Several studies have reported that the insertion (I) allele of the angiotensin-converting enzyme ( ACE) I/deletion (D) polymorphism is associated with enhanced responsiveness to endurance training and is more common in endurance athletes than in sedentary controls. We tested the latter hypothesis in a cohort of 192 male endurance athletes with maximal oxygen uptake ≥75 ml ⋅ kg−1 ⋅ min−1and 189 sedentary male controls. The ACE ID polymorphism in intron 16 was typed with the three-primer polymerase chain reaction method. Both the genotype ( P = 0.214) and allele ( P = 0.095) frequencies were similar in the athletes and the controls. Further analyses in the athletes revealed no excess of the I allele among the athletes within the highest quartile (> 80 ml ⋅ kg−1 ⋅ min−1) or decile (>83 ml ⋅ kg−1 ⋅ min−1) of maximal oxygen uptake. These data from the GENATHLETE cohort do not support the hypothesis that the ACE ID polymorphism is associated with a higher cardiorespiratory endurance performance level.

This informative report focuses on filling information gaps regarding adherence to physical activity and exercise in the health care spectrum of older adults (OA) and an overview of the benefits of physical activity for OA. Healthy People 2000, 2010, and 2020 are public health programs from the U.S. Department of Health and Human Services that set national goals and objectives for promoting health and preventing disease. The programs include 10 leading health indicators that reflect major health problems, which concern OA. Exercise and physical activity are among the most important factors affecting health and longevity, but exercise adherence is a significant hindrance in achieving health goals in the OA. Exercise adherence in OA is a multifactorial problem encompassing many biopsychosocial factors. Factors affecting adherence in the OA include socioeconomic status, education level, living arrangements, health status, pacemakers, physical fitness, and depression. Improving adherence could have a significant impact on longevity, quality of life, and health care costs.

This review presents the 2001 update of the human gene map for physical performance and health-related phenotypes. It is based on scientific papers published by the end of 2001. Association studies with candidate genes, genome-wide scans with polymorphic markers, and single gene defects causing exercise intolerance to variable degrees are included. 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, there were 29 loci depicted on the map. The 2001 map includes 71 loci on the autosomes and two on the X chromosome. Among these genes or markers, 24 are from prior publications on exercise intolerance and four relate to other pathologies. Finally, 13 sequence variants in mitochondrial DNA have been shown to influence relevant fitness and performance phenotypes.