Big Gut Dilemma - Is Insulin to Blame?

HE said it. Finally, someone who cannot be ignored pointed HIS finger at the “600-pound gorilla in the room.” Bodybuilding went from being a pursuit of the physical ideal to a lemming-like plunge toward the most extreme pursuit of mass for the sake of mass. Who is HE? Arnold Schwarzenegger, THE MAN whose physique and personality launched bodybuilding from a niche, California-weird, fringe culture to exemplar of the mainstream male physical ideal. What did HE say? At a symposium held during the 2015 Arnold Classic, while discussing HIS displeasure with the 20-year-plus physique trend among bodybuilders, Arnold stated too many of today’s professional competitors have “bottled-shaped bodies” rather than V-shaped ones, caused by the competitors’ bellies: “Stomachs sticking out … it doesn’t look right anymore.”¹

The cause of a swollen belly has long been attributed to growth hormone excess, which can cause distension by inducing insulin resistance, organomegaly (enlargement of the intestines and other organs) and edema (fluid retention).² However, it appears that too much of the blame has been placed on growth hormone. Around the same time, professional bodybuilders also began experimenting with insulin to promote mass gains. Though growth hormone and insulin are antagonists in the “real world” of human physiology, both contribute to significant mass gains when misused/abused in supraphysiologic amounts. Though growth hormone was noted to provide “next level” mass gains when dosed around three to seven times the therapeutic adult dose, it was inevitably associated with numerous side effects. Replacement doses are effective for soft tissue repair and fat loss.³ Little additional strength gain is noted with growth hormone misuse, despite the size increase.

Insulin also provides “next level” gains in mass, and notably strength gains as well that surpass those experienced with growth hormone doping. Insulin requires a disciplined diet and consistent monitoring to ensure that the gains are not fat, as fat mass is more prone than muscle to increase under the influence of elevated insulin. Further, there are serious consequences that can occur from insulin misuse. Every year, emergency rooms frequently deal with individuals who failed to eat properly, misdosed their prescribed insulin or perhaps had an interaction with another drug, resulting in severe hypoglycemia. This does not sound threatening, but without intervention, this can lead to coma and even death.⁴

Raw Mass, Not Quality Muscle

How does insulin contribute to what has been known as “GH belly” in bodybuilders? Is there any proof it happens? Of course, there has not be a randomized, double-blind, placebo-controlled trial approved by an institutional review board; nor will there ever be. Yet, would the word of another Mr. Olympia legend add credence to the hypothetical association?

In an interview published in Muscular Development, six-time Mr. Olympia Dorian Yates noted his experience with growth hormone and insulin, commenting that whereas growth hormone (8 IU/day) did have a positive effect on his size and condition, insofar as insulin was concerned, “I got bigger than ever, but it wasn’t quality muscle, and my midsection was distended.” In fact, Yates only used insulin one year during the off-season. He further stated, “For me, insulin had a negative overall impact on my physique. It kept me from getting into my usual condition that I prided myself on. Raw mass is not the same thing as quality muscle tissue. I got a bit bigger, but at the expense of my separation, crispness and clear muscle separations. I see that same lack of separation constantly today with the guys, as well as the distended abs.”

Despite the cacophony of disrespect for “broscience” from the wonder boys of academia, there is great relevance and value in the observations of these men. Such “reports from the field” offer insights that more often than not raise questions, but also offer guidance as to the correct direction to explore in the scientific literature. Note, Yates reports that the appearance of today’s competitors is similar to what he experienced while experimenting with insulin.

Insulin’s Double Whammy

This is going to be a deep-end splash into physiology, so hold your hat and look for the general concepts. First, insulin increases adipocyte lipogenesis— basically, fat storage in the fat cell. This is particularly unhealthy in the intra-abdominal fat depots where much of the growth is due to adipocyte hypertrophy.⁵ Further, in the overfed state, cortisol (the “stress” hormone) increases the growth of individual fat cells and increases the rate of lipogenesis from insulin’s signal.⁶ Though testosterone replacement may produce smaller, healthier visceral fat cells in older men with low testosterone, excessively high testosterone may increase adipocyte hypertrophy— bigger but unhealthy fat cells that release harmful hormone-like signals.⁷ In part, this happens because testosterone increases the enzyme that activates cortisol in fat cells.⁸ Also, hypertrophic adipocytes have a higher aromatase activity that converts testosterone to estradiol in the cell, further promoting fat storage.⁹ Insulin resistance is harmful to the overall metabolism, but fat cells and muscle cells that are overloaded with stored fat make cellular modifications to become less sensitive to insulin as a “last resort” act of self-preservation.

So, not only fat cells become more resistant to insulin, but also muscle cells. The increase in cellular energy (ATP/AMP ratio) turns on the anabolic pathway of mTOR and suppresses the metabolically beneficial AMPK pathways.¹⁰ Further, stored fat inside the muscle cells increases just as it does in fat cells. Though this is beneficial if it is a response to chronic aerobic conditioning, where the stored fat is there to be used instead of deposited as overflow from overburdened fat cells, it reduces the activity of insulin in muscle cells.¹¹ Thus, the muscle cell is less efficient. Eventually it becomes less efficient at increasing muscle protein synthesis in response to insulin, similar to aging.¹²

Not only does stored fat interfere with muscle insulin signaling, but also with circulating fat (free fatty acids). Though it has not been studied, the conglomerate of drugs used by professional bodybuilders (e.g., growth hormone, thyroid hormone, clenbuterol, etc.) results in a near-continuous release of free fatty acids. This has been shown to reduce muscle response to insulin.¹³ Competitors seeking continued gains may unwisely increase the insulin dose— increasing not only fat mass, but also the risk of side effects. Lastly, insulin promotes the accumulation of a class of lipids called ceramides in muscle cells by increasing the rate of production of these signaling molecules.¹⁴ The types of ceramides that accumulate in insulin-resistant muscle cells are associated with abdominal obesity and insulin resistance, though they have not been shown to damage muscle function.¹⁵

Water Retention

One final matter to consider with insulin’s effect on appearance is water retention. Perhaps the experience of a puffy face and doughy skin after a three-day buffet binge or just a heavy Thanksgiving meal is familiar to many? Insulin acts on the kidneys, promoting water and sodium retention, among other effects.¹⁶ Edema (water retention) is common among diabetics using prescribed doses of insulin on restricted diets, so one can only imagine the greater effect among bodybuilders using supraphysiologic doses while consuming the number of calories required to maintain the mass and growth they display. Typical to the sport, the response of the bodybuilder is more drugs to treat this side effect— primarily diuretics during the pre-contest preparation. Some might attempt a low-carbohydrate diet, but this increases the vulnerability to hypoglycemia, shock and organ damage.

Bigger Not Always Better

There is little question that insulin has fueled much of the mass differential in modern-day bodybuilders. However, as voiced by Mr. Olympia legends Arnold Schwarzenegger and Dorian Yates, bigger has not resulted in better. Some of the abdominal distension seen is likely due to growth hormone abuse. However, the role of insulin has been underappreciated, adding to the “bottle-shaped bodies” that provoked a comment from Arnold. The professional places himself at great risk by abusing insulin for size gains. However, the greater fear is that impressionable young men are following their lead with little understanding. Further, the anabolic effect of insulin comes at the cost of greater insulin resistance, and edema. Too often, this leads to additional drug seeking to counter these effects, with a greater risk of an adverse drug interaction.

Insulin has not added to the appeal of the sport or the health of its competitors. It is dangerous, even deadly in untrained hands. The only hope is that judging will begin to penalize competitors for failing to develop an aesthetic, as well as muscular, physique.

References:

1. Schwarzenegger A. Arnold Schwarzenegger criticizes today’s bodybuilding - Arnold Classic 2015. https://www.youtube.com/watch?v=pnpt7han0SE, accessed April 7, 2015.

2. Scacchi M, Cavagnini F. Acromegaly. Pituitary 2006;9:297-303.

3. Doessing S, Heinemeier KM, et al. Growth hormone stimulates the collagen synthesis in human tendon and skeletal muscle without affecting myofibrillar protein synthesis. J Physiol 2010;588:341-51.

4. Prescrire Editorial Staff. Insulin use: preventable errors. Prescrire Int 2014;23:14-7.

5. Rydén M, Andersson DP, et al. Adipose tissue and metabolic alterations: regional differences in fat cell size and number matter, but differently: a cross-sectional study. J Clin Endocrinol Metab 2014;99:E1870-6.

6. Gathercole LL, Morgan SA, et al. Regulation of lipogenesis by glucocorticoids and insulin in human adipose tissue. PLoS One 2011;6:e26223. doi: 10.1371/journal.pone.0026223.

7. Abdelhamed A, Hisasue S, et al. Testosterone replacement alters the cell size in visceral fat but not in subcutaneous fat in hypogonadal aged male rats as a late-onset hypogonadism animal model. Res Rep Urol 2015;7:35-40.

8. Zhu L, Hou M, et al. Testosterone stimulates adipose tissue 11beta-hydroxysteroid dehydrogenase type 1 expression in a depot-specific manner in children. J Clin Endocrinol Metab 2010;95:3300-8.

9. Williams G. Aromatase up-regulation, insulin and raised intracellular oestrogens in men, induce adiposity, metabolic syndrome and prostate disease, via aberrant ER-α and GPER signalling. Mol Cell Endocrinol 2012;351:269-78.

10. Mounier R, Lantier L, et al. Antagonistic control of muscle cell size by AMPK and mTORC1. Cell Cycle 2011;10:2640-6.

11. Timmers S, Schrauwen P, et al. Muscular diacylglycerol metabolism and insulin resistance. Physiol Behav 2008;94:242-51.

12. Fujita S, Glynn EL, et al. Supraphysiological hyperinsulinaemia is necessary to stimulate skeletal muscle protein anabolism in older adults: evidence of a true age-related insulin resistance of muscle protein metabolism. Diabetologia 2009;52:1889-98.

13. Kolka CM, Richey JM, et al. Lipid-induced insulin resistance does not impair insulin access to skeletal muscle. Am J Physiol Endocrinol Metab 2015 Apr 7. [Epub, ahead of print]

14. Hansen ME, Tippetts TS, et al. Insulin increases ceramide synthesis in skeletal muscle. J Diabetes Res. 2014;2014:765784(9 pp). doi: 10.1155/2014/765784.

15. De la Maza MP, Rodriguez JM, et al. Skeletal muscle ceramide species in men with abdominal obesity. J Nutr Health Aging 2015;19:389-96.

DISCUSS THIS ARTICLE ON THE MD FORUM

FOLLOW MUSCULAR DEVELOPMENT ON:

FACEBOOK: MuscularDevelopment Magazine

TWITTER: @MuscularDevelop

INSTAGRAM: @MuscularDevelopment

YOUTUBE: http://bit.ly/2fvHgnZ