CIENCIASMEDICASNEWS: Personalized Preventive Medicine: Genetics and the Response to Regular Exercise in Preventive Interventions

lunes, 25 de agosto de 2014

Personalized Preventive Medicine: Genetics and the Response to Regular Exercise in Preventive Interventions

Abstract

Regular exercise and a physically active lifestyle have favorable effects on health. Several issues related to this theme are addressed in this report. A comment on the requirements of personalized exercise medicine and in-depth biological profiling along with the opportunities that they offer is presented. This is followed by a brief overview of the evidence for the contributions of genetic differences to the ability to benefit from regular exercise. Subsequently, studies showing that mutations in TP53 influence exercise capacity in mice and humans are succinctly described. The evidence for effects of exercise on endothelial function in health and disease also is covered. Finally, changes in cardiac and skeletal muscle in response to exercise and their implications for patients with cardiac disease are summarized. Innovative research strategies are needed to define the molecular mechanisms involved in adaptation to exercise and to translate them into useful clinical and public health applications.

Abbreviations and Acronyms

ACSL1, Acyl-CoA synthetase long-chain family member 1;
CREB1, cAMP responsive element binding protein 1;
CHD, Coronary heart disease;
CRF, Cardiorespiratory fitness;
CVD, Cardiovascular disease;
GWAS, Genome-Wide Association Studies;
FMD, Flow-mediated dilation;
HF, Heart failire;
HR50, Heart rate at 50 W;
IGF-1, Insulin-like growth factor 1;
IL, Interleukin;
KIF5B, Kinesin family member 5B;
LFS, Li-Fraumeni syndrome;
mtDNA, Mitochondrial DNA;
MZ, Monozygotic;
NO, Nitric oxide;
NFAT, Nuclear calcineurin/nuclear factor of activated T-cells;
³¹P-MRS, P-31 magnetic resonance spectroscopy;
PA,Physical activity;
PCr, Phosphocreatine;
QTL, Quantitative trait loci;
SERCA2, Sarcoplasmic/endoplasmic reticulum Ca2 + ATPase 2;
SNPs, Single nucleotide polymorphisms;
TNF-α Tumor protein 53 – p53,Tumor necrosis factor-α;
VO_2Max, Maximal oxygen consumption

Keywords

Personalized medicine;
individual differences;
genetics;
mitochondria;
endothelium

Acknowledgements: C Bouchard is partially supported by the John W. Barton, Sr. Chair in Genetics and Nutrition. Research on the HERITAGE Family Study was supported for over 20 years by the National Institutes of Health (HL-45670). PY Wang and PM Hwang are supported by the Division of Intramural Research, National Heart, Lung, and Blood Institutes (NHLBI) and by a Bench-to-Bedside of the National Institutes of Health. LM Antunes-Correa was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo FAPESP (2013/15651-7and 2013/07607-8). CE Negrao was supported by CNPq (301867/2010-0), FAPESP (2010/50048-1 and 2013/07607-8), and, in part, by Fundação Zerbini.

: Address reprint requests to Claude Bouchard, Human Genomics Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA 70806, USA. Tel.: + 1 225 763 2663.