Being sedentary has a cost: your health will most likely be worse, and your life expectancy shorter. One of the metabolic dysfunctions that arises with increasing age is a reduction in insulin sensitivity, most often associated with excess fat tissue and the descent into type 2 diabetes, but lack of exercise is also an important contributing factor. Here researchers look into some of the low-level biological mechanisms involved in the relationship between exercise and insulin metabolism:
Both aging and physical inactivity are associated with increased development of insulin resistance whereas physical activity has been shown to promote increased insulin sensitivity. Here we investigated the effects of physical activity level on aging-associated insulin resistance in myotubes derived from human skeletal muscle satellite cells. Satellite cells were obtained from young (22 yrs) normally active or middle-aged (56.6 yrs) individuals who were either lifelong sedentary or lifelong active.
Human myotubes in culture obtained from middle-aged sedentary individuals have differences in insulin stimulated glucose metabolism that would be expected to be seen due to secondary aging in vivo, including impaired insulin-stimulated glucose uptake. Interestingly, physical activity throughout life seems to protect myotubes from these aspects of secondary aging potentially through adaptations including increased expression of GLUT4 and MYH2.
Additionally, lifelong physical activity exerts positive effects on muscle metabolism (including enhanced GSK3 phosphorylation and GLUT4 expression) when compared to the same parameters in myotubes from young, recreationally active, healthy controls. Life-long physical activity, such as seen in elite athletes, has shown that 60 year old athletes have the same glucose and insulin levels during an oral glucose tolerance test as 26 year olds. It is therefore unlikely that deterioration in insulin sensitivity is an inevitable consequence of aging and is maintained by regular physical activity.