Trends in Endocrinology & Metabolism
Fatty acid mobilization from adipose tissue during exercise
Section snippets
Mobilization of adipose tissue triglycerides during endurance exercise
The increased energy demands during exercise are met in part by an enhanced rate of triglyceride hydrolysis (i.e. lipolysis). Even during low-intensity exercise (25% maximal oxygen consumption; VO2max), adipose tissue lipolysis [measured as the rate of appearance of glycerol in the circulation (Ra glycerol)] increases two- to fivefold above resting levels 1, 2, 3 (Fig. 1). At the same time, the rate of fatty acid re-esterification decreases, resulting in a greater proportion of released fatty
Sources of fatty acids during exercise
Lipolytic activity is heterogeneous in different adipose tissue beds 7, 8. Intra-abdominal adipose tissue is the most lipolytically active adipose tissue depot [9], linking the accumulation of fat in this region to a range of clinical complications [10]. However, in spite of the high rate of lipolysis of intra-abdominal adipocytes, it is unlikely that this fat source is an important contributor to fatty acid oxidation by skeletal muscle during exercise. Fatty acid release from the splanchnic
Regulation of adipose tissue lipolysis
The rate-limiting step for the liberation of fatty acids from adipose tissue triglycerides into the circulation and ultimately for use as fuel during exercise is the activation of the enzyme hormone-sensitive lipase (HSL), via a cascade of cellular signals. Phosphorylated HSL moves from the cytosol of the adipocyte to the surface of the lipid droplet within the cell [29]. The phosphorylation of a family of proteins located on the surface of the lipid droplet (perilipins) is also required before
Influence of catecholamines on adipose tissue lipolysis
Catecholamines activate the lipolytic cascade by binding to β-adrenoceptors (β1, β2 and β3) on the plasma membrane of adipocytes, whereas catecholamine binding to α2-adrenoceptors inhibits lipolytic activity. These adrenoceptors interact with membrane-bound GTP-binding regulatory proteins (G proteins), which modulate the activity of the enzyme adenylate cyclase (Fig. 4). All β-adrenoceptors are coupled with a stimulatory G protein (Gs), and α2-receptors are coupled with inhibitory G proteins (Gi
Influence of insulin on adipose tissue lipolysis
Adipose tissue lipolysis is very sensitive to changes in plasma insulin concentration [38]. Even a very small increase in plasma insulin concentration (i.e. 10–30 μU ml−1) can suppress the lipolytic rate to >50% below basal levels [38]. Conversely, a decrease in plasma insulin concentration, as occurs during exercise, increases lipolysis [39]. Most of the antilipolytic action of insulin has been attributed to stimulating the activity of cellular phosphodiesterase-3 40, 41, which degrades cAMP,
Alternative regulators of lipolysis
Although catecholamines and insulin are the primary factors regulating adipose tissue lipolysis, other hormones and metabolites can also influence lipolytic rate (Table 1). In general, the effects of these factors are not as profound as those of catecholamines and insulin. The response to these agents is often much slower and, in many cases, they act through modulating the effects of catecholamines and/or insulin. In addition, the direct effect of many of these factors on the lipolytic rate is
Regional lipolysis
The variability in lipolytic rate in different adipose tissue beds is related to regional differences in adrenergic and insulin receptor density and function. Lipolytic sensitivity to catecholamines is greater in fat cells obtained from intra-abdominal adipose tissue than in those from subcutaneous adipose tissue 9, 50. In addition, the antilipolytic effect of insulin is greater in fat cells obtained from subcutaneous adipose tissue than in fat cells from intra-abdominal adipose tissue [51].
Endurance exercise training and lipid mobilization
Endurance exercise training increases the use of fat as a fuel during exercise [60]. However, this increase in fat oxidation is not the result of increased availability of fatty acids coming from adipose tissue triglycerides. Lipolytic rates are similar in endurance-trained athletes and untrained volunteers during exercise performed at the same absolute intensity [3]. In addition, data from longitudinal studies indicate that plasma fatty acid mobilization during exercise does not increase [61]
Fatty acid uptake and oxidation in skeletal muscle
Although mobilizing fatty acids from their triglyceride storage sites is the first crucial step for using fat as a fuel during exercise, these fatty acids must still be transported into skeletal muscle and then to the mitochondria before being oxidized. Our understanding of this process has increased tremendously in only the past few years, but still much remains unknown. Until recently, it was believed that all plasma fatty acids traverse the lipid bilayer of the muscle cell membrane by simple
Clinical implications and future directions
Exercise is often prescribed in the prevention and/or treatment of obesity-related disorders, such as type II diabetes and cardiovascular disease. Although exercise is an important part of a successful weight-loss program for these patients, it is the negative energy balance associated with exercise and a low-calorie diet that leads to the weight loss, not alterations in lipid metabolism. Although not directly responsible for reductions in body weight or body fat, alterations in lipid
Conclusion
Adipose tissue triglycerides are a very important source of fuel to meet energy demands during exercise. Increases in lipolytic rate and availability of fatty acids that occur during exercise require the coordination of neural, hormonal and circulatory events, which facilitate delivery of fatty acids from adipose tissue to the working muscle for oxidation. Lipolysis of adipose tissue triglycerides is heterogeneous, and much of the fat used during exercise is derived from abdominal subcutaneous
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2022, ChemosphereCitation Excerpt :Humans utilize both lipids and carbohydrates during exercise; thus, metabolism and utilization of lipids during physical activity is an essential consideration not only in obesity research, but also in obesogen research (Goodpaster et al., 2002). During physical activity, stored triglycerides in adipose tissue and muscle fibers are hydrolyzed to fatty acids, powering the movement of muscle fibers (Horowitz, 2003). However, not all humans oxidize and mobilize triglycerides at the same efficiency (Horowitz and Klein, 2000).