The Effects of Exercise Training on Obesity-Induced Dysregulated Expression of Adipokines in White Adipose Tissue

Figure 3

Schematic model for the effects of exercise training on expression of adipokines in WAT. During endurance training, type I muscle fibers in skeletal muscle are selectively used for the execution of exercises, and therefore, energy expenditure using lipid increases. Triglycerides within the adipocytes are broken down due to the secretion of catecholamines, and the resultant fatty acids are transported to tissues such as skeletal muscle. When exercise is repeated, adipocyte size is lessened. Decreases in adipocyte size are considered to result in the attenuation of dysregulated expression of adipocyte size-sensitive adipokines, such as leptin and oxidative stress in WAT. Moreover, catecholamine itself seems to correct disarray of adiponectin and TNF-α in WAT of obese subjects. In addition, endurance training might suppress oxidative stress and a hypoxic state of WAT due to an enhanced antioxidative system and increases in blood flow, respectively, which lead to the attenuation of the dysregulated expression of inflammatory-related adipokines involving TNF-α and MCP-1. In skeletal muscle, endurance training produces transition to type I muscle fiber following the increase in mitochondria biogenesis and enhances insulin sensitivity. Consequently, enhanced glucose/lipid metabolism in skeletal muscle decreases adipocyte size. On the other hand, resistance and endurance training enhance resting metabolic rate, which is likely to cause the alteration of adipokine expression following WAT mass reduction due to increased energy expenditure in the resting state.