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
- Identify the hormones responsible for controlling adipose accumulation/distribution, and mobilization/oxidation.
- Determine specific strategies to control the adipose-enhancing hormones, while discussing strategies to enhance the adipose-inhibiting hormones.
- 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
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