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How to Control Fat Accumulation: Part 1

Almost every client who works with a trainer wishes to improve their body composition. Besides looking better in a bathing suit, improving body composition reduces mortality risk and chronic diseases like obesity, Type II diabetes, and cardiovascular disease. Different hormones and enzymes control muscular growth and body fat accumulation, distribution, and mobilization. The purpose of this two part article series is to identify the hormones responsible for controlling the regulation of body composition, and offer practical nutritional, exercise, and lifestyle strategies. This information will help trainers educate and assist their clients in effectively improving natural regulation of hormones and facilitate positive changes in body composition, while simultaneously improving long-term health.

Part 2 of this article can be found here: How to Control Fat Accumulation: Part 2

Learning Objectives:

  1. Identify the hormones responsible for controlling adipose accumulation/distribution, and mobilization/oxidation.
  2. Determine specific strategies to control the adipose-enhancing hormones, while discussing strategies to enhance the adipose-inhibiting hormones.
  3. Recognize simple lifestyle changes that can make the biggest impact on body composition and overall health.

Hormones Responsible for Controlling Body Composition

The risk of developing cardiovascular disease, Type II diabetes, and stroke are significantly increased in individuals who accumulate substantial abdominal visceral fat, or central adiposity. Specific hormonal concentrations and interactions have different metabolic effects, which can influence the amount of adiposity and its regional distribution patterns (Roemmich, & Rogol, 1999; Gambacciani et al., 1997). Fat distribution, accumulation, and mobilization is different in every individual, and depends on multiple factors including: gender; serum hormone concentrations; anatomical differences in the location, number, and density of hormone receptors; blood flow; neural innervation; and the activity of the enzymes activating either fat accumulation or mobilization (Björntorp, 1996). 

The enzyme responsible for regulating the accumulation of adipose tissue is lipoprotein lipase (LPL), whereas the mobilization of free-fatty acids from adipose tissue is regulated by the activity of hormone-sensitive lipase (HSL). Cortisol and insulin together produce significant effects on fat accumulation through the up-regulation of LPL, while the sex-steroid hormones along with growth hormone (GH) enhance the effects of lipolysis by stimulating HSL activity (Björntorp, 1997). Other hormones such as leptin and ghrelin can also be culprits for either fat accumulation or mobilization due to their influence on hunger and appetite (Roemmich, & Rogol, 1999).  

Adipose Enhancing Hormones

Insulin is the hormone the body uses to regulate blood sugar. It is released by pancreatic β-cells to maintain homeostatic levels of blood sugar by storing excess glucose in insulin-dependent tissues such as muscle, liver and fat cells (Spiegel, Knutson, Leproult, Tasali, & Van Cauter, 2005). It is a necessary action because excess blood sugar is a toxic environment, and chronically elevated blood sugar can lead to Type II diabetes. Whenever blood sugar is elevated, it triggers the body into ‘storage’ mode because insulin stimulates LPL while simultaneously inhibiting any additional free-fatty acid release from HSL (Ottosson, Lönnroth, Björntorp, & Edén, 2000). 

Diets consistently high in refined carbohydrates and sugar will chronically elevate blood glucose and subsequent plasma insulin levels, potentially leading to hyperinsulinemia. Hyperinsulinemia is suggested to influence the regulation of sex hormones in both men and women. In vitro studies have shown that insulin enhances the effects of luteinizing hormone (LH), which stimulates ovarian androgen synthesis - contributing to abdominal fat accumulation in women, a characterization of hyperinsulinemia. 

In men however, studies have shown direct correlations between serum testosterone (Te) levels and insulin sensitivity (Bhasin, 2003; Haffner, Karhapää, Mykkänen, & Laakso, 1994). Hyperinsulinemia contributes to lowered Te levels by increasing the clearance rate, while simultaneously reducing sex-hormone binding globulin (SHBG) concentrations (Pasquali et al., 1991). 

Prolonged hyperinsulinemia leads to impaired glucose regulation and subsequent hyperglycemia. This constant state of high blood sugar can cause chronic inflammation by which oxidative stress damages the DNA of pancreatic β-cells, therefore contributing to a vicious cycle of greater insulin resistance and hyperglycemia, until finally deteriorating to Type II diabetes (Song et al., 2007). 

Cortisol is the body’s ‘fight or flight’ stress hormone that has major effects on the metabolism of adipose tissue, both in accumulation and mobilization (Björntorp, 1997). Cortisol’s main action is to stimulate glycogen release into the blood stream, which ultimately stimulates pancreatic insulin release. In the presence of insulin, cortisol causes fat accumulation by stimulating LPL (Ottosson, Lönnroth, Björntorp, & Edén, 2000). These effects are most likely pronounced in visceral fat accumulation due to the high density of visceral glucocorticoid receptors. 

It is well documented that Cushing’s Syndrome (a disease characterized by excessive serum cortisol levels) is associated with obesity and typically involves visceral fat accumulation (Noreen et al., 2010; Björntorp, 1997). In normal individuals, serum cortisol concentrations are the highest at the beginning of the day, and gradually reach their lowest levels in the afternoon and night hours. Cortisol levels will increase with any kind of stress to the body whether it is physical, mental, psychological, emotional, etc. This increased stress response of cortisol is related to greater central adiposity as women with higher waist : hip ratios exhibit greater serum cortisol concentrations after experiencing stressful situations (Epel et al., 2000). In women with post-traumatic stress disorder, cortisol concentrations remain elevated up to 24 hours after simply recollecting a traumatic stressful event in their lives (Koopman et al., 2003). This is how high-stress situations can increase fat accumulation due to the lipogenic effects cortisol and insulin have together.

The cortisol response to exercise is affected by the intensity, duration, exercise state (competition vs. practice), psychological stimuli, and the time of day (Azarbayjani, Fatolahi, Rasaee, Peeri, & Babael, 2011). Even though exercise increases cortisol levels, the subsequent rise in growth hormone actually inhibits fat accumulation, shifting activity toward lipid mobilization (Björntorp, 1997).

Strategies for Controlling Insulin

The development of skeletal muscle insulin resistance is believed to be a key progression in the pathogenesis of Type II diabetes, and oxidative stress is thought to play an important role in the pathogenesis of atherosclerosis; linking obesity, insulin resistance and Type II diabetes. Indicators of oxidative stress are significantly higher in obese children who also have increased insulin resistance, which indicates a more severe level of damage in their vascular tissue (Codoñer-Franch et al., 2012). 

The traditional approach to improve insulin sensitivity includes exercise, weight loss, and insulin-sensitizing drugs. Weight loss can be improved by reducing carbohydrate consumption, which increases the body’s efficiency in lipid oxidation and reduces serum triglycerides - which decreases overall fat storage (Parks, 2001) - along with improving countless risk factors for cardiovascular disease (Westman et al., 2007). 

While there can be undesirable side effects with drugs, other alternative nutritional approaches and supplements can be used to improve insulin sensitivity, such as the supplementation of antioxidants (Wright, & Sutherland, 2008). Antioxidants can enhance significant gains in fat-free mass during resistance training programs (even in elderly populations), likely from reducing the damage to muscles and/or increasing protein synthesis stimulated from the muscle contractions during training. However, insulin sensitivity will not improve if exercise does not cause adequate glycogen depletion (Bobeuf, Labonté, Khalil, & Dionne, 2010). So exercise intensity is an important variable to monitor when attempting to improve insulin sensitivity. 

Low levels of both magnesium (Mg) and vitamin D concentrations have been associated with both increased fat mass and BMI among children and adults. Daily supplementation enhances lipid mobilization and improves insulin sensitivity in insulin-resistant subjects. Vitamin D specifically reduces visceral adipose tissue, while Mg can act as a prophylactic for individuals even with normal serum levels, but who may be at risk for developing metabolic syndrome (Mooren et al., 2011; Rosenblum, Castro, Moore, & Kaplan, 2012).

Strategies for Controlling Cortisol

Care must be taken to monitor life-stressors in attempt to maintain normal cortisol regulation, as it is well established that cortisol increases protein catabolism (Noreen et al., 2010).  Although cortisol will increase with any kind of stress, exercise provides the largest stimulus for GH release, which will negate any effects cortisol has on lipid accumulation and shift toward mobilization (Weltman et al., 1992). 

Long-duration aerobic training should be avoided, however, if attempting to decrease cortisol. In a study investigating the hormonal response to strenuous anaerobic running, there were only slight increases in plasma cortisol (Kuoppasalmi, Näveri, Rehunen, Härkönen, & Adlercreutz, 1976). Whereas in studies comparing short-duration, anaerobic exercises to prolonged aerobic exercise, increases in cortisol were consistently greater in the longer-duration exercise protocols (Kindermann et al., 1982; Schwarz & Kindermann, 1990). In trained cyclists, the longer the duration and greater the intensity of the aerobic endurance workout decreased Te levels and changed the hormonal concentrations of GH and cortisol during the subsequent night’s sleep (Kern, Perras, Wodick, Fehm, & Born, 1995).

Therefore, when attempting to control cortisol, exercise type should be more anaerobic (such as resistance training or sprint training) and should ideally be performed in the morning hours to take advantage of the naturally higher levels of cortisol and Te. When combined with the increases in GH, greater lipid mobilization will be stimulated. In higher trained individuals, the cortisol response is less sensitive during matched work output (Azarbayjani, Fatolahi, Rasaee, Peeri, & Babael, 2011), so training variables must constantly be manipulated to avoid plateaus in hormonal responses.   

Omega-3 fatty-acid supplementation has also been shown to decrease serum cortisol concentrations, and stimulate an increase in fat-free mass while decreasing fat mass, likely due to the effects omega-3’s have on suppressing lipogenesis (Noreen et al., 2010). To avoid unnecessary increases in cortisol throughout the day, it is best to consume any caffeine prior to exercise rather than after because caffeine has been shown to increase serum cortisol levels.  In addition, caffeine improves voluntary exercise intensity in both endurance and strength activities, even in a sleep-deprived state, lending a greater hormonal response from cortisol, Te and GH post exercise (Cook, Beaven, Kilduff, & Drawer, 2012).  

Adipose Inhibiting Hormones 

Growth Hormone (GH) & Insulin-like Growth Factor (IGF-1) 
GH is one of the most lipolytic hormones in the body (Weltman et al., 1992). It specifically induces lipolysis, or the release of free-fatty acids from adipocytes, through the activation of HSL while simultaneously inhibiting LPL. Even in the presence of cortisol, the stimulatory effects on LPL are diminished if GH is present (Ottosson, Lönnroth, Björntorp, & Edén, 2000). GH also helps build muscle as it reduces protein degradation while increasing protein synthesis; an effect enhanced even more when combined with Te (Widdowson, Healy, Sönksen, & Gibney, 2009).

GH treatment selectively reduces abdominal visceral fat in GH-deficient children (Björntorp, 1996). Obesity has been shown to reduce serum GH release and the GH treatment reduces the size of subcutaneous fat cells, while decreasing overall percentage of body fat, fat mass, and abdominal visceral fat. Additionally, the GH treatment increases fat-free mass and bone mineral content. Due to maturational and gender differences, there is no general consensus on the fat distribution patterns of GH, likely due to interactions between different sex steroid concentrations and selective oxidation of fat in specific regions (Roemmich, & Rogol, 1999).

When GH is released, insulin-like growth factor-1 (IGF-1) levels also increase, which intercedes most of the anabolic effects of GH. Medically, IGF-1 is often prescribed for patients who have different types of GH receptor defects, and also for diabetics who do not respond well to insulin therapy (Guha, Sönksen, & Holt, 2009; Kuzuya et al., 1993). IGF-I is a hypoglycemic agent that directly affects glucose metabolism as it causes a similar action of insulin by stimulating muscle glycogen synthesis. IGF-1 treatment has been shown to significantly increase the rate of protein synthesis, likely by stimulating amino acid uptake into muscle cells.  Treatment also causes an increase in lipolysis and lipid oxidation, possibly due to an inhibitory effect on circulating insulin (Guha, Sönksen, & Holt, 2009). 

The highest amounts of serum Te and cortisol occur during early morning hours, and gradually decline throughout the day (Azarbayjani, Fatolahi, Rasaee, Peeri, & Babael, 2011). High elevations of testosterone (Te) greatly enhance androgen receptor signaling in skeletal muscle, which plays a key role in regulating muscle protein synthesis and hypertrophy (Willoughby & Taylor, 2004). When Te is coupled with GH, synergistically they increase lipolysis in abdominal adipose tissue through the up-regulation of HSL (Björntorp, 1996) and will also limit any accumulation of visceral abdominal fat by inhibiting LPL (Mårin, Odén, & Björntorp, 1995; Mårin et al., 1992).

Obesity in men is characterized by reduced Te levels which increase the estrogen : androgen ratio, suggesting hyperestrogenemia from the aromatization of androgens in adipose tissue (Pasquali et al., 1991). Consequently low Te creates a vicious cycle. Increased fat accumulation subsequently aromatizes more Te, therefore it decreases more Te while accumulating additional fat. These results are confirmed in hypogonadal men whose accumulation of abdominal visceral fat is reduced upon administration of Te and is accompanied with reductions in plasma insulin levels, blood glucose concentrations, and increased insulin sensitivity (Mårin et al.,1992; Haffner, Karhapää, Mykkänen, & Laakso, 1994). 

In older men, Te can result in substantial increases in lean body mass, muscle strength, and aerobic capacity accompanied with marked decreases in total fat mass and abdominal adiposity. These improvements are enhanced with the concurrent administration of GH, illustrating the synergistic relationship these hormones have with one another (Sattler et al., 2009).

Estrogen tends to play an indirect role in lipolysis and fat distribution. The amount of visceral fat in women is thought to be more dependent on the estrogen : androgen ratio because hyperandrogenic women tend to have greater amounts of abdominal visceral fat (Björntorp, 1996; Kaye, 1991), along with decreased insulin sensitivity (Haffner, Karhapää, Mykkänen, & Laakso, 1994). In early pubertal girls, higher estrogen concentrations are associated with greater gynoid fat distribution patterns (Roemmich, & Rogol, 1999). As women age and transition into menopause, decreases in estrogen selectively accelerate fat accumulation in the abdominal region (Tchernof, Poehlman, & Després, 2000). 

In a study investigating early postmenopausal women treated with estrogen hormone-replacement therapy (HRT), no changes were observed in total body fat or percentage of fat mass when compared to a control group who experienced significant declines in estrogen accompanied with a gain in body weight and BMI. The control group also experienced a shift in body fat accumulation to a more central (android) adiposity with the accumulation of both abdominal visceral and subcutaneous fat, along with increased subcutaneous arm fat using dual x-ray absorbptiometry (DEXA). In the HRT group, there was an increase in the proportion of fat distributed in the legs region after 12 months of treatment but there were no modifications of fat distribution in the abdomen or arms, confirming estrogen prefers a more gynoid pattern of fat distribution (Gambacciani et al., 1997). These postmenopausal changes in fat accumulation and distribution are likely due to the deficiency in estrogen which secondarily up-regulates LPL activity (Toth, Tchernof, Sites, & Poehlman, 2000). Another interesting finding in the HRT study was that the women who had less prominent android fat distribution in basal conditions were the ones who actually noticed a greater increase in android fat distribution after menopause. This suggests changes in fat distribution are less dependent on basal characteristics of adipocytes and more related to the hormonal environment during the menopause transition (Gambacciani et al., 1997). 

There is no doubt that estrogen has functional effects on female metabolism and fat distribution similar to that of Te in men, but because of the absence of estrogen and progesterone receptors in adipose tissue, the effects are likely through indirect interaction with GH secretion or by regulating the density of androgen receptors (Björntorp, 1996).


By understanding the different hormones and enzymes responsible for influencing body composition, trainers can impart sound advice for clients based on individual needs. Controlling serum insulin and cortisol levels can minimize fat accumulation; while decreasing the risk of chronic diseases like obesity, diabetes, and cardiovascular disease.

Continue reading Part 2 of this article here: How to Control Fat Accumulation: Part 2


Azarbayjani, M. A., Fatolahi, H., Rasaee, M. J., Peeri, M., & Babael, R. (2011). The effect of exercise mode and intensity of submaximal physical activities on salivary testosterone to cortisol ratio and a-amylase in young active males. International Journal of Exercise Science, 4(4), 9.

Bélanger, A., Locong, A., Noel, C., Cusan, L., Dupont, A., Prévost, J., & Sévigny, J. (1989). Influence of diet on plasma steroids and sex hormone-binding globulin levels in adult men. Journal Of Steroid Biochemistry, 32(6), 829-833.

Bhasin, S. (2003). Effects of testosterone administration on fat distribution, insulin sensitivity, and atherosclerosis progression. Clinical Infectious Diseases: An Official Publication Of The Infectious Diseases Society Of America, 37 Suppl 2S142-S149.

Biolo, G., Williams, B., Fleming, R., & Wolfe, R. (1999). Insulin action on muscle protein kinetics and amino acid transport during recovery after resistance exercise. Diabetes, 48(5), 949-957.

Björntorp, P. (1996). The regulation of adipose tissue distribution in humans. International Journal Of Obesity And Related Metabolic Disorders: Journal Of The International Association For The Study Of Obesity, 20(4), 291-302.

Björntorp, P. (1997). Hormonal control of regional fat distribution. Human Reproduction (Oxford, England), 12 Suppl 121-25.

Bobeuf, F., Labonté, M., Khalil, A., & Dionne, I. J. (2010). Effects of resistance training combined with antioxidant supplementation on fat-free mass and insulin sensitivity in healthy elderly subjects. Diabetes Research & Clinical Practice, 87(1), e1-e3.

Børsheim, E., Tipton, K., Wolf, S., & Wolfe, R. (2002). Essential amino acids and muscle protein recovery from resistance exercise. American Journal Of Physiology. Endocrinology And Metabolism, 283(4), E648-E657.

Boutcher, S. (2011). High-intensity intermittent exercise and fat loss. Journal Of Obesity, doi:10.1155/2011/868305.

Brilla, L. R., & Conte, V. (2000). Effects of a Novel Zinc-Magnesium Formulation on Hormones and Strength. Journal Of Exercise Physiology Online, 3(4), 26-36.

Brinkley, T., Hsu, F., Beavers, K., Church, T., Goodpaster, B., Stafford, R., & ... Nicklas, B. (2012). Total and abdominal adiposity are associated with inflammation in older adults using a factor analysis approach. Journals Of Gerontology Series A: Biological Sciences & Medical Sciences, 67(10), 1099-1106.

Buxton, O., Pavlova, M., Reid, E., Wang, W., Simonson, D., & Adler, G. (2010). Sleep restriction for 1 week reduces insulin sensitivity in healthy men. Diabetes, 59(9), 2126-2133.

Chandler, R. M., Byrne, H. K., Patterson, J. G., & Ivy, J. L. (1994). Dietary supplements affect the anabolic hormones after weight-training exercise. Journal of Applied Physiology, 76(2), 839-845.

Codoñer-Franch, P., Navarro-Ruiz, A., Fernández-Ferri, M., Arilla-Codoñer, Á., Ballester-Asensio, E., & Valls-Bellés, V. (2012). A matter of fat: insulin resistance and oxidative stress. Pediatric Diabetes, 13(5), 369-376.

Cook, C., Beaven, C., Kilduff, L. P., & Drawer, S. (2012). Acute Caffeine Ingestion's Increase of Voluntarily Chosen Resistance-Training Load After Limited Sleep. International Journal Of Sport Nutrition & Exercise Metabolism, 22(3), 157-164.

Donga, E., van Dijk, M., van Dijk, J., Biermasz, N., Lammers, G., van Kralingen, K., & ... Romijn, J. (2010). Partial sleep restriction decreases insulin sensitivity in type 1 diabetes. Diabetes Care, 33(7), 1573-1577.

Epel, E., McEwen, B., Seeman, T., Matthews, K., Castellazzo, G., Brownell, K., & ... Ickovics, J. (2000). Stress and body shape: stress-induced cortisol secretion is consistently greater among women with central fat. Psychosomatic Medicine, 62(5), 623-632.

Gambacciani, M., Ciaponi, M., Cappagli, B., Piaggesi, L., De Simone, L., Orlandi, R., & Genazzani, A. (1997). Body weight, body fat distribution, and hormonal replacement therapy in early postmenopausal women. The Journal Of Clinical Endocrinology And Metabolism, 82(2), 414-417.

Golf, S., Bender, S., & Grüttner, J. (1998). On the significance of magnesium in extreme physical stress. Cardiovascular Drugs And Therapy, 12 Suppl 2197-202.

Gómez-González, B., Domínguez-Salazar, E., Hurtado-Alvarado, G., Esqueda-Leon, E., Santana-Miranda, R., Rojas-Zamorano, J., & Velázquez-Moctezuma, J. (2012). Role of sleep in the regulation of the immune system and the pituitary hormones. Annals Of The New York Academy Of Sciences, 1261(1), 97-106

Goto, K., Ishii, N., Sugihara, S., Yoshioka, T., & Takamatsu, K. (2007). Effects of resistance exercise on lipolysis during subsequent submaximal exercise. Medicine & Science In Sports & Exercise, 39(2), 308-315.

Guha, N., Sönksen, P., & Holt, R. (2009). IGF-I abuse in sport: Current knowledge and future prospects for detection. Growth Hormone & IGF Research: Official Journal Of The Growth Hormone Research Society And The International IGF Research Society, 19(4), 408-411.

Haffner, S., Karhapää, P., Mykkänen, L., & Laakso, M. (1994). Insulin resistance, body fat distribution, and sex hormones in men. Diabetes, 43(2), 212-219.

Hill, P., & Wynder, E. (1979). Effect of a vegetarian diet and dexamethasone on plasma prolactin, testosterone and dehydroepiandrosterone in men and women. Cancer Letters, 7(5), 273-282.

Kaye, S., Folsom, A., Soler, J., Prineas, R., & Potter, J. (1991). Associations of body mass and fat distribution with sex hormone concentrations in postmenopausal women. International Journal Of Epidemiology, 20(1), 151-156.

Kern, W., Perras, B., Wodick, R., Fehm, H., & Born, J. (1995). Hormonal secretion during nighttime sleep indicating stress of daytime exercise. Journal Of Applied Physiology, 79(5), 1461-1468.

Kindermann, W. W., Schnabel, A. A., Schmitt, W. M., Biro, G. G., Cassens, J. J., & Weber, F. F. (1982). Catecholamines, growth hormone, cortisol, insulin, and sex hormones in anaerobic and aerobic exercise. European Journal Of Applied Physiology & Occupational Physiology, 49(3), 389-399.

Klingenberg, L., Chaput, J., Holmbäck, U., Visby, T., Jennum, P., Nikolic, M., & ... Sjödin, A. (2013). Acute Sleep Restriction Reduces Insulin Sensitivity in Adolescent Boys. Sleep, 36(7), 1085-1090.

Koopman, C., Sephton, S., Abercrombie, H. C., Classen, C., Butler, L. D., Gore-Felton, C., & ... Spiegel, D. (2003). Dissociative Symptoms and Cortisol Responses to Recounting Traumatic Experiences Among Childhood Sexual Abuse Survivors with PTSD. Journal Of Trauma & Dissociation, 4(4), 29-44.

Kraemer, W. J., Vingren, J. L., & Spiering, B. A., (2008). Endocrine responses to resistance exercise. In T. R. Baechle & R. W. Earle (Eds.), Essentials of Strength Training and Conditioning. (41-64). Champaign, IL: Human Kinetics.

Kuoppasalmi, K., Näveri, H., Rehunen, S., Härkönen, M., & Adlercreutz, H. (1976). Effect of strenuous anaerobic running exercise on plasma growth hormone, cortisol, luteinizing hormone, testosterone, androstenedione, estrone and estradiol. Journal Of Steroid Biochemistry, 7(10), 823-829.

Kuzuya, H., Matsuura, N., Sakamoto, M., Makino, H., Sakamoto, Y., Kadowaki, T., & et. al. (1993). Trial of insulin like growth factor I therapy for patients with extreme insulin resistance syndromes. Diabetes, 42(5), 696-705.

Leproult, R., Copinschi, G., Buxton, O., & Van Cauter, E. (1997). Sleep loss results in an elevation of cortisol levels the next evening. Sleep, 20(10), 865-870.

Mäestu, J., Eliakim, A., Jürimäe, J., Valter, I., & Jürimäe, T. (2010). Anabolic and catabolic hormones and energy balance of the male bodybuilders during the preparation for the competition. Journal Of Strength & Conditioning Research, 24(4), 1074-1081.

Mårin, P., Holmäng, S., Jönsson, L., Sjöström, L., Kvist, H., Holm, G., & ... Björntorp, P. (1992). The effects of testosterone treatment on body composition and metabolism in middle-aged obese men. International Journal Of Obesity And Related Metabolic Disorders: Journal Of The International Association For The Study Of Obesity, 16(12), 991-997.

Mårin, P., Odén, B., & Björntorp, P. (1995). Assimilation and mobilization of triglycerides in subcutaneous abdominal and femoral adipose tissue in vivo in men: effects of androgens. The Journal Of Clinical Endocrinology And Metabolism, 80(1), 239-243.

Mooren, F., Krüger, K., Völker, K., Golf, S., Wadepuhl, M., & Kraus, A. (2011). Oral magnesium supplementation reduces insulin resistance in non-diabetic subjects - a double-blind, placebo-controlled, randomized trial. Diabetes, Obesity & Metabolism, 13(3), 281-284.

Noreen, E. E., Sass, M. J., Crowe, M. L., Pabon, V. A., Brandauer, J., & Averill, L. K. (2010). Effects of supplemental fish oil on resting metabolic rate, body composition, and salivary cortisol in healthy adults. Journal of The International Society Of Sports Nutrition, 731-37.

Ottosson, M., Lönnroth, P., Björntorp, P., & Edén, S. (2000). Effects of cortisol and growth hormone on lipolysis in human adipose tissue. The Journal Of Clinical Endocrinology And Metabolism, 85(2), 799-803.

Parks, E. J. (2001). Effect of dietary carbohydrate on triglyceride metabolism in humans. Journal Of Nutrition, 131(10), 2772s-2774s.

Pasquali, R. R., Fabbri, R. R., Capelli, M. M., Bortoluzzi, L. L., Labate, A. M., Casimirri, F. F., & ... Melchionda, N. N. (1991). Effect of obesity and body fat distribution on sex hormones and insulin in men. Metabolism: Clinical And Experimental, 40(1), 101-104.

Pilz, S., Frisch, S., Koertke, H., Kuhn, J., Dreier, J., Obermayer-Pietsch, B., Wehr, E., & Zittermann, A. (2011). Effect of vitamin D supplementation on testosterone levels in men. Hormonal Metabolism Research, 43(3), 223-225.

Raben, A., Kiens, B., Richter, E., Rasmussen, L., Svenstrup, B., Micic, S., & Bennett, P. (1992). Serum sex hormones and endurance performance after a lacto-ovo vegetarian and a mixed diet. Medicine And Science In Sports And Exercise, 24(11), 1290-1297.

Riechman, S., Andrews, R., MacLean, D., & Sheather, S. (2007). Statins and dietary and serum cholesterol are associated with increased lean mass following resistance training. Journals Of Gerontology Series A: Biological Sciences & Medical Sciences, 62A(10), 1164-1171.

Roemmich, J. N., & Rogol, A. D. (1999). Hormonal changes during puberty and their relationship to fat distribution. American Journal Of Human Biology: The Official Journal Of The Human Biology Council, 11(2), 209-224.

Rohleder, N., Aringer, M., & Boentert, M. (2012). Role of interleukin-6 in stress, sleep, and fatigue. Annals Of The New York Academy Of Sciences, 1261(1), 88-96.

Rønnestad, B., Nygaard, H., & Raastad, T. (2011). Physiological elevation of endogenous hormones results in superior strength training adaptation. European Journal Of Applied Physiology, 111(9), 2249-2259.

Rosenblum, J., Castro, V., Moore, C., & Kaplan, L. (2012). Calcium and vitamin D supplementation is associated with decreased abdominal visceral adipose tissue in overweight and obese adults. American Journal Of Clinical Nutrition, 95(1), 101-108.

Rueggeberg, R., Wrosch, C., & Miller, G. (2012). Sleep duration buffers diurnal cortisol increases in older adulthood. Psychoneuroendocrinology, 37(7), 1029-1038.

Salehpour, A., Hosseinpanah, F., Shidfar, F., Vafa, M., Razaghi, M., Dehghani, S., & Gohari, M. (2012). A 12-week double-blind randomized clinical trial of vitamin D₃ supplementation on body fat mass in healthy overweight and obese women. Nutrition Journal, 11 (78)

Sanal, E., Ardic, F., & Kirac, S. (2013). Effects of aerobic or combined aerobic resistance exercise on body composition in overweight and obese adults: gender differences. A randomized intervention study. European Journal Of Physical And Rehabilitation Medicine, 49(1), 1-11.

Sassin, J. F. (1969). Human growth hormone release: relation to slow-wave sleep and sleep-waking cycles. Science, 165513-515.

Sattler, F., Castaneda-Sceppa, C., Binder, E., Schroeder, E., Wang, Y., Bhasin, S., & Azen, S. (2009). Testosterone and growth hormone improve body composition and muscle performance in older men. The Journal Of Clinical Endocrinology And Metabolism, 94(6), 1991-2001.

Song, F., Jia, W., Yao, Y., Hu, Y., Lei, L., Lin, J., & ... Liu, L. (2007). Oxidative stress, antioxidant status and DNA damage in patients with impaired glucose regulation and newly diagnosed Type 2 diabetes. Clinical Science (London), 112(12), 599-606.

Spiegel, K., Knutson, K., Leproult, R., Tasali, E., & Van Cauter, E. (2005). Sleep loss: a novel risk factor for insulin resistance and Type 2 diabetes. Journal Of Applied Physiology, 99(5), 2008-2019.

Spiegel, K., Leproult, R., & Van Cauter, E. (1999). Impact of sleep debt on metabolic and endocrine function. Lancet, 354(9188), 1435-1439.

Schwarz, L. L., & Kindermann, W. W. (1990). B-Endorphin, adrenocorticotropic hormone, cortisol and catecholamines during aerobic and anaerobic exercise. European Journal Of Applied Physiology & Occupational Physiology, 61(3-4), 165-171.

Taheri, S., Ling, L., Austin, D., Young, T., & Mignot, E. (2004). Short Sleep Duration Is Associated with Reduced Leptin, Elevated Ghrelin, and Increased Body Mass Index. Plos Medicine, 1(3), 210-217.

Tchernof, A., Poehlman, E., & Després, J. (2000). Body fat distribution, the menopause transition, and hormone replacement therapy. Diabetes & Metabolism, 26(1), 12-20.

Toth, M., Tchernof, A., Sites, C., & Poehlman, E. (2000). Menopause-related changes in body fat distribution. Annals Of The New York Academy Of Sciences, 904502-506.

Weikel, J., Wichniak, A., Ising, M., Brunner, H., Friess, E., Held, K., & Steiger, A. (2003). Ghrelin promotes slow-wave sleep in humans. American Journal Of Physiology. Endocrinology And Metabolism, 284(2), E407-E415.

Weltman, A., Weltman, J., Schurrer, R., Evans, W., Veldhuis, J., & Rogol, A. (1992). Endurance training amplifies the pulsatile release of growth hormone. Effects of training intensity. Journal Of Applied Physiology, 72(6), 2188-2196.

Westman, E., Feinman, R., Mavropoulos, J., Vernon, M., Volek, J., Wortman, J., & Phinney, S. (2007). Low-carbohydrate nutrition and metabolism. The American Journal Of Clinical Nutrition, 86(2), 276-284.

Widdowson, W., Healy, M., Sönksen, P., & Gibney, J. (2009). The physiology of growth hormone and sport. Growth Hormone & IGF Research: Official Journal Of The Growth Hormone Research Society And The International IGF Research Society, 19(4), 308-319.

Willoughby, D. S., & Taylor, L. (2004). Effects of sequential bouts of resistance exercise on androgen receptor expression. Medicine & Science In Sports & Exercise, 36(9), 1499-1506.

Wren, A., Seal, L., Cohen, M., Brynes, A., Frost, G., Murphy, K., & Bloom, S. (2001). Ghrelin enhances appetite and increases food intake in humans. The Journal Of Clinical Endocrinology And Metabolism, 86(12), 5992.

Wright, D., & Sutherland, L. (2008). Antioxidant supplementation in the treatment of skeletal muscle insulin resistance: potential mechanisms and clinical relevance. Applied Physiological Nutritional Metabolism, 33(1), 21-31.

Yaggi, H. K., Araujo, A. B., McKinlay, J. B. (2006). Sleep duration as a risk factor for the development of type 2 diabetes. Diabetes Care, 29(3), 657-661.

Zeligs, M. A. (1998). Diet and estrogen status: the cruciferous connection. Journal Of Medicinal Food, 1(2), 67-82.