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.
Before continuing to read this article, read Part 1 here: How to Control Fat Accumulation: Part 1
- 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.
Dietary Strategies for Improvement
If weight loss is not a major concern, the post-exercise period is one of the best opportunities to nutritionally take advantage of the anabolic effects insulin has on muscle. By ingesting carbohydrates in combination with essential amino acids (EAA) immediately post-exercise, protein breakdown is significantly reduced while also increasing muscle glycogen synthesis (Børsheim, Tipton, Wolf, & Wolfe, 2002; Biolo, Williams, Fleming, & Wolfe, 1999). This combination of EAA and carbohydrates during recovery has also been shown to elevate growth hormone (GH) concentrations up to six hours post-exercise; significantly longer than protein ingestion alone (Chandler, Byrne, Patterson, & Ivy, 1994).
If weight loss is a concern, then overall dietary carbohydrate consumption should be kept low throughout the entire day to help stabilize insulin levels and improve insulin sensitivity. However, extremely prolonged reductions in dietary carbohydrates should be avoided in athletes who compete in weight classes and need to maintain a certain amount of muscle mass (body builders, wrestlers, martial artists). Extreme reductions not only decrease circulating insulin, but also IGF-1, which may ultimately lead to muscle loss because post-exercise protein synthesis is reduced without adequate concentrations of insulin and IGF-I (Mäestu, Eliakim, Jürimäe, Valter, & Jürimäe, 2010).
Eating foods high in dietary cholesterol is a simple way to increase serum testosterone (Te). Dietary cholesterol does not correlate to serum cholesterol, and the greater intake of dietary cholesterol correlates to greater increases in strength and lean mass when resistance training. This is because cholesterol seems to aid in the production of Te and estrogen (Riechman, Andrews, MacLean, & Sheather, 2007). Vegetarian diets are often low in dietary cholesterol, and are associated with lower Te compared to omnivores (Hill & Wynder, 1979; Bélanger et al., 1989; Raben et al., 1992).
Supplementing with vitamin D also proves beneficial for body composition. In overweight and obese women, total body fat mass decreased as vitamin D serum concentrations increased (Salehpour et al., 2012). Vitamin D is also necessary for muscle growth, and when healthy overweight men with low Te levels were given ~3,300 iu of vitamin D a day for one year, a significant increase in total Te was observed when compared to baseline levels and a placebo group (Pilz et al., 2011).
Zinc and Magnesium
Zinc and Mg supplementation have also been correlated to increased IGF-I levels and zinc specifically can increase serum Te concentrations. In trained football players, zinc and Mg supplementation improved muscle function along with the anabolic hormone profile after seven weeks of training (Brilla & Conte, 2000). In competitive triathletes supplementing with Mg for four weeks, they experienced greater work capacity along with decreased levels of cortisol before and after exhaustive exercise, indicating the improvement in efficiency compared to a control group (Golf, Bender & Grüttner, 1998).
In those attempting to decrease their amount of estrogen (men with lower Te: estrogen ratios, and women with excessive lower-extremity body fat accumulation), evidence is building in the efficacy of cruciferous vegetables to not only alter body composition but also reduce the risk of cancers associated with estrogen. The phytochemicals contained in broccoli, Brussels sprouts, cabbage, and cauliflower seem to favorably modify and balance the metabolism of estrogen. Diindolylmethane (DIM), the most potent inducer of estrogen metabolism, has been shown to reduce the risk of certain cancers (Zeligs, 1998). Supplementing with DIM may prove to be a viable strategy to reduce serum estrogen and its effects on fat distribution.
Exercise Strategies for Improvement
Within the first 10 minutes of a workout, growth hormone (GH) steadily increases; eventually peaking at the end of a workout, yet remains elevated above basal conditions for up to 2 hours. GH directly stimulates and increases lipolysis up to 3-fold in normal individuals once exercise begins, much from the effects of GH increasing free-fatty acid availability in the blood stream, while improving the oxidation of those fatty acids. The GH response to exercise is dependent on many variables including: age, gender, body composition, fitness level, and the type, duration, and intensity of training. Blood lactate levels, blood pH, and body temperature can all impact the GH response, with a proportional reduction in the GH response when exercising in cold conditions (Widdowson, Healy, Sönksen, & Gibney, 2009).
Running and other forms of aerobic exercise are popular choices for many people to engage in with the thought that aerobic exercise "burns fat." Lipolysis does increase with aerobic exercise due to moderate increases in catecholamine hormones (epinephrine and norepinephrine), but for optimal body composition, high-intensity anaerobic exercise greatly increases the catecholamine response. This response plays a significant role in lipolysis for both subcutaneous fat and intramuscular fat stores (Boutcher, 2011).
With any cardiovascular exercise program, it is imperative to include resistance-training exercises. Combining aerobic exercise with anaerobic-resistance exercise leads to greater total fat loss and greater increases in fat-free mass. In men, it preferentially decreases abdominal fat, and in women it preferentially decreases lower body fat when compared to aerobic exercise alone (Sanal, Ardic, & Kirac, 2013). If performing both resistance and endurance exercises on the same day, it is wise to perform the resistance exercise first because fat oxidation will be greatly enhanced in the subsequent endurance exercise due to an increase in plasma free-fatty acids, especially when performed with a small amount of rest between the exercise bouts (Goto, Ishii, Sugihara, Yoshioka, & Takamatsu, 2007).
In regard to resistance training, total Te and the free-Te: cortisol ratio is affected by exercise modes and the intensity of that exercise (Azarbayjani, Fatolahi, Rasaee, Peeri, & Babael, 2011). Manipulating the following variables has been shown to create optimal hormonal responses to training:
- Train large muscle groups early in the workout (i.e. deadlift, squats). Performing leg exercises prior to arm exercises increases transient levels of serum GH and Te, resulting in greater strength and muscle growth (Rønnestad, Nygaard, & Raastad, 2011).
- Use moderate to heavy resistance (75-95% of 1RM)
- Use multiple sets with moderate to high volume
- Use short rest periods
- Train the anaerobic glycolysis energy system to increase lactate and hydrogen ion concentrations
As training experience increases, the total hormonal response will also improve, likely due to higher intensity exercise (Kraemer, Vingren, & Spiering, 2008).
Discussion: The Miracle of Sleep
Sleep is probably the most underestimated and underutilized strategy to control body composition. The hormonal flux of the entire endocrine system is affected by the circadian sleep/wake cycle (Gómez-González et al., 2012). Over the past 40 years, the average self-reported sleep duration of Americans has declined by 1.5-2 hours to the point where many only sleep 5-6 hours per night. While this may not seem like much, it is interesting to note in those same 40 years America’s average BMI and chronic disease rates of obesity and Type II diabetes have also increased. Evidence continually demonstrates a link between reduced sleep duration and increases in BMI, insulin resistance, diabetes, obesity, and mortality rates (Spiegel, Knutson, Leproult, Tasali, & Van Cauter, 2005).
Elevated Interleukin-6 and C-reactive Protein
There are many explanations for this impact sleep has on overall health. Both acute and chronic sleep reduction or reduced sleep quality have been shown to create persistent over-secretion of inflammatory cytokines, which are messenger molecules of the immune system that communicate between different immune cells and tissues. Specifically interleukin-6 (IL-6) and C-reactive protein (CRP), biomarkers for low-grade inflammation, are significantly elevated in sleep-deprived states (Rohleder, Aringer, & Boentert, 2012). They are also markers for potential fat gain and muscle loss, and have been shown to be good indicators of disease severity which is directly related to impaired physical functioning in older adults with various diseases/conditions (Brinkley et al., 2012).
Reduced Leptin and Ghrelin
The opposing hormones that regulate appetite, leptin and ghrelin, also become altered with reduced sleep durations. Leptin is produced in adipocytes that signal satiety to the metabolism centers of the brain, and in children who lack adequate leptin secretions or have nonfunctional leptin receptors tend to also have a decreased secretion of GH and they rapidly become obese because their brain never receives the signal they are full (Roemmich, & Rogol, 1999). Ghrelin is a stomach peptide that influences food intake, promotes sleep, and contributes to energy balance and weight gain (Weikel, Wichniak, Ising, Brunner, Friess, Held, & Steiger, 2003). In individuals infused with ghrelin, increased appetite along with significantly greater food consumption occurred at a food buffet when compared to a control group (Wren, Seal, Cohen, Brynes, Frost, Murphy, & Bloom, 2001). In the Wisconsin Sleep Cohort Study, data from 1,024 volunteers revealed that short sleep duration (<8 hours) was proportional to increases in BMI. Blood tests taken upon wakening revealed those who experienced approximately 5 hours of sleep had 14.9% greater increases in ghrelin levels, and a 15.5% reduction in leptin concentrations which directly correlated to weight gain (Taheri, Ling, Austin, Young, & Mignot, 2004).
Sleep duration also negatively affects carbohydrate metabolism. Decreased sleep duration (<5 hr/nght) significantly reduces insulin sensitivity (Buxton et al., 2010; Donga et al., 2010; Klingenberg et al., 2013), and even partial sleep loss causes an elevation in evening cortisol levels, which can chronically alter metabolic and cognitive functions (Leproult, Copinschi, Buxton, & Van Cauter, 1997; Spiegel, Leproult, & Van Cauter, 1999; Yaggi, Araujo, McKinlay, 2006). Reduced insulin sensitivity, or insulin resistance, will force the body to release greater amounts of insulin to clear the necessary amount of glucose from the blood stream to remain in homeostatic ranges; yet increased insulin means greater fat storage. In a study performed on older adults, longer sleep durations not only help restore endocrine functions but also prevent abnormal increases in daily cortisol concentrations (Rueggeberg, Wrosch, & Miller, 2012).
Finally, the normal 24-hour flux of GH consistently spikes within 90 minutes of the onset of sleep. Although there is individual variability, most will notice an initial spike early in the sleep cycle, and then notice an additional spike toward the later stages of sleep close to wakefulness. If sleep is cut short, they will not get the benefit of the second, albeit smaller spike in GH, and if laying in bed with eyes closed but not asleep, one might actually never experience any spike in GH (Sassin, 1969).
All of these factors contribute to explaining why sleep duration is such a prominent risk factor for chronic disease, and why it plays such an important role in maintaining normal metabolic and cognitive functioning. Sleep deprivation causes increased systemic inflammation and cortisol levels throughout the day which signals increased stress on the body. A sleep-deprived individual is hungrier and likely to eat greater amounts due to the impact on serum leptin and ghrelin concentrations, and when they do eat their body is more insulin resistant; all of which contribute to increased fat accumulation. Learning how to engineer a good night’s sleep may have the biggest impact and may be the easiest strategy to implement when controlling body composition.
Nutrition and exercise strategies can be used to improve the sex-steroid hormones and GH, all of which contribute to mobilizing and oxidizing greater amounts of fat to favorably change body composition. Additionally, a lifestyle strategy of increasing nightly sleep duration is a simple, practical way to improve long-term health by lowering the stress response on the body while regulating the normal circadian rhythm of the endocrine system.
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