Abstract
Increased physical activity is an optimal way to maintain a good health. During exercise, triacylglycerols, an energy reservoir in adipose tissue, are hydrolyzed to free fatty acids (FAs) which are then released to the circulation, providing a fuel for working muscles. Thus, regular physical activity leads to a reduction of adipose tissue mass and improves metabolism. However, the reduction of lipid reservoir is also associated with many other interesting changes in adipose tissue FA metabolism. For example, a prolonged exercise contributes to a decrease in lipoprotein lipase activity and resultant reduction of FA uptake. This results in the improvement of mitochondrial function and upregulation of enzymes involved in the metabolism of polyunsaturated fatty acids. The exercise-induced changes in adipocyte metabolism are associated with modifications of FA composition. The modifications are adipose tissue depot-specific and follow different patterns in visceral and subcutaneous adipose tissue. Moreover, exercise affects adipokine release from adipose tissue, and thus, may mitigate inflammation and improve insulin sensitivity. Another consequence of exercise is the recently described phenomenon of adipose tissue “beiging,” i.e., a switch from energy-storing white adipocyte phenotype to thermogenic FA oxidizing beige adipocytes. This process is regulated by myokines released during the exercise. In this review, we summarize published evidence for the exercise-related changes in FA metabolism and adipokine release in adipose tissue, and their potential contribution to beneficial cardiovascular and metabolic effects of physical activity.
Highlights
In the 21st century, when obesity is recognized as a civilization-related, economic and social burden and the numbers of obese and overweight individuals still increase, we need new strategies to prevent and treat those conditions
Designed training simulates lipolysis, i.e., the hydrolysis of triacylglycerols stored in adipose tissue (AT), which results in the release of free fatty acids (FFAs) to circulation and their oxidation in muscles and other tissues
Exercise contributes to an increase in the number of mitochondria in white AT (WAT) and stimulates the expression of brown adipocyte-specific genes, which leads to “beiging” of WAT and amelioration of glucose intolerance induced by a high-fat diet (Sutherland et al, 2009; Xu et al, 2011; Roberts et al, 2014) (Figure 1)
Summary
In the 21st century, when obesity is recognized as a civilization-related, economic and social burden and the numbers of obese and overweight individuals still increase, we need new strategies to prevent and treat those conditions. Exercise contributes to an increase in the number of mitochondria in white AT (WAT) and stimulates the expression of brown adipocyte-specific genes, which leads to “beiging” of WAT and amelioration of glucose intolerance induced by a high-fat diet (Sutherland et al, 2009; Xu et al, 2011; Roberts et al, 2014) (Figure 1). These effects of exercise on AT are associated with significant changes in metabolism and composition of fatty acids (FAs), the main components of adipocytes. We discuss the exercise-induced changes in the composition and metabolism of FAs in AT, with particular emphasis on AT depotspecific differences
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