Recent studies have identified a remarkable association between indices of athletic performance and optimal health of the general public. Both high aerobic capacity and high skeletal muscle strength are associated with lower mortality. Furthermore, higher aerobic capacity and often higher skeletal muscle strength are associated with lower prevalence of most chronic diseases. Finally, maintenance of aerobic capacity and skeletal muscle strength by lifelong physical activity delays the biological aging in most organ systems, therefore, delaying premature death. These facts raise the fascinating question: Are associations between high aerobic capacity and muscle strength with either metabolic health or elite performance causally or associatively related? If a causal relationship was noted at the molecular level it would have major public health implications. In this review, we provide evidence for the assertion that research on elite athletes and chronic disease prevention by exercise is actually addressing the same biochemical, physiological and genomic phenomena.
We contend that many of the same inherited genes whose proteins functioned to maximize aerobic capacity and skeletal muscle strength for survival during selection set the physiological norm for fluxes in metabolic pathways, anabolic events for hypertrophied skeletal muscle mass, high endothelial function, healthy storage of intramuscular fat, etc. Remarkably, the loss of our ancestral norm for physical activity reverses the aforementioned processes and contributes to chronic disease risk. Knowledge of the natural gene expression that allows one individual to excel in elite athletics can be applied to non-athletes to prevent chronic disorders, delay decline in most organ systems (biological aging), and improve health.
Hopefully the realization that the genetic mechanisms in those who inherited genes allowing elite athletic performance with training may be similar, if not the same, to those that improve health by daily physical activity would promote a better quality of life for those living today and for future generations. Alternatively, understanding changes in molecular pathways that link detraining and reductions in free-living daily physical activity to increased risk factors for disease will delineate the primary molecular events that contribute to many chronic diseases.
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