The Underappreciated Power of Exercise and Training to Prevent Diabetes
In the United States and Europe, between 5% and 8% of the adult population is estimated to suffer from T2D, and in genetically prone subpopulations, the prevalence may be as high as approximately 50% (Frøsig & Richter, 2009). That translates to between 53 and 132 million diabetic adults in 2011. Central to development of T2D is the impaired capacity of insulin to regulate blood glucose. This is caused primarily by resistance to insulin action in liver, adipose tissue, and skeletal muscle. In the liver, insulin is less effective in suppressing hepatic glucose production. In the adipose tissue, insulin is less effective in suppressing lipolysis, and in skeletal muscle, the capacity of insulin to reduce plasma glucose concentration through muscle glucose uptake and oxidative and nonoxidative disposal is diminished. Insulin resistance also is the core symptom of metabolic syndrome, a cluster of three or more metabolic abnormalities characterized by inflexibility in metabolizing carbohydrate and fat. Metabolic inflexibility increases the risk of cardiovascular disease and affects approximately one third of overweight and obese individuals (Ervin, 2009; Grundy et al., 2004). T2D amplifies the risk of cardiovascular and cerebrovascular disease and impairs circulation in the retina, extremities, and kidneys. It is clear that it inflicts great personal suffering and imposes high medical costs.
A wider understanding of the power of exercise and exercise training to improve glucose tolerance and reduce insulin resistance would allow the implementation of simple exercise strategies for preventing and treating diabetes. Only three facts need to be appreciated. First, the skeletal muscle constitutes between 35% and 40% of body mass and can utilize between 50% and 75% of glucose produced by the liver. Once the muscle takes up glucose, glucose can no longer return to circulation. Utilization of glucose by muscle during exercise plays a central role in the removal of glucose from the blood.
Second, the local events in contracting muscle (e.g., muscle glycogen depletion) allow up to a 20-fold increase in glucose uptake by the muscle, depending on exercise duration and intensity, without the need for insulin (Richter et al., 1985; Rose & Richter, 2005). The magnitude of the increase in glucose uptake during or immediately after an exercise bout is independent of the insulin action (Garetto et al., 1984). After the termination of exercise, this effect lasts for between 1 and 2.5 h, after which it wanes. That means that individuals with T2D in whom insulin action is defective experience lowered blood glucose while they exercise and for a short period of time after exercise.
The third and perhaps most important fact is that, again depending on the duration and intensity of exercise, a few hours after the termination of exercise, muscle sensitivity to insulin increases for between 2.5 and 48 h, whereas no increase in glucose uptake occurs in the absence of insulin (Garetto et al., 1984; Maarbjerg et al., 2011). This means that individuals with T2D and prediabetics can maintain increased insulin sensitivity by simply engaging in physical activity every 2 d. This increase in insulin sensitivity also is specific to the muscles that underwent contraction. Thus, lower insulin concentration is needed to elicit the same glucose uptake in the exercised leg compared with the nonexercised leg (Richter et al., 1989; Wojtaszewski et al., 2002). Overall, increased postexercise insulin sensitivity allows for increased glucose uptake by the muscle, increased glucose oxidation, and nonoxidative means of glucose disposal that involves muscle glycogen synthesis.