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About Kevin Murnane

I am a cognitive scientist, a freelance writer and author (Nutrition for Cyclists: Eating and Drinking Before, During and After the Ride), a musician (Parametric Monkey - stream on Spotify, Soundcloud and YouTube), a bookstore owner (Monkey Books - first edition mystery, science fiction, fantasy and more, listed on ABE books, Amazon and Biblio), and a retired house painter, children's theater actor & owner, and university professor. I'm also a regular contributor to the technology section at Forbes and I write a cycling blog called Tuned In To Cycling. You can follow me on twitter @TheInfoMonkey and contact me at murnane.kevin@gmail.com.

Human Growth Hormone and Cycling

This post is mainly oriented toward the cyclist who is concerned with taking Human growth hormone (HGH) or so-called “HGH releasers” orally as a dietary supplement.  Intravenous injection of HGH  is a much more serious and much more expensive proposition and deserves a more detailed analysis than the one that will be given here.

HGH has been offered as something like a universal miracle drug for everything from building muscle mass and recovery from exercise to enhancing virility, curing depression and combating the effects of aging.  One of the ideas that is promoted by the HGH industry is that there is a two hour period after exercise, which is sometimes referred to as a “synergy window”, when consumption of  foods that are high in glucose or carbohydrates disrupts the release of HGH by the body and hence should be avoided because of all of the benefits claimed for HGH. A comment on our Eating After the Ride post  pointed out that the advice to consume a fairly large amount of carbohydrate in the first 30 to 40 minutes after exercise that is given in Eating After the Ride is in direct conflict with the recommendation to avoid carbohydrates during the Synergy Window.

Is this an important conflict that cyclists should take into account?  What can be said about the “synergy window” based on reputable research?  Are the claims made about the benefits of HGH accurate and reliable?  Should cyclists be concerned with HGH?

It is important to keep in mind that – like virtually every issue in the field of nutrition for athletes – knowledge about HGH that is based on well-designed and carefully carried out scientific research is a story in progress.  Much remains to be discovered about how chemical information carriers (i.e, hormones and neurotransmitters) affect function, how the human body processes nutrients and macronutrients (like carbs, fats and proteins), and how all of this affects exercise and athletic performance.

That being said, the HGH industry is a cesspool of outright fraud, ignorance, scams and ridiculous claims based on no scientific evidence whatsoever.  The problem isn’t that scientifically well-supported information about HGH is hard to come by; 20 minutes, google, and an open mind are about all it takes to at least raise the suspicion that many of the claims made about HGH on numerous websites and blogs are complete nonsense.  The problem is that too many people are making too much money selling quack nostrums to gullible people who are ignorant of the science involved and who aren’t willing to spend the time or effort to look beyond what the hucksters are pitching at them.

What about the concern that ingesting carbohydrates will interfere with the two hour HGH “synergy window”?

If, at the time of this writing, you google “synergy window” and “HGH”, you get several pages of hits from many, many websites and blogs that all reproduce the same text.  Many of these pages are headed “Two foods you should never eat after exercise”.  The text copied on all of these websites and blogs claims, among some other things, that sugars (i.e., carbohydrates) must be avoided during the two hour synergy window in order to reap the supposed benefits of increased  HGH production after exercise. This advice is accompanied by a citation to a well-designed and well-executed research study and gives the impression that the research study supports the claims being made about HGH, the “synergy window” and avoiding carbohydrates in the form of sugars after exercise.

The research cited in the “synergy window” blurb was carried out by S.A. Newsom and colleagues and appeared in the March 2010 Journal of Applied Physiology.  You can read it for yourself here.  The study contains research that may be of interest to cyclists and is described in detail in Eating After the Ride Part 2.

Our question here is how much support does the cited research give to the claims being made about HGH, the “synergy window” and avoiding carbohydrates after exercise?

The answer is – none whatsoever.

The Newsom study has nothing at all to do with HGH.  The investigators are interested in the consequences of replacing calories lost during exercise by ingesting either fats or carbohydrates after exercise.  They don’t consider, or even mention, HGH.

What about a two hour window after exercise?  In the study, participants ate meals with carefully controlled amounts of fats and carbohydrates 30 minutes, 5 hours and 10 hours after exercise.  Nothing was manipulated nor measured at a two hour interval.  Nothing can be concluded from this study about the consequences of eating or not eating carbs, fats, proteins or anything else during the two hours after exercise because the study doesn’t have anything to do with a two hour post exercise period.

In short, while the Newsom research contains much of interest to people who are engaged in regular exercise, it provides no support whatsoever for the claims about HGH, the so-called “synergy window”, or the advice to avoid carbs after exercise that appear on all of the websites and blogs that cite the research. The people who are posting this “synergy window” nonsense all over the internet either didn’t read the research paper they cite, read it and didn’t understand it, or read it, understood it and are making fraudulent claims based on it with the expectation that their readers won’t bother to check their source.

The websites telling you not to consume carbs after exercise because it will interfere with HGH have nothing  to offer in the way of scientific evidence to support their stories.  Does HGH provide some other benefits for cyclists? Or any other basically healthy person for that matter?

The first thing to keep in mind is that for HGH to have any effect at all, it must be taken intravenously. HGH is a peptide and peptides are broken down by gastric acid in the digestive tract which means that taking HGH orally is pointless.  It is most likely to be destroyed before it enters the bloodstream.  This is fairly elementary biochemistry and you would expect people who are recommending and selling dietary supplements to know it.  The HGH mongers apparently didn’t, however, and at first they were hawking HGH as a dietary supplement.  Now they are hawking “HGH releasers” which aren’t HGH but are supposed to trigger the release of HGH by the body.  What they are in fact selling are branched-chain amino acids which account for approximately 35% of the amino acids found in muscle proteins.  You can get a roughly equivalent amount of branched chain amino acids as are present in high-priced “HGH releasers” by eating a piece of steak.  There is no credible evidence that these so called “HGH releasers” have any of the beneficial effects claimed for them.  If you are taking HGH or an “HGH releaser” orally as a dietary suplement, you are throwing your money away on a scam.

When pressed for evidence by fraud litigation or by consumers who want evidence rather than unsubstantiated advertising claims before they take dietary supplements, the HGH industry has consistently pointed to a study published by D. Rudman and colleagues entitled “Effects of Human Growth Hormone in Men over 60 Years Old” in the New England Journal of Medicine (NEJM) in 1990.  You can read the Rudman study for yourself here.

What Rudman et. al found was that a six month program of  high-dose intravenous injections of HGH reduced the percentage of body fat and increased the percentage of lean muscle mass and bone density in a group of men aged 61 to 81. This study has been so widely misunderstood, misinterpreted or used in support of outright fraudulent claims about HGH that the editors of the New England Journal of Medicine took the highly unusual step of attaching editorials written by Dr. Mary Lee Vance (who was the editor of NEJM when the Rudman study was originally published) and Dr. Jeffrey M. Drazen (who was the editor when the decision to add the attachments was made) that pointed out that the research reported in the Rudman article does not providence evidence to support the claims about the benefits of HGH or “HGH releasers”  made by the people in the HGH industry who cite the study as scientific support for their products.  You can read Dr. Vance’s editorial here, and Dr. Drazen’s editorial here.

Subsequent research published in the Journal of the American Medical Association (an Abstract can be found here) that has followed up on the Rudman study and which is cited in the Vance editorial has replicated Rudman’s results with regard to HGH producing a decrease in body fat and an increase in lean muscle mass.  While the Rudman study did not examine differences in muscle function as a consequence of HGH treatment the follow up study did and what was found is of great interest to cyclists who are considering taking HGH.  The increase in lean muscle mass was not accompanied by any increase in either strength or endurance (as measured by maximal oxygen uptake, i.e., VO(2)max) in women.  Strength increased slightly and VO(2)max increased in men but only if the HGH treatment was accompanied by testosterone injections.   HGH without testosterone produced increases in lean muscle mass but no increases in either strength or endurance.  Negative side effects, primarily diabetes and glucose intolerance, were frequent in both men and women who were administered HGH.

These results may sound encouraging for some body builders for whom the increase in muscle mass combined with a decrease in body fat (which makes the musculature easier to see) may contribute to the goal of displaying muscle development.  Body builders are essentially developing muscles to serve as decoration or ornament.  Their competition does not involve using muscle strength in any way and so the lack of increase in strength or endurance accompanied by the increase in muscle mass that is produced by HGH alone would not hurt them when they compete.  For athletes who are interesting in building stronger muscles as opposed to bigger muscles the story is entirely different.  For the cyclist, increased muscle mass that is not accompanied by an increase in strength or endurance is simply dead weight that has to be carried uphill.

So, what’s the story on HGH for cyclists?

HGH or “HGH releasers” taken as orally administered dietary supplements are scams.  There is no credible scientific evidence that these products have any of the benefits that are claimed for them.

Intravenous injection of HGH increases lean muscle mass without an increase in either endurance or strength.  It adds weight without improving function which is something every cyclist wants to avoid.

HGH injections that are accompanied by testosterone injections increase endurance and marginally increase strength in men.  While the increase in VO(2)max may be of value to competitive cyclists, the HGH injections have serious negative consequences such as the development of diabetes and glucose intolerance (which will more than offset the competitive benefits gained through HGH use).  HGH is also banned as a performance enhancing drug.  Patrick Sinkewitz tested positive for HGH and was the first rider banned from the pro peloton for HGH use.

For professional cyclists there is a temptation to inject HGH and hope to avoid a positive drug test.  For the non-professional cyclist there is no reason whatsoever to take HGH and many reasons to avoid it.

For cyclists, HGH is an epic fail

Eating After the Ride Part 2

A streamlined version of the information presented in this post can be found in Nutrition for Cyclists: Eating and Drinking Before, During and After the Ride which can be purchased on Amazon.com.  For information about the book and how it relates to what I’ve posted to Tuned In To Cycling, please check out this post.

A comment on our Eating After the Ride post raised the question of whether the recommendation to consume one half gram of carbohydrate for each pound of body weight during the 30 minutes after you finish a bike ride is contradicted by recommendations to avoid all carbohydrates immediately after exercise because carbs supposedly disrupt a two hour “synergy window” during which the release of human growth hormone (HGH) by the body is claimed to produce a wide range of miraculous effects.  The HGH industry is a cesspool of fraud, ignorance, scams and ridiculous claims that are completely unsupported by scientific research (more on this can be found in Human Growth Hormone and Cycling).

One piece of HGH-related nonsense about the so-called “synergy window” that has been copied and reproduced on many, many websites and blogs cites a study published in the Journal of Applied Physiology as evidence in support of its claims.  The research that is cited has nothing whatsoever to do with HGH or a two-hour post exercise window but it is relevant to concerns of cyclists who are concerned with what to eat after a ride.

The study was carried out by S.A. Newsom and colleagues. It is titled “Energy deficit after exercise augments lipid mobilization but does not contribute to the exercise-induced increase in insulin sensitivity” and you can read it for yourself here.  The investigators were interested in the consequences of replacing the energy stores burned during exercise with either fats or carbohydrates.  They carried out a carefully controlled study that involved different groups of experimental subjects engaging in a period of controlled exercise followed by the ingestion of carefully controlled meals and snacks for the rest of the day.  The investigators varied whether energy stores were replaced by carbs or fats and measured insulin sensitivity (an indicator of the degree to which the system is primed and ready to process glucose into glycogen) and lipid metabolism (an indicator of the extent to which adipose tissue, i.e., fat, is being mobilized or broken down) the following day.

Here’s what they did.

Nine men between 28 and 30 years of age participated in the study.  There were four experimental conditions and each participant took part in each of the four conditions over four different experimental sessions.

The following general procedure was carried out in each of the four experimental sessions:

*  Participants fasted over night and were admitted to the hospital where testing would take place the next morning.

*  After admission and a 30 minute rest period, oxygen consumption and carbon dioxide production were measured.

*  This was followed by approximately 90 minutes of exercise in 3 of the 4 conditions.  The 4th condition was a control where participants did not exercise.  The exercise was split evenly between a treadmill and an exercise bike and each participant burned approximately 800 kilocalories (kcal) during the exercise period.  Oxygen consumption and carbon dioxide production were measured at several points throughout the exercise period to insure participants were exercising at the required rate and expending the required amount of energy.

*  The participants ingested meals at periods of 30 minutes, 5 hours, and 10 hours after exercise.  The experimental manipulation was in the nutritional make-up of these meals.

* Three hours after the last meal all of the participants ingested an identical snack to control for any effects of the last food eaten.

*  The participants then spent the night at the hospital and a variety of physiological measures were taken the following morning.

There were four experimental conditions in the study.  These were:

1. A Control condition in which participants did not exercise.  Participants were fed meals that maintained their fat and carbohydrate balance.

2. A Balanced condition in which participants were fed enough carbohydrate to replace the glycogen lost during exercise and enough fats to replace the fats lost during exercise.

3. A Low Carbohydrate condition in which participants were fed meals that did not contain enough carbohydrate to replace the glycogen burned during the exercise period.  The total energy loss of the exercise (kcal burned from both fats and glycogen stores in the body) was offset by increasing the amount of fat in the meals.

4. A Low Energy condition in which participants were fed enough carbohydrate to replace the glycogen lost during exercise but were not fed enough fat to replace the fat burned during exercise.

There are two important comparisons to consider with regard to the consequences of failing to replace either fats or glycogen (by ingesting carbs) after exercise.

(A) In the Control condition no exercise takes place and energy balance is maintained by replacing energy lost (during rest) to fat metabolism with fat in the diet and energy lost to burning glucose with carbohydrate in the diet.  In the Low Carbohydrate condition energy balance is also maintained but it is accomplished by shorting the amount of carbohydrate in the diet and replacing the missing carbohydrates with fats.  Testing the next day showed that the amount of glycogen stored in muscle tissue was significantly lower in the Low Carbohydrate condition than in the Control condition.  Insulin sensitivity was also higher in the Low Carbohydrate condition than in the Control condition.  This means that insulin was more active the following day in the Low Carbohydrate condition.  Insulin plays a critical role in converting blood glucose into glycogen that can be stored in the muscles (and liver) and the system would be expected to show higher sensitivity to insulin when it is in glycogen debt and operating to replace lost glycogen stores.

(B) In the Balanced condition exercise take place and energy balance is maintained by replacing energy lost (during exercise) to fat metabolism with fat in the diet and energy lost to burning glucose with carbohydrate in the diet. In the Low Energy condition energy lost to burning glucose is replaced by carbohydrates in the diet (in other words, muscle glycogen lost to exercise is completely replaced) but energy lost to burning fats is not.  Testing the next day showed no differences in muscle glycogen between the two groups.  However, there was an increase in plasma fatty acid mobilization and oxidation and an increase in plasma triacylglycerol concentration the next day in the Low Energy condition as compared to the Balanced condition.  This means that fat metabolism was higher in the Low energy group.

What does this mean for the active cyclist?

The results discussed in (A) above provide another source of evidence that failure to ingest enough carbohydrate following exercise results in lower stores of muscle glycogen the next day.  A deficit in muscle glycogen translates into less energy on the bike, lower performance levels, and an increased tendency to bonk on the ride.  The critical need to replace muscle glycogen after exercise is the basis for the recommendation made in Eating After the Ride to ingest a heavy carbohydrate load during the first 30 minutes after you get off the bike in order to take advantage of the brief period during which a high-efficiency glycogen storage process take place that allows blood glucose to be stored as muscle glycogen without the use of insulin.

Note that this study by Newsom et. al. provides evidence that muscle glycogen is depleted the day after exercise if carbohydrates are not consumed in sufficient quantity during the 12 hours or so after exercise.  Although the investigators made sure that participants were fed a meal withing 30 minutes of exercise, the study is not concerned with the brief period of enhanced, efficient glycogen storage that takes place immediately after exercise and provides no evidence one way or the other about the consequences of ingesting or failing to ingest sufficient carbohydrates immediately after exercise.

The results discussed in (B) provide evidence that fat metabolism is higher the day after exercise if fat intake in the hours after exercise is depressed.  This is of interest to cyclists who are concerned with losing weight.  Body fat is being burned at a higher rate the day after exercise if the fats burned during exercise are not replaced with fat in the diet.  Note that there is no indication here one way or the other whether the increased amount of fat metabolism shown the following day is sufficient to produce noticeable weight loss.  However, if you are interested in losing weight through the loss of body fat, increased levels of fat metabolism have to be better than no increase in fat metabolism in the long run.  Note also that fat metabolism was increased in the Low Energy condition even though carbohydrate intake was kept high enough to replace the muscle glycogen lost to exercise.  Taking in enough carbohydrate after exercise to replenish glycogen stores allows you to be ready for an exercise session the next day and does not stop fat metabolism that is breaking down body fat to supply energy.

In summary, what you eat after a ride makes a difference.  It isn’t the case that calories ingested from fats are equivalent to calories ingested from carbohydrates when replacing the calories burned during exercise.  Eating carbs after a ride replaces lost muscle glycogen, gets you ready to ride the next day, and does not stop fat metabolism.  Refraining from eating fats after a ride increases the burning of body fat the day after the ride and does not interfere with glycogen storage.  The take home message seems simple: Replace glycogen by ingesting carbs after a ride; metabolize fat and possibly lose weight by not eating fats after a ride.