Opening Comments

Today I want to talk about growth hormone. From what I’ve gathered over the past couple of weeks, there seems to be a prevailing notion that eating carbohydrates at night will somehow prevent natural growth hormone release from occurring and therefore hinder muscle protein synthesis. This is presumably due to carbohydrates causing insulin to be raised and therefore causing growth hormone to be inhibited. As some of you may already be aware, growth hormone secretion is at its maximum during sleep. It makes sense to want to maximize your natural hormonal milieus in order to promote anabolism.  However, what proponents of this misconstrued theory choose to forget – or just flat out don’t know – is that insulin, too, is anabolic. Nonetheless, for argument’s sake, I will solely focus on growth hormone and how a carbohydrate meal at night might – potentially (never?) – lead to less muscle protein synthesis.

For starters, it is true that when insulin is elevated (via ingested carbohydrate), growth hormone is inhibited and therefore low in concentration. However, this hardly deserves much attention given the numerous other factors that go into muscle hypertrophy. Nevertheless, some still translate this single piece of information into meaning that growth hormone will somehow be blunted to the point of no release and therefore inhibiting muscle protein synthesis altogether. This is just plain ridiculous and completely misleading, not to mention that there is not ONE study which even slightly suggests this. Nevertheless, in lieu of today’s topic, I’ll start by describing some of the physiology behind growth hormone and it’s functions and then follow it up with some research studies that will put everything into perspective (hopefully). However, before we begin, be warned, today’s article will be quite lengthy and somewhat sciency.

Growth Hormone Secretion  

Growth hormone (GH) is a peptide hormone secreted from the anterior pituitary of the brain. GH is secreted throughout life but is most important during childhood wherein peak concentrations are the highest they will ever be [1]. For the purposes of today’s article, we will just discuss GH as it pertains to muscle growth and hypertrophy.

In skeletal muscle, GH promotes a positive protein balance by increasing muscle protein uptake/synthesis and by potentially preventing muscle protein breakdown [2]. There are various stimuli which affect the release and inhibition of GH, namely nutrients (such as carbs, protein, and fats), age, stress (exercise), gender, circadian rhythm, and the presence of other, counter-regulatory hormones such as insulin [1, 3]. To say that the regulation of GH is simple is a complete understatement. In fact, the interplay between exercise, diet and GH regulation is not fully understood [3]. It is at this point that I want to discuss what controls GH secretion and inhibition and the relative impacts of the various macronutrients on GH regulation. After all, that’s what you came for, right?

Growth Hormone Regulation

GH is primarily acted on by growth hormone-releasing hormone (GHRH) – aptly named – which signals GH to be released into circulation. In opposition to GHRH is another hormone called somatostatin (SS) which inhibits GHRH and therefore prevents GH to be secreted. Throughout the day both GHRH and SS control the release and inhibition of GH and inevitably dictate the overall magnitude of GH release [3]. This manner of release and inhibition is often termed a pulsatile pattern wherein the largest release happens within the first two hours of sleep (see below). This is thought to be prime time for anabolism.

Like many biochemical and physiological mechanisms GH, too, has feedback inhibition. This simply means that the products of a pathway also turn that pathway off once sufficient levels of product are made. The inhibitory products for GH include, glucose, free fatty acids, IGF-1 and potentially GH itself [3].

IGF-1 (insulin-like growth factor-1) is stimulated when GH is released and acts on the liver and muscle tissue. This causes insulin-like growth factor-1 to be released into circulation where it can act of various tissues such as muscle. It is through IGF-1 that GH indirectly mediates some its anabolic effects. Therefore, it may not be GH per se that causes muscle protein synthesis, but rather IGF-1. However, to date, there is still some controversy as to which one is the primary stimulator of muscle protein synthesis. Nevertheless, as I already mentioned, IGF-1 causes GH to stop being secreted once sufficient levels of IGF-1 have been made. The same applies for glucose and free fatty acids which are also products of GH release. During exercise, GH optimizes the body’s fuel sources by decreasing tissue glucose uptake, stimulating lipolysis, and increasing gluconeogenesis [4]. This makes sure that blood glucose levels are preserved during exercise.

An important thing to keep in mind when talking about GH release and inhibition is that SS causes GH secretion to be inhibited BUT does not cause GH to stop being produced. Therefore, even though GH may not be released into circulation, the pituitary gland is still synthesizing more GH which will inevitably be released once the inhibition is removed. This concept is very important because there seems to be a ‘rebound’ effect for GH secretion after the inhibition is taken away [5].

Therefore the real question is whether or not the initial inhibition presented by a carbohydrate meal will actually reduce the amount of total GH secreted over the course of the day. If this ‘rebound’ effect holds true than GH will just be secreted in higher levels than it would have originally been and therefore reaching its daily quota, so to speak. To my knowledge, there are no studies which directly look at this theory in respect to a nighttime carbohydrate meal and subsequent levels of GH over the course of the night. Moreover, there also needs to be evidence that shows that muscle protein synthesis is somehow reduced because of this inhibition. Because a study like this does not exist, not only is the original argument completely speculative, but it is also founded on very little fact. Nevertheless, let us take a look at some effects of food on GH after a meal and see if we can’t postulate some conclusions about diet and GH.

Post-prandial GH Response to Feeding

Carbohydrates

It has been shown multiple times that an oral glucose tolerance test results in reduced levels of GH [6-9]. Furthermore, another study demonstrated that carbohydrate alone or in conjunction with protein also caused GH levels to be decreased [10]. However, this study was done in a group of sedentary diabetics who may not serve as the best example for what might occur in a non-sedentary, athletic population. Furthermore, it has also been shown that hypoglycemia is a potent stimulator of GH [7, 11].  Although interesting, this is virtually irrelevant given that hypoglycemia is not something likely to occur in most athletes/bodybuilders who consume anywhere from 4-6 meals a day. Nevertheless, as insulin levels tend to go down, GH levels tend to increase [12].

Protein

Next we will consider protein, and more specifically amino acids. Amino acids have come under scrutiny for their potential to increase levels of GH. Although certain amino acids (arginine, ornithine, lysine) taken orally and intravenously in gram doses have been shown to increase levels of GH in sedentary participants, this is not the case in bodybuilders and those who consume high protein diets [13]. Sorry guys.

Fat

In 1993, Cappon et al. wanted to test the effects of a high fat drink consumed 45 minutes before a 10 minute bout of intense exercise on subsequent GH levels [14]. Researchers found that, compared to a non-caloric placebo, GH was reduced by 54% and blood concentrations of SS were significantly elevated. The authors postulated a potential link between fat and somatostatin (SS). In fact, in a separate study done a few years earlier, a group of researchers found that both a mixed meal and a fat-rich meal had the greatest effects on elevating SS levels with carbohydrate having the least effects [15].

Conclusions?

Obviously keeping SS low and GH high would be the best case scenario in terms of body composition; however, as is life, things are not that simple. The relative impact and relevance of the aforementioned studies on body composition are essentially worthless and at best speculative. They are acute studies which tell us nothing about long-term effects of diet on hormonal responses. Not to mention many of these studies were done with macronutrients in isolation; a situation not relevant to normal eating behaviors to begin with. Finally, there was no direct measurement of lean body mass in any of the studies. Therefore they really tell us little about the potential effects of food on GH in relation to body composition. So where do we go from here?

Well, it just so happens that there is one study which comes close to answering the question at hand, although not entirely. Nevertheless, it draws upon some of the themes I’ve already laid out so far, so let’s see if we can’t inch one step closer to a definitive answer and drive a nail into this coffin.

Effects of Heavy Weightlifting on GH Release at Night

A study done in 2001 looked the effects of heavy resistance exercise on the pulsatile released of GH in humans [16]. At that point, it was well established that exercise was a potent stimulator of GH; however, it was not fully understood on how resistance exercise affected GH throughout the rest of the day, specifically during the nighttime. What the researchers found, contrary to their original hypothesis, was that heavy resistance exercise – completed in the afternoon – actually decreased overnight maximum GH concentrations (see below).

In spite of this overall reduction in maximal GH concentration, they saw that total GH concentration by the end of the night was not significantly reduced when compared to the control. AHA! To put it another way, GH was lower during the first half of sleep (perhaps what might happen if one ate a carbohydrate meal) but remained elevated during the second half of sleep to maintain normal GH concentrations (think about the ‘rebound’ effect I mentioned earlier). As you can see, when faced with lower than normal secretion patterns, most likely due to SS inhibition, GH was released at higher concentrations during the rest of the night in order to meet its ‘quota.’ As I mentioned earlier SS does not affect GH synthesis, only release. In fact, the researchers postulated that the temporal changes in GH over the course of the night were possibly due to the ‘rebound effect’ of SS on GH secretion.

So, if you got nothing from what I just stated, remember this: it appears that GH release has some form of homeostatic mechanism which maintains a certain quota for GH concentrations over the course of the day. Therefore, when something like exercise interacts and alters the normal release pattern of GH, the brain is smart enough to save it and release it later when the inhibition is gone. This presumably keeps GH concentrations unchanged over a 24-hr period. My guess is that this is also true for something as trivial as a carbohydrate meal consumed at night wherein GH might be slightly inhibited by the time you fall asleep. This is probably not something to get worried about at all.

Unfortunately, this study provides very little insight into what would happen with chronic patterns of nightly carbohydrates. What it does do, however, is provide evidence for the ‘rebound’ effect postulated earlier, which seems to be a good model for maintaining normal levels of GH over a 24-hr period. Obviously more studies are needed, especially ones that pertain to nutrition. This also brings me to something I should have mentioned earlier. Had this topic of carbs and GH been such a revelation in the field nutritional science, don’t you think more studies would have been done on it? Usually scientific interest is a good indicator of the importance of a given nutritional topic. Just some food for thought.

Rapid Suppression of GH from Overeating

There is one more study which I would like to cover, and it has to deal with the possibility of GH being completely suppressed by food intake. Obviously this is what nighttime Carbophobics are worried about, so it makes sense to look at the closest study I could find that mimics this question. In a recent study done in 2011, researchers looked to see if GH secretion could be significantly suppressed by the act of overeating [17]. There were essentially three phases of the study; baseline, 3 days post-overeating, and 2 weeks post-overeating. During the entire study period following baseline, researchers had participants consume ~175% of their daily caloric needs while limiting their daily activity to 1500 steps per day (not very active). At baseline GH levels were essentially normal. By day 3, GH levels had significantly dropped by ~80% wherein they remained relatively unchanged during the remaining 2-week period (see below).

Obviously these conditions are not relevant to normal consumption patterns, even among those who are bulking. However, as you can see, GH can be suppressed, although this relates little to our argument because I doubt a single carbohydrate meal at night will reproduce anything like what was seen during this study, even under chronic conditions of nighttime carb meals.

Nevertheless, the question remains; will this negatively affect gains in lean body mass? Well, here’s the kicker! Even with GH being suppressed by up to 80%, participants actually increased their lean body mass (~2lb increase)! Let me repeat that; they actually increased their lean body mass. Now, I will admit that it wasn’t statistically significant, although it was bordering significant, and that the LBM gains could have been tissue other than skeletal muscle. Nonetheless, the fact still remains that protein synthesis wasn’t completely inhibited, even in the face of dramatically low GH levels and almost complete inactivity. Would greater gains in LBM have been seen if GH wasn’t reduced as much? Would activity have nullified the results and attenuated the drop in GH levels? Who knows? The key thing to keep in mind is that muscle protein synthesis is a complex system that involves multiple players. Singling out two factors amongst a host of others is flat out ridiculous.

Concluding Remarks

The fact of the matter is that those who fear carbs at night are basing their fear off of one piece of information that holds little scientific backing. Hopefully by now I’ve convinced you that GH regulation is a complex system with many factors that each plays a role. To say that carbs at night will reduce the capacity to build muscle is completely ludacris and unfounded – that is unless that meal is part of a diet which comprises 175% of your daily needs. So, in the end, there is no scientific evidence whatsoever to suggest that carbs consumed at night will reduce one’s goal of gaining muscle, and I doubt there ever will be. The main thing to keep in mind is that there is much more to building muscle than splitting-hairs. The people who care the most about this stuff are the ones who should care the least, and those who capitulate to stupid misinformation like that are worse off than they were when they knew nothing at all. If you learned nothing, remember this:

Lift heavy, eat right, rest up, and most importantly don’t concern yourself with trivial aspects of dieting that are at best speculative and at worst completely false. Dichotomous thinking never did anyone any good. Ever.

References

1. Silverthorn DU. Endocrine control of growth and metabolism. In: Human physiology: an integrated approach, 5^th ed. Pearson Education, Inc.: San Francisco, CA, 2010.

2. Rooyackers OE, Nair KS. Hormonal regulation of human muscle protein metabolism. Annu Rev Nutr. 1997;17:457-85.

3. Kraemer WJ, Nindl BC, Gordon SE. Resistance exercise: acute and chronic changes in growth hormone concentrations. In: The endocrine system in sports and exercise. Blackwell Publishing: Malden, MA, 2005.

4. McArdle WD, Katch FI, Katch VL. The endocrine system: organization and acute and chronic responses to exercise. In: Exercise physiology: energy, nutrition, and human performance, 6^th ed. Lippincott, Williams and Wilkins: Baltimore, MD, 2007.

5. Giustina A, Veldhuis JD. Pathophysiology and neuroregulation of growth hormone secretion in experimental animals and the human. Endocrine Reviews 1998;19(6):717-797.

6. Bernardi F, Petraglia F, Seppala M, et al. GH, IGFBP-1, and IGFBP-3 response to oral glucose tolerance test in perimenopausal women: no influence of body mass index. Maturitas 1999;33:163-179.

7. Frystyk J, Grofte T, Skjaerbaek C, Orskov H. The effect of oral glucose on serum free insulin-like growth factor-I and –II in healthy adults. J Clin Endocrinol Metab. 1997;82:3124-3127.

8. Hjalmarsen A, Aasebo U, Aakvaag A, Jorde R. Sex hormone responses in healthy men and male patients with chronic obstructive pulmonary disease during an oral glucose load. Scand J Clin Lab Invest. 1996;56:635-640.

9. Nakagawa E, Nagaya N, Okumura H, et al. Hyperglycaemia suppresses the secretion of ghrelin, a novel growth hormone-releasing peptide: responses to the intravenous and oral administration of glucose. Clin Science 2002;103:325-328.

10. van Loon LJ, Saris WH, Verhagen H, Wagenmakers AJ. Plasma insulin responses after ingestion of different amino acid or protein mixtures with carbohydrates. Am J Clin Nutr. 2000;72:96-105.

11. Roth et al. 1963.

12. Volek JS, Sharman MJ. Diet and hormonal responses: potential impact on body composition. In: The endocrine system in sports and exercise. Blackwell Publishing: Malden, MA, 2005.

13. Chromiak JA, Antonio J. Use of amino acids as growth hormone-releasing agents by athletes. Nutrition 2002;18:657-661.

14. Cappon JP, Ipp E, Brasel JA, Cooper DM. Acute effects of high-fat and high-glucose meals on the growth hormone response to exercise. J Clin Endocrinol Metab. 1993;76-1418-1422.

15. Ensinck JW, Vogel RE, Laschansky EC, Francis BH. Effect of ingested carbohydrate, fat, and protein on the release of somatostatin-28 in humans. Gastroenterology 1990;98(3):633-638.

16. Nindl BC, Hymer WC, Deaver DR, Kraemer WJ. Growth hormone pulsatility profile characteristics following acute heavy resistance exercise. J Appl Physiol. 2001;91:163-172.

17. Cornford AS, Barkan AL, Horowitz JF. Rapid suppression of growth hormone concentration by overeating: potential mediation by hyperinsulinemia. J Clin Endocrinol Metab. 2011;96(3):824-830.