Sports Med 2005; 35 (5): 393-412

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 393 1. Hormonal Regulation of Lipid Metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395 2. Hormonal Interrelationships . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 396 3. Obesity-Induced Modifications of Hormonal Interactions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 399 4. Energy Restriction and Metabolic Hormones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 401 5. Exercise-Induced Changes in Lipid Metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 402 6. Exercise-Induced Changes in Adiposity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 403 7. Exercise-Induced Modifications of Hormones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 403 7.1 Acute Exercise: Normal Weight Individuals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 403 7.2 Acute Exercise: Obese Individuals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 404 7.3 Training . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 404 8. Relationship Between Exercise-Induced Hormonal Changes and Body Fat . . . . . . . . . . . . . . . . . . . . . 406 9. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 406 Physiological and psychological systems work together to determine energy Abstract intake and output, and thus maintain adipose tissue. In addition, adipose tissue secretes leptin and cytokines, which induces satiety and has been linked to catecholamines, cortisol, insulin, human growth hormone, thyroid hormones, gonadotropin and lipolysis. Thus, adipose tissue is acted upon by a number of physiological stimuli, including hormones, and simultaneously, is an active component in the regulation of its own lipid content. All of the hormones mentioned above are associated with each other and respond to exercise and exercise training. Thus, exercise is one of the major links between the hormonal modulators of energy intake and output. It appears that the sympathetic nervous system and the catecholamines are key components facilitating the lipolytic activity during exercise. These two neuroendocrine factors directly affect adipose metabolism and metabolic hormones that influence adipose metabolism. Acute lowand moderate-intensity exercise causes hormonal changes that facilitate lipolytic activity. Exercise training reduces these hormonal responses, but the sensitivity to these hormones increases so that lipolysis may be facilitated. Large amounts of adipose tissue blunt the metabolic hormonal responses to exercise, but the sensitivity of these hormones is increased; thus maintaining normal lipolytic activity. Although the physiological role of the endocrine system during exercise 394 McMurray & Hackney and training is significant, other training effects may have as great, or greater influence on lipolytic activity in adipose tissue. Adipose tissue is maintained by a complex internot as convincing.[6,7] Leptin has been linked to action of a number of physiological and psychologiseveral other hormones[3,8,9] that have direct effects cal systems that regulate energy intake and energy on carbohydrate and lipid metabolism. In addition, output (figure 1). Typically, energy intake is conadipose tissue releases a number of cytokines (e.g. trolled by hunger, appetite and satiety.[1] Hunger and adiponectin, interleukin [IL]-6, tumour necrosis satiety appear to be genetic or physiological in nafactor-α [TNFα], resistin) that can influence insuture, receiving input from blood glucose, splanchnic lin,[10,11] stimulate corticotropin-releasing hormone neurons, endogenous opiates, neurotransmitters, the (CRH)[12] and ultimately cortisol,[13] which in turn gastrointestinal system and leptin.[2] Conversely, apincreases lipolysis.[11,14] Leptin may also be affected petite appears to be psychological or cultural, and is by exercise.[15,16] Thus, adipose tissue is an active a learned response to foods. Energy output is related component in the regulation of the body’s overall fat to metabolic rate, which, at rest, is controlled by content. various hormones and genetic factors. Physical acFrom an endocrine perspective, a number of hortivity (e.g. exercise) increases energy output directmones regulate lipid metabolism including, catecholy, but also affects a number of hormones that conlamines, corticosteroids, human growth hormone trol metabolic rate and hunger. Thus, exercise ap(hGH), thyroid hormones and gonadotropins (anpears to be the one perturbation that has the potential drogens and estrogens). All of these hormones can, to influence both sides of the energy balance equatherefore, have an influence on adipose tissue and all tion (i.e. energy intake and energy output). of these hormones have been in some way related to, Adipose tissue is not passive, as it influences or associated with, leptin.[3,9] In addition, these hormetabolic activity in other tissues including muscle mones appear responsive to exercise and exercise and liver.[3] Adipose tissue secretes the hormone training.[17] Thus, exercise is one of the major links leptin, which has a controlling effect on satiety and between the hormonal modulators of energy intake hunger. In animals, leptin has also been shown to and output. This article will attempt to explore the influence spontaneous activity levels and increase relationship between these hormones and adipose energy expenditure.[4,5] In humans, studies on the tissue with emphasis on how exercise influences this effects of leptin on spontaneous activity levels are relationship. A vast body of literature has shown relationships between androgens, catecholamines, cortisol, hGH, insulin and thyroid hormones. Most of this information has come from studies of isolated cell, animal, disease states, drugs and correlation studies in humans. In addition, the relationship between these hormones at rest, during stress and exercise is influenced by the sex of the individual.[17] These sex-related effects in turn, influence energy substrate metabolism. The role of sex is a treatise beyond the scope of this article. This topic is addressed in a recent article by Braun and Horton.[18] Finally, many other factors besides exercise influence these hormones, such as circadian rhythm, thermoregulaGlucose Adiposity Energy intake Energy output Leptin cytokines