was observed in the sedentary or moderately active subjects but not in subjects who participated in vigorous physical activities (54).
A lifestyle intervention utilizing both dietary and physical activity programs resulted in a significant reduction in the incidence of diabetes in middle-aged, overweight subjects with impaired glucose tolerance (164). A G-308A polymorphism of the tumor necrosis factor (TNF) gene was significantly associated with the risk of developing Type 2 diabetes during the follow-up. Carriers of the −308A allele showed 1.8 times greater risk than the G/G homozygotes. Interestingly, the lower diabetes risk associated with the G/G genotype was seen only in the lifestyle intervention group: the incidence of Type 2 diabetes was 5.0% and 18.2% in the GG homozygotes and the A allele carriers (odds ratio 4.22), respectively, whereas the corresponding values in the control group were 20.8% and 22.7% (72).
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 2003. Even those who know little about molecular biology realize that exciting advances have been made in the understanding of the molecular and cellular regulation of the adaptation to activity and inactivity in the last decade. Although we have a long way to go, we are beginning to understand which genes and pathways are contributing to the response of various tissues and organs to acute or repeated exposures to exercise or muscle contractions. These studies are of paramount importance if we are to understand the true biological determinants of physical performance and of the role of regular exercise in disease prevention or of physical inactivity in common chronic diseases and premature death.
In contrast, little progress has been made with respect to the genetic basis of human variation in performance and health-related fitness. Indeed the biological basis of human individuality is a very different topic that has received only very limited attention to date. The current stagnation on the genetic front needs to benefit from the advances that are taking place in the molecular and cellular biology of exercise. The focus of these yearly reviews is on the genetic basis of human individuality for relevant traits and biological properties.
The 2003 map includes 109 autosomal entries, 2 X chromosome assignments, and 15 mt DNA markers. There are 19 nuclear genome markers more than in 2002. 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. As in previous years, we are forced to conclude that advances in this field are registered at a very modest pace.
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2. Akbulut, T., T. Bilsel, S. Terzi, et al. Relationship between ACE gene polymorphism and ischemic chronic heart failure in Turkish population. Eur. J. Med. Res.
3. Alvarez, R., N. Terrados, R. Ortolano, et al. Genetic variation in the renin-angiotensin system and athletic performance. Eur. J. Appl. Physiol.
4. 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.
5. Andreu, A. L., C. Bruno, S. Shanske, et al. Missense mutation in the mtDNA cytochrome b gene in a patient with myopathy. Neurology
6. 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.
7. Andreu, A. L., K. Tanji, C. Bruno, et al. Exercise intolerance due to a nonsense mutation in the mtDNA ND4 gene. Ann. Neurol.
8. Barbieri, M., L. Ferrucci, E. Ragno, et al. Chronic inflammation and the effect of IGF-I on muscle strength and power in older persons. Am. J. Physiol. Endocrinol. Metab.
9. Bernstein, M. S., M. C. Costanza, R. W. James, et al. No physical activity x CETP 1b.-629 interaction effects on lipid profile. Med. Sci. Sports Exerc.
10. 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.
11. 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.
12. 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.
13. Bouchard, C., T. Rankinen, Y. Chagnon, et al. Genomic scan for maximal oxygen uptake and its response to training in the HERITAGE Family Study. J. Appl. Physiol.
14. Brull, D., S. Dhamrait, S. Myerson, et al. Bradykinin B2BKR receptor polymorphism and left-ventricular growth response. Lancet
15. Brull, D. J., S. Dhamrait, R. Moulding, et al. The effect of fibrinogen genotype on fibrinogen levels after strenuous physical exercise. Thromb. Haemost.
16. 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.
17. 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
18. 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.
19. 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.
20. Campos, Y., A. Garcia, A. Lopez, et al. Cosegregation of the mitochondrial DNA A1555G and G4309A mutations results in deafness and mitochondrial myopathy. Muscle Nerve
21. 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.
22. Comi, G. P., F. Fortunato, S. Lucchiari, et al. Beta-enolase deficiency, a new metabolic myopathy of distal glycolysis. Ann. Neurol.
23. Corbalan, M. S. The 27Glu polymorphism of the beta2-adrenergic receptor gene interacts with physical activity influencing obesity risk among female subjects. Clin. Genet.
24. 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
25. 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.
26. Delanghe, J., M. Langlois, D. Duprez, M. De Buyzere, and D. Clement. Haptoglobin polymorphism and peripheral arterial occlusive disease. Atherosclerosis
27. Dengel, D. R., M. D. Brown, R. E. Ferrell, T. Ht. Reynolds, and M. A. Supiano. Exercise-induced changes in insulin action are associated with ACE gene polymorphisms in older adults. Physiol. Genomics
28. Dhamrait, S. S., L. James, D. J. Brull, et al. Cortical bone resorption during exercise is interleukin-6 genotype-dependent. Eur. J. Appl. Physiol.
29. 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.
30. 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.
31. 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. Folland, J., B. Leach, T. Little, et al. Angiotensin-converting enzyme genotype affects the response of human skeletal muscle to functional overload. Exp. Physiol.
33. Franks, P. W., I. Barroso, J. Luan, et al. PGC-1alpha genotype modifies the association of volitional energy expenditure with VO2max. Med. Sci. Sports Exerc.
34. Frederiksen, H., L. Bathum, C. Worm, K. Christensen, and L. Puggaard. ACE genotype and physical training effects: a randomized study among elderly Danes. Aging Clin. Exp Res.
35. Frederiksen, H., D. Gaist, L. Bathum, et al. Angiotensin I-converting enzyme (ACE) gene polymorphism in relation to physical performance, cognition and survival–a follow-up study of elderly Danish twins. Ann. Epidemiol.
36. 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.
37. 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
38. 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.
39. Garenc, C., L. Perusse, Y. C. Chagnon, et al. Effects of beta2-adrenergic receptor gene variants on adiposity: the HERITAGE Family Study. Obes. Res.
40. 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.
41. Gerson, M. C., L. E. Wagoner, N. McGuire, and S. B. Liggett. Activity of the uptake-1 norepinephrine transporter as measured by I-123 MIBG in heart failure patients with a loss-of-function polymorphism of the presynaptic alpha2C-adrenergic receptor. J. Nucl. Cardiol.
42. 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.
43. 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.
44. Grunig, E., B. Janssen, D. Mereles, et al. Abnormal pulmonary artery pressure response in asymptomatic carriers of primary pulmonary hypertension gene. Circulation
45. 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.
46. 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
47. 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. Hagberg, J. M., R. E. Ferrell, S. D. McCole, K. R. Wilund, and G. E. Moore. VO2 max is associated with ACE genotype in postmenopausal women. J. Appl. Physiol.
49. 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.
50. Hagberg, J. M., S. D. McCole, R. E. Ferrell, et al. Physical activity, hormone replacement therapy and plasma lipoprotein-lipid levels in postmenopausal women. Int. J. Sports Med.
51. 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
52. 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.
53. Hao, H., E. Bonilla, G. Manfredi, S. DiMauro, and C. T. Moraes. Segregation patterns of a novel mutation in the mito-chondrial tRNA glutamic acid gene associated with myopathy and diabetes mellitus. Am. J. Hum. Genet.
54. Hokanson, J. E., M. I. Kamboh, S. Scarboro, R. H. Eckel, and R. F. Hamman. Effects of the hepatic lipase gene and physical activity on coronary heart disease risk. Am. J. Epidemiol.
55. 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.
56. 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
57. Kahara, T., T. Takamura, T. Hayakawa, et al. PPARgamma gene polymorphism is associated with exercise-mediated changes of insulin resistance in healthy men. Metabolism
58. Kahara, T., T. Takamura, T. Hayakawa, et al. Prediction of exercise-mediated changes in metabolic markers by gene polymorphism. Diabetes Res. Clin. Pract.
59. 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.
60. 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.
61. 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
62. 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
63. 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.
64. 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
65. 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
66. 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.
67. 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.
68. Kimura, T., T. Yokoyama, Y. Matsumura, et al. NOS3 genotype-dependent correlation between blood pressure and physical activity. Hypertension
69. King, M. C., J. H. Marks, and J. B. Mandell. Breast and ovarian cancer risks due to inherited mutations in BRCA1 and BRCA2. Science
70. Kitagawa, I., Y. Kitagawa, T. Nagaya, and S. Tokudome. Interplay of physical activity and vitamin D receptor gene polymorphism on bone mineral density. J. Epidemiol.
71. 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.
72. Kubaszek, A., J. Pihlajamaki, V.Komarovski, et al. Promoter polymorphisms of the TNF-alpha (G-308A) and IL-6 (C-174G) genes predict the conversion from impaired glucose tolerance to type 2 diabetes: the Finnish Diabetes Prevention Study. Diabetes
73. 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
74. 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.
75. Laitinen, P. J., K. M. Brown, et al. Mutations of the cardiac ryanodine receptor (RyR2) gene in familial polymorphic ventricular tachycardia. Circulation
76. 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
77. 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.
78. 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.
79. 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
80. 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.
81. 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.
82. 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.
83. 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.
84. Mancuso, M., M. Filosto, J. C. Stevens, et al. Mitochondrial myopathy and complex III deficiency in a patient with a new stop-codon mutation (G339X) in the cytochrome b gene. J. Neurol. Sci.
85. 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.
86. Martinuzzi, A., E. Sartori, M. Fanin, et al. Phenotype modulators in myophosphorylase deficiency. Ann. Neurol.
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