Get_Swole
MuscleChemistry Registered Member
Exercise and Fat Loss - Mechanisms of Action
Page 2
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Page 1 of 2
The guidance most often given to people seeking to lose weight is to eat less and exercise more. This is wonderful advice for the couch potatoes who get motivated only during the Super Bowl or while watching "Rocky" marathons.
Bodybuilders know that exercise and diet are key ingredients to their success in reducing body fat down to the lowest possible level. Never is it questioned among those who practice a dedicated lifestyle whether the dual approach of diet and exercise aid fat loss. Acknowledging that both work in fat loss, medicine and science are aggressively investigating exactly how this happens.
Is Starving Away Fat the Answer?
At the most basic level, fat loss occurs when energy intake (calories consumed as food and drink) is less than energy expended (metabolic rate and exercise).1 Dieting decreases the number of calories consumed and exercise increases the number of calories burned; seems simple and many assume the equation ends there. If fat loss were merely a matter of dropping calories, then slimming down would be a simple matter of just starving away the fat. Bodybuilders know this is not the case. Lower the calories too far and your energy drops until getting through the day is a challenge due to persistent fatigue and lethargy. Additionally, not only does weight loss slow down until it seems to stop, much of the weight loss appears to come from muscle rather than fat.2
It is really a shame that severe dieting carries so many negative side effects, as it's much simpler to cut calories than to burn more. Hundreds of calories can be dropped by switching to diet soft drinks or refusing dessert. In contrast, a half hour on the treadmill or a fairly intense session in the gym can be negated by a couple of cold beers.
Beyond the immediate impact on energy balance (calories in versus calories out), dieting and exercise affect the body's metabolism, which affects the balance between fat storage and fat burning.3 Overall metabolism includes both the resting metabolic rate and activity-related energy expenditure; in other words, the number of calories burned while resting and while working.
Metabolic rate is controlled to some degree by a number of hormones circulating through the bloodstream. In addition to the rate at which calories are burned, it's important to consider what substrate (type of calories- fat vs. carbohydrates) is burned. Using up sugar stores (glucose and glycogen) forces the body to catabolize (break down) protein, including muscle mass, in order to provide amino acids that are converted into glucose through a process known as gluconeogenesis.
Exercise and Fat Burning
A recent paper reviewed many of the effects of exercise on the storage and oxidation (calorie burning) of dietary fat.3 Exercise burns calories, but the intensity, duration and type (aerobic vs. resistance training) of exercise determines not only the number of calories burned, but also what percent of those calories come from fat. The more intense the exercise, the more total calories burned. However, there is a bell-shaped curve in regard to the percent of those calories burned coming from fat. Moderate-intensity exercise, defined as 65 percent of VO2 max, burns the most fat.4 VO2 is not measurable in the gym, but 65 percent VO2 equates to 74 percent maximal heart rate (220 minus age times 0.74). For a 30-year-old, this would be exercising at a rate that maintains the pulse at 140 beats per minute.
The fat burned during exercise comes from two sources: stores contained within muscle and fatty acids circulating in the blood. Fatty acid levels in the blood appear to be able to modulate the degree of fat oxidation (burning). When a high-fat meal is eaten 90 minutes prior to exercise, fat oxidation is increased.5 Conversely, a low-fat diet decreases lipolysis and fat oxidation.6 This might be explained in part by the fatty acid-glucose cycle- a relationship describing fatty acids' ability to decrease glucose uptake and glucose oxidation in the presence of high fatty acid levels.7 A long-term, high-fat diet changes the body's physiology, causing it to burn fat more so than compared to a high- carbohydrate diet.
A great part of the benefit of exercise, relative to fat loss, comes not from the immediate calorie burning due to the increase in activity, but to the increase in fat burning during recovery. In contrast to the immediate effect of exercise, which had shown differences based upon intensity, the delayed effects of exercise on fat metabolism are based upon the total amount of exercise.8-10 In other words, relative to delayed fat burning, you get the same benefit working half as hard and twice as long, as you do working twice as hard and half as long.
In one experiment, researchers learned walking at 60 percent of VO2 for an hour increased dietary fat burning significantly for the next 20 hours.10 In other studies, it was determined that 30 minutes of walking burns approximately 25 grams of fat over the next 12 hours, about half during the exercise, the remainder during the 12 hour recovery period.11,12
Both the immediate and delayed fat metabolism effects of exercise offer clear benefits, but what about long-term benefits in people who adopt an exercise-based lifestyle? Unfortunately, much of the research depends upon aerobic exercise (running, cycling and aerobics), but similar effects have been noted with resistance training, though to a lesser degree.
Metabolism and Hormones
Metabolism is determined by the balance of a number of hormones. Two hormones dominate in determining fat metabolism: leptin and catecholamines.3 A third, insulin, plays a major role in suppressing lipolysis and fat oxidation.13,14 Leptin is a hormone released by fat cells that helps the body regulate energy stores. Leptin is related to both the total amount of fat stores and recent food availability. Catecholamines include both the neurotransmitter norepinephrine, as well as adrenalin- the fight or flight hormone released from the adrenal medulla. Leptin and catecholamines both affect fat loss by decreasing appetite (reducing food intake) and increasing metabolism (burning more calories quicker).3,15 Insulin is a hormone released from the pancreas that regulates blood sugar. Insulin also promotes fat storage and inhibits fat release from adipocytes (fat cells).13,14
Additional hormones involved in fat metabolism include testosterone, estradiol, thyroid hormone, growth hormone, glucagon and cortisol.16-18 With the exception of insulin, all these hormones are involved in increasing fat oxidation. Estradiol, an estrogen, has been shown to increase fat oxidation in women, but may increase fat stores in men.19,20
Evidence from numerous studies has shown exercise alters the body's physiology, making it easier to utilize fat for energy, preserving sugar stores and protecting against the catabolic effects of exercise. Athletes' bodies are different in that they are much more efficient at releasing fat and burning fat for energy in muscle. Though common sense would suggest that if athletes burn more fat, they must have higher levels of the hormones involved in fat oxidation; it's actually the reverse that appears to be true.3
Compared to normal-weight sedentary people and the obese, athletes actually have lower levels of most hormones at rest. However, this does not represent a global hormone deficiency, rather it demonstrates that athletes are more sensitive to the hormones and respond more vigorously when exposed to lower levels of the hormones. This phenomenon was relatively unappreciated until the discovery of leptin. When leptin was being developed as a drug, it was believed to represent the great hope in combating obesity. Unfortunately, clinical trials failed, as it was discovered that most obese people generate plenty of leptin- since it's generated by fat cells- but they are resistant to its effects.21,22 Administering additional leptin had minimal effect. Athletes and those exposed to exercise training develop greater leptin sensitivity.23
Catecholamines are more immediately potent and respond rapidly to changes in activity. In sedentary people, this promotes fat oxidation, but it does not have a direct impact on subcutaneous fat (the stores of fat directly under the skin). This is due to what is known as tissue-specific effects of catecholamines. Different receptors respond to catecholamines; some promote fat loss, others constrict blood vessels closing off blood flow. In fat cells and muscle, ß-receptors dominate, which turn on the fat-burning machinery in a cell. In blood vessels, especially those in the subcutaneous fat tissue, α2-receptors dominate, which constrict the blood vessels, preventing hormones from getting into the subcutaneous area to stimulate fat release and preventing the released fat from reaching the circulation.24-26
One might wonder why the body prevents sedentary people from tapping into the subcutaneous fat, but allows athletes to access these energy stores. Likely, the matter is incidental to another function of the skin: thermoregulation. As athletes generate a lot of body heat during exercise, they have to release the heat through the skin.27 By conditioning the body to open the subcutaneous and dermal circulation during exercise, athletes now have the ability to tap into their subcutaneous fat stores. This is due to lower α2-receptor sensitivity.
In contrast, it appears the fat oxidizing effects of catecholamines are increased through higher ß-receptor sensitivity.25,26 Thus, relative to catecholamines, athletes have more fat oxidation.
The Role of Insulin
Insulin shows a similar pattern. Obese people are prone to type II diabetes and metabolic syndrome. These conditions include a pronounced resistance to insulin. As insulin strongly inhibits lipolysis, even at normal physiologic levels, chronically elevated insulin levels can rapidly lead to increased fat storage and a predisposition toward obesity.28 Athletes, as a group, have a much better degree of insulin sensitivity, so their insulin levels remain low.3 Thus, under similar conditions, athletes have less resistance to releasing and burning stored fat during exercise.
The other hormones mentioned- testosterone, estradiol, thyroid hormone, growth hormone and cortisol- demonstrate similar features. Immediately during exercise, these hormones peak, but at rest, athletes have similar or lower levels than their sedentary counterparts.3 Primarily, this is due to improved sensitivity and the body's ability to respond to the hormone stimulus.
Another interesting feature noted in some exercise studies is a change in the cellular structure of athletes. The mitochondria, the part of the cell where fat oxidation occurs, actually increases in size and number.29 This means not only does the active muscle of athletes receive more fatty acids to burn as energy, the muscle also has more "furnaces," increasing the body's ability to rely upon fat stores for energy instead of the more fragile carbohydrate stores.
The ideal for fitness fanatics would be to have a physiology that burned fat almost exclusively for most of the body's resting and exercise needs. This would preserve carbohydrate stores for immediate, high-energy work and protect protein stores from the catabolic demands of gluconeogenesis. Unfortunately, the human body is relatively inefficient at burning fat.30
Fortunately, the body adapts to a training lifestyle, making changes that improve the amount of fat made available for energy and offering a greater potential for burning fat for energy. This includes changes in the levels of several key metabolic hormones and a general increase in the sensitivity to the hormonal stimuli. These adaptations allow for a greater mobilization of stored fat, preservation of carbohydrate stores (especially during the recovery/replenishment period after exercise) and protection against muscle breakdown.
For dedicated athletes, the fat loss benefits of exercise go well beyond the mathematical equation of calories in minus calories burned. The bodybuilding lifestyle creates a physiology that improves health and works on physique enhancement even while you sleep.
References
1. Hansen K, Shriver T, et al. The effects of exercise on the storage and oxidation of dietary fat. Sports Med, 2005;35(5):363-73.
2. Miller WC, Koceja DM, et al. A meta-analysis of the past 25 years of weight loss research using diet, exercise or diet plus exercise intervention. Int J Obes Relat Metab Disord, 1997 Oct;21(10):941-7.
3. McMurray RG, Hackney AC. Interactions of metabolic hormones, adipose tissue and exercise. Sports Med, 2005;35(5):393-412.
4. Achten J, Gleeson M, et al. Determination of the exercise intensity that elicits maximal fat oxidation. Med Sci Sports Exerc, 2002: Jan;34(1):92-7.
5. Hawley JA, Burke LM, et al. Effect of altering substrate availability on metabolism and performance during intense exercise. Br J Nutr, 2000 Dec;84(6):829-38.
6. Coyle EF, Jeukendrup AE, et al. Low-fat diet alters intramuscular substrates and reduces lipolysis and fat oxidation during exercise. Am J Physiol Endocrinol Metab, 2001 Mar,280(3):E391-8.
7. Randle P, Hales C, et al. The glucose fatty acid cycle. Lancet, 1963;I:785-9.
8. Tsetsonis NV, Hardman AE. Reduction in postprandial lipemia after walking: influence of exercise intensity. Med Sci Sports Exerc, 1996 Oct;28(10):1235-42.
9. Tsetsonis NV, Hardman AE. Effects of low and moderate intensity treadmill walking on postprandial lipaemia in healthy young adults. Eur J Appl Physiol Occup Physiol, 1996;73(5):419-26.
10. Thompson DL, Townsend KM, et al. Substrate use during and following moderate- and low-intensity exercise: implications for weight control. Eur J Appl Physiol Occup Physiol, 1998 Jun;78(1):43-9.
11. Romijn JA, Coyle EF, et al. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Am J Physiol, 1993 Sep;265(3 Pt 1):E380-91.
12. Votruba SB, Atkinson RL, et al. Prior exercise increases subsequent utilization of dietary fat. Med Sci Sports Exerc, 2002 Nov;34(11):1757-65.
13. Stumvoll M, Jacob S, et al. Suppression of systemic, intramuscular, and subcutaneous adipose tissue lipolysis by insulin in humans. J Clin Endocrinol Metab, 2000 Oct;85(10):3740-5.
14. Jacob S, Hauer B, et al. Lipolysis in skeletal muscle is rapidly regulated by low physiological doses of insulin. Diabetologia, 1999 Oct;42(10):1171-4.
15. Mohamed-Ali V, Pinkney JH, et al. Adipose tissue as an endocrine and paracrine organ. Int J Obes Relat Metab Disord, 1998;22:1145-58.
16. Jeukendrup AE, Saris WHM, et al. Fat metabolism during exercise: a review - part I: fatty acid mobilization and muscle metabolism. Int J Sports Med, 1998;19(6):231-44.
17. Jeukendrup AE, Saris WHM, et al. Fat metabolism during exercise: a review - part II: regulation of metabolism and the effects of training. Int J Sports Med, 1998;19:293-302.
18. Steinacker JM, Lormes W, et al. New aspects of the hormone and cytokine response to training. Eur J Appl Physiol, 2004 Apr;91(4):382-91.
19. Ruby BC, Robergs RA, et al. Effects of estradiol on substrate turnover during exercise in amenorrheic females. Med Sci Sports Exerc, 1997;29(9):1160-9.
20. Longcope C, Baker R, et al. Androgen and estrogen metabolism: relationship to obesity. Metabolism, 1986;35(3):235-7.
21. Sahu A. Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance. Front Neuroendocrinol, 2003 Dec;24(4):225-53.
22. El-Haschimi K, Lehnert H. Leptin resistance - or why leptin fails to work in obesity. Exp Clin Endocrinol Diabetes, 2003 Feb;111(1):2-7.
23. Koutsari C, Karpe F, et al. Plasma leptin is influenced by diet composition and exercise. Int J Obes Relat Metab Disord, 2003 Aug;27(8):901-6.
24. Astrup A. The sympathetic nervous system as a target for intervention in obesity. Int J Obes Relat Metab Disord, 1995;19 Suppl 7:S24-8.
25. Harant I, Marion-Latard F, et al. Effect of a long-duration physical exercise on fat cell lipolytic responsiveness to adrenergic agents and insulin in obese men. Int J Obes Relat Metab Disord, 2002;26(10):1373-8.
26. Martin WH, Coyle EF, et al. Effects of stopping exercise training on epinephrine-stimulated lipolysis in humans. J Appl Physiol, 1984;56:845-8.
27. Yanagimoto S, Kuwahara T, et al. Intensity-dependent thermoregulatory responses at the onset of dynamic exercise in mildly heated humans. Am J Physiol Regul Integr Comp Physiol, 2003 Jul;285(1):R200-7.
28. Greenfield JR, Campbell LV. Insulin resistance and obesity. Clin Dermatol, 2004 Jul-Aug;22(4):289-95.
29. Coggan AR, Williams BD. Metabolic adaptations to endurance training: substrate metabolism during exercise. In: Hargreaves M, editor. Exercise metabolism. Champaign (IL): Human Kinetics Publisher Inc. 1995:177-210.
30. Lange KH. Fat metabolism in exercise - with special reference to training and growth hormone administration. Scand J Med Sci Sports, 2004 Apr;14(2):74-99.
Page 2
All Pages
Page 1 of 2
The guidance most often given to people seeking to lose weight is to eat less and exercise more. This is wonderful advice for the couch potatoes who get motivated only during the Super Bowl or while watching "Rocky" marathons.
Bodybuilders know that exercise and diet are key ingredients to their success in reducing body fat down to the lowest possible level. Never is it questioned among those who practice a dedicated lifestyle whether the dual approach of diet and exercise aid fat loss. Acknowledging that both work in fat loss, medicine and science are aggressively investigating exactly how this happens.
Is Starving Away Fat the Answer?
At the most basic level, fat loss occurs when energy intake (calories consumed as food and drink) is less than energy expended (metabolic rate and exercise).1 Dieting decreases the number of calories consumed and exercise increases the number of calories burned; seems simple and many assume the equation ends there. If fat loss were merely a matter of dropping calories, then slimming down would be a simple matter of just starving away the fat. Bodybuilders know this is not the case. Lower the calories too far and your energy drops until getting through the day is a challenge due to persistent fatigue and lethargy. Additionally, not only does weight loss slow down until it seems to stop, much of the weight loss appears to come from muscle rather than fat.2
It is really a shame that severe dieting carries so many negative side effects, as it's much simpler to cut calories than to burn more. Hundreds of calories can be dropped by switching to diet soft drinks or refusing dessert. In contrast, a half hour on the treadmill or a fairly intense session in the gym can be negated by a couple of cold beers.
Beyond the immediate impact on energy balance (calories in versus calories out), dieting and exercise affect the body's metabolism, which affects the balance between fat storage and fat burning.3 Overall metabolism includes both the resting metabolic rate and activity-related energy expenditure; in other words, the number of calories burned while resting and while working.
Metabolic rate is controlled to some degree by a number of hormones circulating through the bloodstream. In addition to the rate at which calories are burned, it's important to consider what substrate (type of calories- fat vs. carbohydrates) is burned. Using up sugar stores (glucose and glycogen) forces the body to catabolize (break down) protein, including muscle mass, in order to provide amino acids that are converted into glucose through a process known as gluconeogenesis.
Exercise and Fat Burning
A recent paper reviewed many of the effects of exercise on the storage and oxidation (calorie burning) of dietary fat.3 Exercise burns calories, but the intensity, duration and type (aerobic vs. resistance training) of exercise determines not only the number of calories burned, but also what percent of those calories come from fat. The more intense the exercise, the more total calories burned. However, there is a bell-shaped curve in regard to the percent of those calories burned coming from fat. Moderate-intensity exercise, defined as 65 percent of VO2 max, burns the most fat.4 VO2 is not measurable in the gym, but 65 percent VO2 equates to 74 percent maximal heart rate (220 minus age times 0.74). For a 30-year-old, this would be exercising at a rate that maintains the pulse at 140 beats per minute.
The fat burned during exercise comes from two sources: stores contained within muscle and fatty acids circulating in the blood. Fatty acid levels in the blood appear to be able to modulate the degree of fat oxidation (burning). When a high-fat meal is eaten 90 minutes prior to exercise, fat oxidation is increased.5 Conversely, a low-fat diet decreases lipolysis and fat oxidation.6 This might be explained in part by the fatty acid-glucose cycle- a relationship describing fatty acids' ability to decrease glucose uptake and glucose oxidation in the presence of high fatty acid levels.7 A long-term, high-fat diet changes the body's physiology, causing it to burn fat more so than compared to a high- carbohydrate diet.
A great part of the benefit of exercise, relative to fat loss, comes not from the immediate calorie burning due to the increase in activity, but to the increase in fat burning during recovery. In contrast to the immediate effect of exercise, which had shown differences based upon intensity, the delayed effects of exercise on fat metabolism are based upon the total amount of exercise.8-10 In other words, relative to delayed fat burning, you get the same benefit working half as hard and twice as long, as you do working twice as hard and half as long.
In one experiment, researchers learned walking at 60 percent of VO2 for an hour increased dietary fat burning significantly for the next 20 hours.10 In other studies, it was determined that 30 minutes of walking burns approximately 25 grams of fat over the next 12 hours, about half during the exercise, the remainder during the 12 hour recovery period.11,12
Both the immediate and delayed fat metabolism effects of exercise offer clear benefits, but what about long-term benefits in people who adopt an exercise-based lifestyle? Unfortunately, much of the research depends upon aerobic exercise (running, cycling and aerobics), but similar effects have been noted with resistance training, though to a lesser degree.
Metabolism and Hormones
Metabolism is determined by the balance of a number of hormones. Two hormones dominate in determining fat metabolism: leptin and catecholamines.3 A third, insulin, plays a major role in suppressing lipolysis and fat oxidation.13,14 Leptin is a hormone released by fat cells that helps the body regulate energy stores. Leptin is related to both the total amount of fat stores and recent food availability. Catecholamines include both the neurotransmitter norepinephrine, as well as adrenalin- the fight or flight hormone released from the adrenal medulla. Leptin and catecholamines both affect fat loss by decreasing appetite (reducing food intake) and increasing metabolism (burning more calories quicker).3,15 Insulin is a hormone released from the pancreas that regulates blood sugar. Insulin also promotes fat storage and inhibits fat release from adipocytes (fat cells).13,14
Additional hormones involved in fat metabolism include testosterone, estradiol, thyroid hormone, growth hormone, glucagon and cortisol.16-18 With the exception of insulin, all these hormones are involved in increasing fat oxidation. Estradiol, an estrogen, has been shown to increase fat oxidation in women, but may increase fat stores in men.19,20
Evidence from numerous studies has shown exercise alters the body's physiology, making it easier to utilize fat for energy, preserving sugar stores and protecting against the catabolic effects of exercise. Athletes' bodies are different in that they are much more efficient at releasing fat and burning fat for energy in muscle. Though common sense would suggest that if athletes burn more fat, they must have higher levels of the hormones involved in fat oxidation; it's actually the reverse that appears to be true.3
Compared to normal-weight sedentary people and the obese, athletes actually have lower levels of most hormones at rest. However, this does not represent a global hormone deficiency, rather it demonstrates that athletes are more sensitive to the hormones and respond more vigorously when exposed to lower levels of the hormones. This phenomenon was relatively unappreciated until the discovery of leptin. When leptin was being developed as a drug, it was believed to represent the great hope in combating obesity. Unfortunately, clinical trials failed, as it was discovered that most obese people generate plenty of leptin- since it's generated by fat cells- but they are resistant to its effects.21,22 Administering additional leptin had minimal effect. Athletes and those exposed to exercise training develop greater leptin sensitivity.23
Catecholamines are more immediately potent and respond rapidly to changes in activity. In sedentary people, this promotes fat oxidation, but it does not have a direct impact on subcutaneous fat (the stores of fat directly under the skin). This is due to what is known as tissue-specific effects of catecholamines. Different receptors respond to catecholamines; some promote fat loss, others constrict blood vessels closing off blood flow. In fat cells and muscle, ß-receptors dominate, which turn on the fat-burning machinery in a cell. In blood vessels, especially those in the subcutaneous fat tissue, α2-receptors dominate, which constrict the blood vessels, preventing hormones from getting into the subcutaneous area to stimulate fat release and preventing the released fat from reaching the circulation.24-26
One might wonder why the body prevents sedentary people from tapping into the subcutaneous fat, but allows athletes to access these energy stores. Likely, the matter is incidental to another function of the skin: thermoregulation. As athletes generate a lot of body heat during exercise, they have to release the heat through the skin.27 By conditioning the body to open the subcutaneous and dermal circulation during exercise, athletes now have the ability to tap into their subcutaneous fat stores. This is due to lower α2-receptor sensitivity.
In contrast, it appears the fat oxidizing effects of catecholamines are increased through higher ß-receptor sensitivity.25,26 Thus, relative to catecholamines, athletes have more fat oxidation.
The Role of Insulin
Insulin shows a similar pattern. Obese people are prone to type II diabetes and metabolic syndrome. These conditions include a pronounced resistance to insulin. As insulin strongly inhibits lipolysis, even at normal physiologic levels, chronically elevated insulin levels can rapidly lead to increased fat storage and a predisposition toward obesity.28 Athletes, as a group, have a much better degree of insulin sensitivity, so their insulin levels remain low.3 Thus, under similar conditions, athletes have less resistance to releasing and burning stored fat during exercise.
The other hormones mentioned- testosterone, estradiol, thyroid hormone, growth hormone and cortisol- demonstrate similar features. Immediately during exercise, these hormones peak, but at rest, athletes have similar or lower levels than their sedentary counterparts.3 Primarily, this is due to improved sensitivity and the body's ability to respond to the hormone stimulus.
Another interesting feature noted in some exercise studies is a change in the cellular structure of athletes. The mitochondria, the part of the cell where fat oxidation occurs, actually increases in size and number.29 This means not only does the active muscle of athletes receive more fatty acids to burn as energy, the muscle also has more "furnaces," increasing the body's ability to rely upon fat stores for energy instead of the more fragile carbohydrate stores.
The ideal for fitness fanatics would be to have a physiology that burned fat almost exclusively for most of the body's resting and exercise needs. This would preserve carbohydrate stores for immediate, high-energy work and protect protein stores from the catabolic demands of gluconeogenesis. Unfortunately, the human body is relatively inefficient at burning fat.30
Fortunately, the body adapts to a training lifestyle, making changes that improve the amount of fat made available for energy and offering a greater potential for burning fat for energy. This includes changes in the levels of several key metabolic hormones and a general increase in the sensitivity to the hormonal stimuli. These adaptations allow for a greater mobilization of stored fat, preservation of carbohydrate stores (especially during the recovery/replenishment period after exercise) and protection against muscle breakdown.
For dedicated athletes, the fat loss benefits of exercise go well beyond the mathematical equation of calories in minus calories burned. The bodybuilding lifestyle creates a physiology that improves health and works on physique enhancement even while you sleep.
References
1. Hansen K, Shriver T, et al. The effects of exercise on the storage and oxidation of dietary fat. Sports Med, 2005;35(5):363-73.
2. Miller WC, Koceja DM, et al. A meta-analysis of the past 25 years of weight loss research using diet, exercise or diet plus exercise intervention. Int J Obes Relat Metab Disord, 1997 Oct;21(10):941-7.
3. McMurray RG, Hackney AC. Interactions of metabolic hormones, adipose tissue and exercise. Sports Med, 2005;35(5):393-412.
4. Achten J, Gleeson M, et al. Determination of the exercise intensity that elicits maximal fat oxidation. Med Sci Sports Exerc, 2002: Jan;34(1):92-7.
5. Hawley JA, Burke LM, et al. Effect of altering substrate availability on metabolism and performance during intense exercise. Br J Nutr, 2000 Dec;84(6):829-38.
6. Coyle EF, Jeukendrup AE, et al. Low-fat diet alters intramuscular substrates and reduces lipolysis and fat oxidation during exercise. Am J Physiol Endocrinol Metab, 2001 Mar,280(3):E391-8.
7. Randle P, Hales C, et al. The glucose fatty acid cycle. Lancet, 1963;I:785-9.
8. Tsetsonis NV, Hardman AE. Reduction in postprandial lipemia after walking: influence of exercise intensity. Med Sci Sports Exerc, 1996 Oct;28(10):1235-42.
9. Tsetsonis NV, Hardman AE. Effects of low and moderate intensity treadmill walking on postprandial lipaemia in healthy young adults. Eur J Appl Physiol Occup Physiol, 1996;73(5):419-26.
10. Thompson DL, Townsend KM, et al. Substrate use during and following moderate- and low-intensity exercise: implications for weight control. Eur J Appl Physiol Occup Physiol, 1998 Jun;78(1):43-9.
11. Romijn JA, Coyle EF, et al. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Am J Physiol, 1993 Sep;265(3 Pt 1):E380-91.
12. Votruba SB, Atkinson RL, et al. Prior exercise increases subsequent utilization of dietary fat. Med Sci Sports Exerc, 2002 Nov;34(11):1757-65.
13. Stumvoll M, Jacob S, et al. Suppression of systemic, intramuscular, and subcutaneous adipose tissue lipolysis by insulin in humans. J Clin Endocrinol Metab, 2000 Oct;85(10):3740-5.
14. Jacob S, Hauer B, et al. Lipolysis in skeletal muscle is rapidly regulated by low physiological doses of insulin. Diabetologia, 1999 Oct;42(10):1171-4.
15. Mohamed-Ali V, Pinkney JH, et al. Adipose tissue as an endocrine and paracrine organ. Int J Obes Relat Metab Disord, 1998;22:1145-58.
16. Jeukendrup AE, Saris WHM, et al. Fat metabolism during exercise: a review - part I: fatty acid mobilization and muscle metabolism. Int J Sports Med, 1998;19(6):231-44.
17. Jeukendrup AE, Saris WHM, et al. Fat metabolism during exercise: a review - part II: regulation of metabolism and the effects of training. Int J Sports Med, 1998;19:293-302.
18. Steinacker JM, Lormes W, et al. New aspects of the hormone and cytokine response to training. Eur J Appl Physiol, 2004 Apr;91(4):382-91.
19. Ruby BC, Robergs RA, et al. Effects of estradiol on substrate turnover during exercise in amenorrheic females. Med Sci Sports Exerc, 1997;29(9):1160-9.
20. Longcope C, Baker R, et al. Androgen and estrogen metabolism: relationship to obesity. Metabolism, 1986;35(3):235-7.
21. Sahu A. Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance. Front Neuroendocrinol, 2003 Dec;24(4):225-53.
22. El-Haschimi K, Lehnert H. Leptin resistance - or why leptin fails to work in obesity. Exp Clin Endocrinol Diabetes, 2003 Feb;111(1):2-7.
23. Koutsari C, Karpe F, et al. Plasma leptin is influenced by diet composition and exercise. Int J Obes Relat Metab Disord, 2003 Aug;27(8):901-6.
24. Astrup A. The sympathetic nervous system as a target for intervention in obesity. Int J Obes Relat Metab Disord, 1995;19 Suppl 7:S24-8.
25. Harant I, Marion-Latard F, et al. Effect of a long-duration physical exercise on fat cell lipolytic responsiveness to adrenergic agents and insulin in obese men. Int J Obes Relat Metab Disord, 2002;26(10):1373-8.
26. Martin WH, Coyle EF, et al. Effects of stopping exercise training on epinephrine-stimulated lipolysis in humans. J Appl Physiol, 1984;56:845-8.
27. Yanagimoto S, Kuwahara T, et al. Intensity-dependent thermoregulatory responses at the onset of dynamic exercise in mildly heated humans. Am J Physiol Regul Integr Comp Physiol, 2003 Jul;285(1):R200-7.
28. Greenfield JR, Campbell LV. Insulin resistance and obesity. Clin Dermatol, 2004 Jul-Aug;22(4):289-95.
29. Coggan AR, Williams BD. Metabolic adaptations to endurance training: substrate metabolism during exercise. In: Hargreaves M, editor. Exercise metabolism. Champaign (IL): Human Kinetics Publisher Inc. 1995:177-210.
30. Lange KH. Fat metabolism in exercise - with special reference to training and growth hormone administration. Scand J Med Sci Sports, 2004 Apr;14(2):74-99.
